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The present study examined the synergistic impact of exogenous hydrogen sulfide (H2S) and nitric oxide (NO) in mitigating nickel (Ni; 1 µM) induced toxicity in two paddy field cyanobacteria, namely Nostoc muscorum ATCC 27893 and Anabaena sp. PCC 7120. The evaluation encompasses growth, photosynthetic pigments (chlorophyll a, carotenoids and phycocyanin), oxidative biomarkers, and enzymes and metabolites involved in the ascorbate–glutathione (AsA-GSH) cycle. Cellular Ni accumulation resulted in elevated reactive oxygen species (ROS) production, reduced pigment levels, and impeded growth. The augmented activities of AsA-GSH cycle enzymes (ascorbate peroxidase, glutathione reductase, and dehydroascorbate reductase) were unable to counteract these toxic effects. However, exogenous supplementation of 8 µM H2S and 10 µM NO significantly reduced Ni-induced toxicity. This amelioration involved decreasing ROS levels, minimizing cellular Ni accumulation, enhancing photosynthetic pigments level, and elevating the AsA-GSH cycle's potential, thereby functioning as promoters of the metal detoxification system. The SEM analysis depicted Ni-accumulation on the surface of both cyanobacterial cells. Furthermore, introducing scavengers (PTIO for NO and HT for H2S) and inhibitors (L-NAME for NO and PAG for H2S) reversed the positive effects of H2S and NO, exacerbating damages under Ni-induced stress. This study proposed a cross-talk mechanism between H2S and NO, wherein H2S downregulates signaling on NO-mediated alleviation under Ni stress in both cyanobacteria. Additionally, the present work suggests that utilizing a lower dose of H2S and NO (cost-effective) in paddy fields could enhance the growth of cyanobacteria (as a significant biofertilizer), even under existing stressful conditions. This approach aims to support sustainable agriculture and uphold rice crop productivity. [ABSTRACT FROM AUTHOR]

AbstractUltrastructural changes and visual symptoms resulting from nutritional disorders involving boron, manganese, iron, zinc, copper, molybdenum, and nickel depend on the species of the plant, and are unknown in passion fruit plants (Passiflora edulis Sims). A hydroponic experiment evaluated the symptoms of nickel addition and micronutrient deficiency in passion fruit seedlings “BRS Gigante Amarelo” and determined the micronutrient contents in leaf and root tissue, root development, ultrastructural changes (leaf tissue deformations) and dry matter accumulation when visual symptoms were observed. Results showed that the order of manifestation of deficiencies was Fe > Mn > Zn > Cu > Mo > B. Nickel toxicity appeared 40 days after the experiment was started, presenting chlorosis in the new leaves followed by general yellowing and some white parts. Boron omission of resulted in deformations in the leaf limbus and loss of apical dominance, showing deformation of the growth points. Mn omission caused reduction of growth and generalized chlorosis of young leaves with a thick reticulum. Iron omission of resulted in internerval chlorosis with a fine lattice appearance. Omission of zinc and copper resulted in deformation and elongation of the leaves, reducing height and root development. Molybdenum omission caused chlorosis in the older leaves, which was observed to spread over time. Iron was the nutrient that most reflected symptoms of deficiency by the formation of root hairs. The findings of this research suggest that the knowledgement of plant micronutrients status permits an understanding of the physiological responses of passion fruit plants to crop fertilization. [ABSTRACT FROM AUTHOR]

The release of nickel "Ni(II)" into aquatic environments is of great concern because of environmental and health issues. Metal-organic frameworks (MOFs) are one of the most promising technologies for removing heavy metals from water. In this work, an octahedral Co-based MOF (Co-MOF) was synthesized with a high Ni(II) removal capacity (qmax of 1534.09 ± 45.49 mg g−1) in aqueous media. For the first time, the effect of Co-MOF alone and in co-exposure with Ni(II) on nitrifying microbial consortium was assessed using dynamic microrespirometry. A single concentration of Co-MOF had no significant effects on nitrifying microbial consortium, while the concentration of Ni(II) exerted non-competitive inhibition on the nitrifying microbial consortium with an IC50 of 1.67 ± 0.03 mg L−1. In addition, the theoretical speciation analysis showed a decrease of 40% of IC50 when the free Ni(II) concentration was considered. Co-exposure of Co-MOF and Ni(II) during the nitrifying process allowed us to conclude that Co-MOF is an effective adsorbent for Ni(II) and can be used to mitigate the inhibitory effects of nickel on nitrifying microbial consortia, which is crucial for maintaining the good operation of wastewater treatment and balance of nitrogen cycle. [ABSTRACT FROM AUTHOR]

Abstract Nickel (Ni), a component of urease, is a micronutrient essential for plant growth and development, but excess Ni is toxic to plants. Tomato (Solanum lycopersicum L.) is one of the important vegetables worldwide. Excessive use of fertilizers and pesticides led to Ni contamination in agricultural soils, thus reducing yield and quality of tomatoes. However, the molecular regulatory mechanisms of Ni toxicity responses in tomato plants have largely not been elucidated. Here, we investigated the molecular mechanisms underlying the Ni toxicity response in tomato plants by physio-biochemical, transcriptomic and molecular regulatory network analyses. Ni toxicity repressed photosynthesis, induced the formation of brush-like lateral roots and interfered with micronutrient accumulation in tomato seedlings. Ni toxicity also induced reactive oxygen species accumulation and oxidative stress responses in plants. Furthermore, Ni toxicity reduced the phytohormone concentrations, including auxin, cytokinin and gibberellic acid, thereby retarding plant growth. Transcriptome analysis revealed that Ni toxicity altered the expression of genes involved in carbon/nitrogen metabolism pathways. Taken together, these results provide a theoretical basis for identifying key genes that could reduce excess Ni accumulation in tomato plants and are helpful for ensuring food safety and sustainable agricultural development.

Heavy metals cause environmental pollution and produce toxic effects on organisms. Nickel (Ni) is a common metallic pollutant of aquatic ecosystems and potentially can produce multifarious changes in the body of aquatic organisms. The average nickel content in rivers is about 0.7 μg/l. As a result, the homeostasis of the affected organism is disturbed, and processes that can counteract the changes are activated. To better understand the effects of Ni in the freshwater environment and its fauna, it is important to establish whether all changes caused in cells and tissues by Ni exposure are reversible when the animal returns to the non-polluted environment. Thus, the main aim of the study was to analyze changes that occur after Ni exposure and after it is returned to non-contaminated water at various levels of the animal's body. The freshwater shrimp Neocaridina davidi (Crustacea) was selected as the subject of the study. As the organ for studies, we chose the midgut because it is a barrier against stressors that enter the organism. A concentration of 3.63 mg Ni/l was selected for the experiment, at which approximately 50% mortality of the population was observed after 14 days. The midgut was analyzed using light and transmission electron microscopy (TEM), confocal microscopy, and flow cytometry for qualitative and quantitative results. When the organisms were transferred to clean water, a prolong exposure resulted in a decrease in the values of the analyzed parameters (e.g. ROS, cell death, etc.) proportional to the purification time. The recovery time was insufficient to return to control values in most analyzed groups. Nevertheless, the occurrence of regenerative changes suggests that freshwater shrimps are relatively tolerant to nickel, when the exposure time is short and the recovery time is long. [ABSTRACT FROM AUTHOR]

The new technological applications of nickel (Ni) raise concerns over its harmful effects on the environment and human health. Pomiferin isolated from Osage orange is evaluated in in vitro and in vivo laboratory bioassays. This study focused the effects of pomiferin on Ni-caused hepatic injury and its underlying mechanisms. With this aim, Sprague–Dawley rats received 10 mg/kg nickel chloride (NiCl2) for 7 d by intraperitoneal injections. Pomiferin was given orally once a day at different doses (75, 150, and 300 mg/kg) for 20 d after exposure to NiCl2. Animals were anesthetized and livers were carefully collected to evaluate oxidative stress, inflammation, vascular injury, and hepatic function. Also, immunofluorescence analysis of apoptosis and DNA damage was performed on rat hepatic tissues. NiCl2 increased MDA production while reducing SOD, CAT, and GPx activity. NiCl2 induced the production of inflammatory cytokines and also platelet activation in hepatic tissue. Moreover, there were significant increases in AST, ALT, and LDH levels. NiCl2 also caused significant pathological changes in hepatic. Additionally, it remarkably induced up-regulations of apoptotic marker and 8-OHdG expressions by immunofluorescence labeling in liver cells. Whereas, pomiferin significantly attenuated lipid peroxidation and increased antioxidant defense system in liver. Also, the use of pomiferin prevented deregulated inflammatory process by signaling pathways nuclear factor kappa B (NFκB)/COX-2/TNF-α/IL-1β/IL-6. In addition, pomiferin diminished histopathologic evidence of hepatic toxicity and significantly lower expressions of caspase 3 and 8-OHdG were observed in liver cells. Pomiferin seems to counteract the deleterious effects of NiCl2 on hepatic tissue through different cellular and signaling mechanisms. NiCl2 induced the production of inflammatory cytokines and also platelet activation in hepatic tissue. NiCl2 increased MDA production while reducing SOD, CAT, and GPx activity. NiCl2 induced the production of inflammatory cytokines and also platelet activation in hepatic tissue. NiCl2 caused significant pathological changes in the liver and also up-regulation of apoptotic marker and 8-OHdG expressions by immunofluorescence staining. Pomiferin attenuated lipid peroxidation and increased antioxidant defense system in liver. The use of pomiferin prevented deregulated inflammatory process by signaling pathways nuclear factor kappa B (NFκB)/COX-2/TNF-α/IL-1β/IL-6. Pomiferin diminished histopathologic evidence of hepatic toxicity and significantly lower expressions of caspase 3 and 8-OHdG were observed in liver cells. Pomiferin seems to counteract the deleterious effects of NiCl2 on hepatic tissue through different cellular and signaling mechanisms and thus can be used as a therapeutic practice against metal toxicity. [ABSTRACT FROM AUTHOR]

Melatonin (MT) plays an important role in alleviating the stress of soil heavy metal pollution on plants. However, its ability to improve the tolerance of Rhus typhina to Ni stress and its mechanism of action are still unclear. Therefore, MT (0, 50, 100, and 200 μmol·L−1) was sprayed on the leaf surface of R. typhina seedlings under Ni (0 and 250 mg·kg−1) stress to study the differences in growth, physiology, and gene expression. The results showed that exogenous MT could improve the ability of R. typhina to resist Ni stress by inhibiting the degradation of chlorophyll and carotenoid, enhancing photosynthesis, and augmenting the activity of antioxidant enzymes. Moreover, 100 μmol·L−1 MT could increase the Ni concentration in R. typhina seedlings and reduce the translocation factor. Transcriptome analysis showed that MT mainly regulated the expression of related genes in plant hormone signal transduction, starch and sucrose metabolism, and various amino acid metabolism pathways. This study combined physiological and transcriptomic analysis to reveal the molecular mechanism of MT enhancing Ni resistance in R. typhina, and provides a new direction for expanding its application in phytoremediation. [ABSTRACT FROM AUTHOR]

Nickel (Ni), a component of urease, is a micronutrient essential for plant growth and development, but excess Ni is toxic to plants. Tomato (Solanum lycopersicum L.) is one of the important vegetables worldwide. Excessive use of fertilizers and pesticides led to Ni contamination in agricultural soils, thus reducing yield and quality of tomatoes. However, the molecular regulatory mechanisms of Ni toxicity responses in tomato plants have largely not been elucidated. Here, we investigated the molecular mechanisms underlying the Ni toxicity response in tomato plants by physio-biochemical, transcriptomic and molecular regulatory network analyses. Ni toxicity repressed photosynthesis, induced the formation of brush-like lateral roots and interfered with micronutrient accumulation in tomato seedlings. Ni toxicity also induced reactive oxygen species accumulation and oxidative stress responses in plants. Furthermore, Ni toxicity reduced the phytohormone concentrations, including auxin, cytokinin and gibberellic acid, thereby retarding plant growth. Transcriptome analysis revealed that Ni toxicity altered the expression of genes involved in carbon/nitrogen metabolism pathways. Taken together, these results provide a theoretical basis for identifying key genes that could reduce excess Ni accumulation in tomato plants and are helpful for ensuring food safety and sustainable agricultural development. [ABSTRACT FROM AUTHOR]

Heavy metals cause environmental pollution and produce toxic effects on organisms. Nickel (Ni) is a common metallic pollutant of aquatic ecosystems and potentially can produce multifarious changes in the body of aquatic organisms. The average nickel content in rivers is about 0.7 μg/l. As a result, the homeostasis of the affected organism is disturbed, and processes that can counteract the changes are activated. To better understand the effects of Ni in the freshwater environment and its fauna, it is important to establish whether all changes caused in cells and tissues by Ni exposure are reversible when the animal returns to the non-polluted environment. Thus, the main aim of the study was to analyze changes that occur after Ni exposure and after it is returned to non-contaminated water at various levels of the animal’s body. The freshwater shrimp Neocaridina davidi (Crustacea) was selected as the subject of the study. As the organ for studies, we chose the midgut because it is a barrier against stressors that enter the organism. A concentration of 3.63 mg Ni/l was selected for the experiment, at which approximately 50% mortality of the population was observed after 14 days. The midgut was analyzed using light and transmission electron microscopy (TEM), confocal microscopy, and flow cytometry for qualitative and quantitative results. When the organisms were transferred to clean water, a prolong exposure resulted in a decrease in the values of the analyzed parameters (e.g. ROS, cell death, etc.) proportional to the purification time. The recovery time was insufficient to return to control values in most analyzed groups. Nevertheless, the occurrence of regenerative changes suggests that freshwater shrimps are relatively tolerant to nickel, when the exposure time is short and the recovery time is long.

The objective of this study was to investigate the defensive influence of methanol fraction and crude extract of cocoplum (Chrysobalanus icaco L.) on nickel toxicity in male Wistar rats. Biochemical analyses in the serum and tissues (liver and kidney) were carried out using standard procedures. Significant (p < 0.05) increase were observed in aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), creatinine, urea, fragmented deoxyribose nucleic acid (DNA), and decrease in albumin and total protein in serum and tissues of Group 2 when compared with Group 1. The oral administration of C. icaco methanol fraction and crude extract significantly decreased AST, ALT, ALP, creatinine, urea, fragmented DNA and increased albumin and total protein in the serum and tissues when compared with Group 2. The histology of various organs (liver and kidney) of Group 2 revealed inflammation of portal vein and degeneration of hepatocytes. The renal tubules showed inflammation of glomerulus and tubular cell. The administration of C. icaco extract markedly reduced the histological alterations of various organs studied. However, these efficacies were shown to be better in the methanol crude extract than the methanol fraction of C. icaco. [ABSTRACT FROM AUTHOR]

Aquatic animals are prone to extinction due to metal pollution and global climate change. Even though the fish and their products are also unsafe for human consumption, their exports have been rejected due to inorganic and organic contaminants. Nickel (Ni) is a metal that induces toxicity and accumulates in the aquatic ecosystem, posing health threats to humans, animals, and fish. In light of the above, our present investigation aimed to determine the median lethal concentration (96 h-LC50) of nickel alone and concurrent with high temperature (34 °C) (Ni + T) using static non-renewable bioassay toxicity test in Pangasianodon hypophthalmus. The groups treated under exposure to Ni reared under control condition (25–28.9 °C) and Ni + T exposure group reread under 34 °C. In this study, chose the definitive dose of Ni and Ni + T as 17, 18, 19, and 20 mg L−1 after the range finding test. The median lethal concentration of Ni and Ni + T was determined as 19.38 and 18.75 mg L−1, respectively at 96 h. Oxidative stress viz. catalase (CAT), superoxide dismutase (SOD), glutathione-s-transferase (GST), and glutathione peroxidase (GPx) in the liver, gill, and kidney were noticeably elevated with Ni and Ni + T during 96 h. Whereas, the CAT, GPx, and SOD gene expressions were significantly upregulated with Ni and Ni + T. Trilox equivalent anti-oxidant capacity (TEAC), cupric reducing anti-oxidant capacity (CUPRIC), ferric reducing ability of plasma (FRAP), ethoxy resorufin-O-deethylase (EROD), and acetylcholine esterase (AChE) were reduced due to exposure to Ni and Ni + T. Cellular metabolic stress and lipid peroxidation were highly affected due to Ni and Ni + T exposure. The immunological status, as indicated by total protein, albumin, globulin, A:G ratio, and nitro blue tetrazolium chloride (NBT), was severely affected by the toxicity of Ni and Ni + T. Moreover, the gene expression of interleukin (IL), tumor necrosis factor (TNFα), toll-like receptor (TLR), and total immunoglobulin (Ig) was remarkably downregulated following exposure to Ni and Ni + T. HSP 70, iNOS expression, ATPase, Na + /K + -ATPase, cortisol, and blood glucose was significantly elevated with Ni and Ni + T in P. hypophthalmus. The bioaccumulation of Ni in fish tissues and experimental water was determined. The kidney and liver tissues were highly accumulated with Ni, whereas DNA damage was reported in gill tissue. Interestingly, depuration study revealed that at the 28th day, the Ni bioaccumulation was below the maximum residue limit (MRL) level. Therefore, the present study revealed that Ni and Ni + T led to dysfunctional gene and metabolic regulation affecting physiology and genotoxicity. The bioaccumulation and depuration results also indicate higher residual occurrence of Ni in water and aquatic organisms for longer periods. [ABSTRACT FROM AUTHOR]

Nickel (Ni) contamination hinders plant growth and yield. Nitric oxide (NO) and thiourea (Thi) aid plant recovery from heavy metal damage, but their combined effects on pepper (Capsicum annuum) plant tolerance to Ni stress need more study. Sodium nitroprusside (0.1 mM, SNP) and 400 mg L−1 Thi, alone and combined, were studied for their impact on pepper growth under Ni toxicity. Ni stress reduces chlorophyll, PSII efficiency and leaf water and sugar content. However, SNP and Thi alleviate these effects by increasing leaf water, proline and sugar content. It also increased the activities of superoxide dismutase, catalase, ascorbate peroxidase and peroxidase. Nickel stress lowered nitrogen assimilation enzymes (nitrate reductase, nitrite reductase, glutamine synthetase, glutamate synthase and glutamate dehydrogenase) and protein content, but increased nitrate, ammonium and amino acid content. SNP and Thi enhanced nitrogen assimilation, increased protein content and improved pepper plant growth and physiological functions during Ni stress. The combined treatment reduced Ni accumulation, increased Ni in leaf cell walls and potentially in root vacuoles, and decreased Ni concentration in cell organelles. It effectively mitigated Ni toxicity to vital organelles, surpassing the effects of SNP or Thi use alone. This study provides valuable insights for addressing heavy metal contamination in agricultural soils and offers potential strategies for sustainable and eco-friendly farming practices. Nickel contamination hinders plant growth and yield. Nitric oxide (NO) and thiourea aid plant recovery from heavy metal damage, but their combined effects on pepper (Capsicum annuum) tolerance to Ni stress need more study. Combined use of NO and thiourea alleviates Ni stress effects on pepper by enhancing leaf water, proline, sugar content, antioxidant enzyme activities and Ni distribution. These findings contribute valuable insights for addressing heavy metal contamination in agricultural soils and promoting sustainable and eco-friendly farming practices. [ABSTRACT FROM AUTHOR]

Melatonin (MT) plays an important role in alleviating the stress of soil heavy metal pollution on plants. However, its ability to improve the tolerance of Rhus typhina to Ni stress and its mechanism of action are still unclear. Therefore, MT (0, 50, 100, and 200 μmol·L−1) was sprayed on the leaf surface of R. typhina seedlings under Ni (0 and 250 mg·kg−1) stress to study the differences in growth, physiology, and gene expression. The results showed that exogenous MT could improve the ability of R. typhina to resist Ni stress by inhibiting the degradation of chlorophyll and carotenoid, enhancing photosynthesis, and augmenting the activity of antioxidant enzymes. Moreover, 100 μmol·L−1 MT could increase the Ni concentration in R. typhina seedlings and reduce the translocation factor. Transcriptome analysis showed that MT mainly regulated the expression of related genes in plant hormone signal transduction, starch and sucrose metabolism, and various amino acid metabolism pathways. This study combined physiological and transcriptomic analysis to reveal the molecular mechanism of MT enhancing Ni resistance in R. typhina, and provides a new direction for expanding its application in phytoremediation.

Recent literature has raised concerns over crop safety due to nickel (Ni) contamination of irrigation water and agricultural soil in Pakistan. Consequently, wheat crop has suffered in terms of nutrient disbalance and yield reduction. Therefore, it is important to screen tolerant wheat cultivars against Ni toxicity with the ability to accumulate low concentration in grains. In this regard, two wheat cultivars (SKD-1 and Borlaug-16) were exposed to Ni stress (100 mg/L) in a pot experiment for 21 days. In the present study, trace elements (As, Cr, Cu, Cd, Mn, Hg, Ni, Pb, and Zn) and mineral nutrients (Ca, Fe, K, Mg, Na, and P) were tested by ICP-OES. To understand tolerance mechanisms, wheat tissues were tested for morphological parameters, anatomical alteration, oxidative stress, and antioxidant capacity. The translocation of Ni was higher in SKD-1 (0.62) compared to Borlaug-16 (0.45) due to low Ni accumulation in roots of Borlaug-16. In the roots of Borlaug-16, trace elements (Cr, Cu, Mn, Pb, and Zn) were comparatively higher than SKD-1. On the contrary, nutrients (Ca, Fe, Mg, Na, and P) were higher in leaves of SKD-1. Under Ni stress, the root anatomy of Borlaug-16 exhibited a marked increase in the cellular thickness of the cortex by 130.38% and stele by 46.2%. Conversely, the bundle sheath cell thickness rose by 68.36% in the SKD-1. In terms of leaf anatomy, Borlaug-16 showed enhanced thickness in the xylem by 13.01% and bundle sheath cells by 84.95%. Meanwhile, the upper epidermis and phloem of SKD-1 registered thickness increases of 21.80% and 24.47% under Ni stress. Oxidative stress (MDA and H2O2) was comparatively highly induced in SKD-1 tissues compared to Borlaug-16. On the other hand, antioxidants (SOD, CAT, and APX) were comparatively higher in root and leaf tissues of Borlaug-16. The lower Ni uptake, less cellular damage, and high antioxidant capacity of Borlaug-16 makes it more tolerant to Ni stress. Such findings will pave the way towards sustainable crop production.

Plants antioxidative system is the first line of defense against oxidative stress caused secondarily by toxic ions under salinity. Plants with pre-activated antioxidative system can better adapt to salinity and can result in higher growth and yield. The current experiment was conducted to assess the adaptation of two tomato genotypes (Riogrande and Green Gold) with pre-activated antioxidative enzymes against salt stress. Tomato seedlings were exposed to mild stress (Ni: 0, 15 and 30 mg L−1) for three weeks to activate the antioxidative enzymes. The seedlings with pre-activated antioxidative enzymes were then grown under severe stress in hydroponics (0, 75 and 150 mM NaCl) and soil (control, 7.5 and 15 dS m−1) to check the adaptation, growth and yield. The results showed that Ni toxicity significantly enhanced activities of antioxidant enzymes (SOD, CAT, APX and POX) in both the genotypes and reduced growth with higher values in genotype Riogrande than Green Gold. The seedlings with pre-activated antioxidant enzymes showed better growth, low Na+ and high K+ uptake and maintained higher antioxidative enzymes activity than non-treated seedlings after four weeks of salt stress treatment in hydroponics. Similarly, the results in soil salinity treatment of the Ni pretreated seedlings showed higher yield characteristics (fruit yield per plant, average fruit weight and fruit diameter) than non-treated seedlings. However, Ni pretreatment had nonsignificant effect on tomato fruit quality characteristics like fruit dry matter percentage, total soluble solids, fruit juice pH and titratable acidity. The genotype Riogrande showed better growth, yield and fruit quality than Green Gold due to higher activity of antioxidant enzymes and better ion homeostasis as a result of Ni pretreatment. The results suggest that pre-activation antioxidant enzymes by Ni treatment proved to be an effective strategy to attenuate salt stress for better growth and yield of tomato plants. [ABSTRACT FROM AUTHOR]

• Nickel at 80 mg kg−1 of soil showed deleterious effects on fenugreek plants. • Calcium application showed encouraging effects on the Ni-affected plants. • Calcium successfully repairs the damage caused by Ni toxicity in plants. • Calcium significantly enhanced all growth & physiological attributes under Ni stress. Nickel (Ni) toxicity has a wide range of metabolic effects on plants, and various anatomical and morphological modifications occur that consequently diminish growth and productivity of plants. Different means of nutrient delivery in plants are being used to combat the harmful effects of Ni stress. The purpose of this study was to determine how the fenugreek plant (Trigonella foenum-graecum L.) responds to exogenous supplementation of calcium (Ca) in stress free and stressed conditions (Ni stress). The plants were supplemented with different concentrations of calcium (0, 40, 80, 120 and 160 mg kg−1) as CaCl 2 under Ni stress. The selected concentration of Ni was applied in the form of NiCl 2 with 80 mg kg−1 of soil to the plants and one set was kept as control. Nickel applied at highest concentration (80 mg kg−1) exhibited maximum inhibition in most of the parameters studied. In this study, Ni at 80 mg kg−1 reduced all the growth attributes (shoot and root lengths, plant fresh and dry weights and leaf area) as well as physiological attributes (chlorophyll (Chl) and carotenoid (Car) content, maximum quantum efficiency (Fv/Fm), carbonic anhydrase (CA) and nitrate reductase (NR) activities). The antioxidant enzymes viz. superoxide dismutase (SOD), catalase (CAT), peroxidase (POX), and other oxidative stress markers such as hydrogen peroxide (H 2 O 2), malondialdehyde (MDA) content, proline (PRO) content and electrolyte leakage (EL) substantially increased as compared to the control in Ni-exposed plants. However, all growth characteristics as well as the level of other functional attributes viz. Chl, Car, fv/fm, CAT, POX, and SOD, PRO, H 2 O 2 , MDA and EL improved significantly in plants supplied with CaCl 2 at 120 mg kg−1 of soil The exogenous application of Ca exhibited a significant and synergistic effect on the overall growth and physiological and metabolic processes of the plant without stress. Furthermore, exogenously-applied Ca also proved effective in countering Ni toxicity and protected fenugreek plant by strengthening antioxidant defense system and other factional attributes. [ABSTRACT FROM AUTHOR]

The global warming and environmental pollution are two crucial contemporary concerns. As both are strongly connected with urbanisation and anthropogenic impact on the environment, they often affect the ecosystem simultaneously. Aquatic habitats are particularly susceptible to thermal and chemical pollution. Temperature influences nearly all physical and chemical features of water bodies and trace metals are known for their toxicity to aquatic organisms. However, effects of multiple stressors, cumulative effects as well as response and possible adaptations of organisms are still open questions. Thus, the aim of this study was to characterize the combined effect of temperature and two trace metals (Co and Ni) on the metal bioaccumulation and viability of a model aquatic macrophyte Elodea canadensis Michx. We exposed shoots of E. canadensis to three temperatures and four metal concentrations (together and separately) applied at environmentally relevant levels. Shoot growth and metal concentration in plants were measured after 120 h. Moreover, after 24, 72 and 120 h the changes in leaf cell morphology and viability were analysed. The results showed that metal accumulation was dose-dependent and was not affected by temperature. The growth of plants was not affected by temperature nor metals. On the other hand, the exposure to Co and Ni and the elevated temperature negatively affected cell viability of E. canadensis leaves which manifested by increased permeability of plasma membranes and visible necroses. The greatest damaged leaf areas were determined after 120 h in the highest concentration of both metals and the highest temperature which indicates synergistic impact of trace metals and temperature on performance of macrohydrophytes. The observed phenomena suggest that global warming and/or thermal pollution may have implications for the performance of aquatic macrophytes in chemically polluted waters, their ability to spread and colonize polluted habitats and their suitability in phytoremediation., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

As the primary reservoir of heavy metals in nature, soil is highly susceptible to significant co-contamination with Cd-As-Ni. In current study, extracellular polymeric substances (EPS) from Bacillus subtilis were utilized as a novel improver to simultaneously enhance soil property and restrain ecotoxicity in Cd-As-Ni co-contaminated soil. Our findings revealed that EPS effectively bound and immobilized free Cd, As, and Ni in soil and decreased 49.73 % of soil available Cd, 79.16 % of As and 77.87 % of Ni contents by increasing soil pH, soil organic matter and cation exchange capacity. The EPS was also found to inhibit the Cd-As-Ni induced ecotoxicity in Caenorhabditis elegans by increasing the activities of antioxidant enzymes including superoxide dismutase, glutathione, and catalase. The remediation of EPS showed progressive improvement over time, and maintained a lasting effect after achieving peak efficiency. Our results might provide a new perspective on the potential of EPS in remediation of soil heavy metal pollution and the development and utilization of microbial biomass resources in a wider range., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

The excessive presence of polystyrene microplastic (PS-MPx) and nickel oxide nanomaterials (NiO-NPs) in agriculture ecosystem have gained serious attention about their effect on the legume root-nodule symbiosis and biological nitrogen fixation (BNF). However, the impact of these contaminants on the root-nodule symbiosis and biological N 2 -fixation have been largely overlooked. The current findings highlighted that NiO-NMs at 50 mg kg -1 improved nodule formation and N 2 -fixation potential, leading to enhanced N 2 uptake by both roots and shoots, resulting in increased plant growth and development. While single exposure of PS-MPx (500 mg kg -1 ) significantly reduced the photosynthetic pigment (8-14 %), phytohormones (9-25 %), nodules biomass (24 %), N 2 -related enzymes (12-17 %) that ultimately affected the N 2 -fixation potential. Besides, co-exposure of MPx and NiO at 100 mg kg -1 altered the nodule morphology. Additionally, single and co-exposure of MPx and NiO-NMs at 100 mg kg -1 reduced the relative abundance of Proteobacteria, Gemmatimonadota, Actinobacteria, Firmicutes, and Bacteroidetes is associated with N 2 -cycling and N 2 -fixation potential. The findings of this study will contribute to understanding the potential risks posed by MPx and NiO-NMs to leguminous crops in the soil environment and provide scientific insights into the soybean N 2 -fixation potential., Competing Interests: Declaration of Competing Interest The authors declare that they have no financial or personal relationships that could influence the research work presented in this manuscript. There are no conflicts of interest regarding the publication of this research., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Nickel (Ni) is an important micronutrient, but excess Ni is toxic to many plant species. Currently, relatively little is known about the genetic basis of the plant responses to Ni toxicity. Here, we demonstrate that NAC32 transcription factor functions as a core genetic hub to regulate the Ni toxicity responses in Arabidopsis. NAC32 negatively regulates root-Ni concentration through the IREG2 (IRON REGULATED2) encoding a transporter. NAC32 also induces local auxin biosynthesis in the root-apex transition zone by upregulating YUCCA 7 (YUC7)/8/9 expression, which results in a local enhancement of auxin signaling in root tips, especially under Ni toxicity, thereby impaired primary root growth. By analyses of various combinations of nac32 and ireg2 mutants, as well as nac32 and yuc7/8/9 triple mutants, including high-order quadruple mutant, we demonstrated that NAC32 negatively regulates Ni stress tolerance by acting upstream of IREG2 and YUC7/8/9 to modulate their function in Ni toxicity responses. ChIPqPCR, EMSA (electrophoretic mobility shift assay) and transient dual-LUC reporter assays showed that NAC32 transcriptionally represses IREG2 expression but activates YUC7/8/9 expression by directly binding to their promoters. Our work demonstrates that NAC32 coordinates Ni compartmentation and developmental plasticity in roots, providing a conceptual framework for understanding Ni toxicity responses in plants., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

The fundamental goal of this study was to determine the potential utility of a novel humanized Toll-like receptor-4 (hTLR-4) mouse model for future in vivo studies of nickel allergy. First, mice of both sexes and hTLR-4 expression profiles were incorporated into a Local Lymph Node Assay (LLNA) to assess skin sensitization. Next, a set of hTLR-4 hTLR-4-positive mice (female and male groups) was similarly exposed to vehicle control (VC) or 10% NiSO 4 on Days 1, 2, and 3. Mice were euthanized on Day 10, lymph node (LN) cellularity was assessed, LN and spleen cells were phenotyped, and serum was collected to quantify circulating cytokine and IgE levels. In the LLNA, hTLR-4-positive mice of both sexes exhibited enhanced responsivity to nickel. NiSO 4 (10%) had a stimulation index (SI) of 3.7 (females) and 3.8 (males) in hTLR-4-positive animals, and an SI of 0.5 (females) and 0.8 (males) in hTLR-4 hTLR-4-negative mice. In the 10d study, hTLR-4-positive mice exposed to 10% NiSO 4 exhibited increased LN cellularity (6.0× increase in females, 3.2× in males) and significantly higher concentrations of circulating IgE (4.1× increase in females, 3.4× in males). Significant increases in serum interferon (IFN)-γ, interleukin (IL)-4, and IL-5 levels were seen in female mice, while altered concentrations of IL-4 and IL-10 were detected in male mice. The results of this study ultimately demonstrate that murine expression of hTLR-4 confers enhanced susceptibility to dermal sensitization by nickel, and consequently, the hTLR-4 mouse model represents a viable approach for future studies of nickel allergy in vivo .

The present study rigorously examined the toxicological effects of nanoparticles (NPs), specifically nickel (Ni) and chromium oxide (Cr 3 O 4 ) NPs, synthesized under controlled conditions and characterized. To evaluate their potential environmental impact exposed the freshwater fish Labeo rohita ( L. rohita ) to environmentally relevant concentrations of both NPs within a controlled laboratory conditions. Vital organs, including gills and liver were subjected to histopathological analysis, revealing profound alterations in tissue architecture that were distinctly correlated with pathological damage. The lesions exhibited moderate to severe changes that are further correlated with the semi-quantitative mean alteration value (MAV). Furthermore, conducted a quantitative assessment of tissue-specific morphological changes. Notably, there was a significant reduction in critical hematological changes, including red blood cell (RBC) and white blood cell (WBC) counts, hemoglobin concentrations and other parameters. All of which exhibited significant fluctuations in relation to increasing NPs concentrations. These findings underscore the critical necessity for continued investigation into the ecological risks associated with these nanoparticles.

Nickel is an essential micronutrient for plant growth and development. However, in excessive amounts caused by accidental pollution of soils, this heavy metal is toxic to plants. Although silicon is a non-essential nutrient, it accumulates in most monocots, particularly the vital crop maize (corn, Zea mays). In fact, this metalloid mineral can alleviate the toxicity of heavy metals, though the mechanism is not entirely clear yet. Herein, we measured proteome, gene expression, enzyme activities, and selected sugars to investigate such effect thoroughly. Deep proteomic analysis revealed a minor impact of 100 µM Ni, 2.5 mM Si, or their combination on roots in 12-day-old hydroponically grown maize seedlings upon 9 days of exposure. Nonetheless, we suggested plausible mechanisms of Si mitigation of excessive Ni: Chelation by metallothioneins and phytochelatins, detoxification by glycine betaine pathway, and restructuring of plasma membrane transporters. Higher activity of glutathione S-transferase confirmed its plausible involvement in reducing Ni toxicity in combined treatment. Accumulation of sucrose synthase and corresponding soluble sugars in Ni and combined treatment implied high energy requirements both during heavy metal stress and its mitigation. Expression analysis of genes coding a few differentially accumulated proteins failed to reveal concordant changes, indicating posttranscriptional regulation. Proposed mitigation mechanisms should be functionally validated in follow-up studies., Competing Interests: Declaration of Competing Interest The authors have no relevant financial or non-financial interests to disclose., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

According to comprehensive research, the cardiovascular system is damaged by nickel exposure. The present study selected rat cardiomyocytes (H9c2 cells) and subjected them to varying doses of sodium nickel sulfate (NiSO 4 ) for 24 hours to better understand the mechanism of cardiovascular damage caused by NiSO 4 exposure. The relevant indicators were detected employing biochemical analysis, real-time quantitative polymerase chain reaction (RT-qPCR), and western blot, and flow cytometry was used to detect the cell apoptosis rate. The study revealed that the survival rate of H9c2 cells fell significantly when the concentration of NiSO 4 exposure rose. Moreover, it caused oxidative stress in H9c2 cells by raising the expression of reactive oxygen species and the concentration of LDH in the cell supernatants. After NiSO 4 exposure, the levels of ASC, NLRP3, gasdermin D, and caspase-1 in H9c2 cells increased, suggesting that H9c2 cells underwent pyroptosis induced by NiSO 4 . In addition, NiSO 4 exposure also led to inflammation, with increased levels of interleukin [IL]-18, IL-1β. After adding the antioxidant N-Acetyl-L-cysteine (NAC), the level of ROS indicated that the oxidative stress level in H9c2 cells was reduced, western blot inhibited inflammation, the level of pyroptosis was reduced, and the activity of the NLRP3/caspase1 signaling pathway was reduced. To examine the connection between pyroptosis and apoptosis, the cells were treated with the caspase1 inhibitor Z-YVAD-Fluoromethyl Ketone (Z-YVAD-FMK, YVAD), which resulted in a significant decrease in the rate of cell apoptosis as well as a reduction in the activity of the related protein in the signaling pathway, which in turn decreased the level of pyroptosis. NiSO 4 could induce pyroptosis in H9c2 cells through the ROS/NLRP3/caspase-1 axis. Furthermore, NiSO 4 -induced apoptosis and pyroptosis were found to be reduced by the addition of the caspase-1 inhibitor., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Our previous study found a positive relationship between fetal nickel exposure and the risk of OFCs. The teratogenic mechanism of nickel is not clear. In this study, we aim to examine the mediating effect of DNA methylation on the association of nickel(Ni) exposure with NSOFC in fetuses. 10 cases and 10 controls was used for screening target gene by Illumina Infinium Methylation EPIC(850k) BeadChip. 36 cases and 78 controls was conducted to determine DNA methylation level of selected gene in umbilical cord blood by Mass spectrometry assay. Mediation analysis was used to evaluate the potential mediating effect of selected gene methylation on the relation between concentrations of Ni and the risk for NSOFC. In the discovery stage, ZEB1 gene was identified to be hypermethylated in both nickel exposure and NSOFC group for validation. In the verification stage, the overall average methylation level of ZEB1 was significant higher in NSOFC cases(median = 8.70, interquartile range(IQR): 5.75-11.53) as compared to controls (median = 5.35, IQR: 4.30-7.78). The risk for NSOFC was increased by 1.43-fold with hypermethylation of ZEB1. Significant correlation was observed between concentrations of Ni in umbilical cord and methylation level of ZEB1. The hypermethylation of ZEB1 had a mediating effect by 20.47 % of total effect of Ni on NSOFC risk. Hypermethylation of ZEB1 is associated with the risk for NSOFC and may partially explain the association between Ni exposure and NSOFC risk. Our findings provide new insights into the epigenetic mechanisms underlying NSOFC and suggesting potential targets for future therapeutic interventions., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Silica nanoparticles (SiNPs) have been touted for their role in the management of non-communicable diseases. Their neuroprotective benefits against heavy metal-induced neurotoxicity remain largely unexplored. This is a comparative evaluation of the oxido-inflammatory and neurotrophic effects of Ni, Al, and Ni/Al mixture on the cerebellum of male albino rats with or without treatment with SiNPs generated from melon seed husk. The study complied with the ARRIVE guidelines for reporting in vivo experiments. A total of 91, 7-9 week-old weight-matched male Sprague rats (to avoid sex bias) were randomly divided into 13 different dosing groups where Group 1 served as the control. Other groups received 0.2 mg/kg Ni, 1 mg/kg Al, and 0.2 mg/kg Ni + 1 mg/kg Al mixture with or without different doses of SiNP for 90 days. Rotarod performance was carried out. Oxidative stress markers, Ni, Al, Ca, Fe, Mg, neurotrophic factors, amyloid beta (Aβ-42), cyclooxygenase-2 (COX-2), and acetylcholinesterase (AChE) were determined in the cerebellum. SiNPs from melon seed husk caused a significant decrease in Aβ-42 level and activities of AChE and COX-2 and a significant increase in brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) mediated by Ni, Al, and Ni/Al mixture exposure in rats. Neurotoxicity of the Ni/Al mixture is via heightened neuronal lipoperoxidative damage, decreased Mg, and increased Fe, and co-administration of SiNPs from melon seed husk with the Ni/Al mixture attenuated some of these biochemical changes in the cerebellum., Competing Interests: Declarations. Ethics Approval: The University Committee on Use and Care of Animals, University of Port Harcourt, Nigeria approved (UPH/CEREMAD/REC/MM86/027) the animal procedure protocols. Consent to Participate: Not Applicable. Consent for Publication: All authors gave final approval and agreed to be accountable for all aspects of work ensuring integrity and accuracy. Competing Interests: The authors declare no competing interests., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Nanotechnology is grabbing great attention all over the world because of its stimulating use in numerous fields, and the nanosilica (nSi) and carbon nanoparticles (CNPs) application has been examined in various studies. Conversely, the nSi and CNPs combinatorial use is a new method and researched in limited literature. For this purpose, a pot experiment was conducted to examine various growth and biochemical parameters in barley (Hordeum vulgare L.) under the toxic concentration of nickel (Ni) i.e., 200 mg kg -1 which were primed with combined application of two NPs of nSi at 3 mM and CNPs i.e., 200 μM respectively. The results showed that the Ni toxicity in the soil showed a significantly (P < 0.05) declined in the growth, gas exchange attributes, sugars, AsA-GSH cycle, cellular fractionation, proline metabolism in H. vulgare. However, Ni toxicity significantly (P < 0.05) increased oxidative stress biomarkers, enzymatic and nonenzymatic antioxidants including their gene expression in H. vulgare. Although, the application of nSi and CNPs showed a significant (P < 0.05) increase in the plant growth and biomass, gas exchange characteristics, enzymatic and non-enzymatic compounds and their gene expression and also decreased the oxidative stress, and Ni uptake. In addition, individual or combined application of nSi and CNPs enhanced the cellular fractionation and decreases the proline metabolism and AsA-GSH cycle in H. vulgare. These results open new insights for sustainable agriculture practices and hold immense promise in addressing the pressing challenges of heavy metal contamination in agricultural soils., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Snails are effective bioindicators due to their prolific distribution, high level of endemism, and capacity to accumulate contaminants. Freshwater snails have unique ecological niches which are imperiled by land-use change and the introduction of hazardous chemicals. To assess how environmental alterations affect gastropods, lab-based studies are needed to characterize the toxicity of specific stressors. This can help guide policy decisions and remediation efforts. The aim of this research was to characterize acute toxicity of nickel (Ni) on endemic snails (Somatogyrus georgianus [Walker, 1904], Elimia cahawbensis [Lea, 1861], and Elimia spp.) and measure the accumulation of Ni and mineral elements including calcium (Ca), magnesium, potassium, and sodium (Na). Snails were exposed to six concentrations (25-800 µg/L) of Ni for 96 h. Among the studied snail species, E. cahawbensis was the most sensitive to Ni, with the lowest lethal concentration where 50% of the organisms died (LC50) at 88.88 µg/L Ni after 96 h. The LC50 at 96 h for S. georgianus was 167.78 µg/L Ni, and 393.13 μg/L Ni for Elimia spp. Except for Elimia spp., mortality of the other two snail species corresponded to the whole-body uptake of Ni. Nickel exposure also influenced Ca and Na uptake for Elimia spp. All three endemic species are potential candidate species for evaluating localized effects of human activities, and the present study provides a first step in characterizing how snails would be affected by environmental alterations. More research could further characterize potential effects of other human stressors on these endemic snail species. Future research into subindividual responses and routes of exposure can further elucidate variations in species sensitivity. Environ Toxicol Chem 2024;43:2578-2588. © 2024 SETAC. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA., (© 2024 SETAC. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA.)

Previous studies have demonstrated that the hippocampus, a crucial region for memory and cognitive functions, is particularly vulnerable to adverse effects of exposure to heavy metals. Nickel (Ni) is a neurotoxic agent that, primarily induces oxidative stress, a process known to contribute to cellular damage, which consequently affects neurological functions. The antioxidant properties of melatonin are a promising option for preventing the adverse effects of Ni, especially by protecting cells against oxidative stress and related damage. In our investigation of the potential neuroprotective effects of melatonin against Ni-induced neurotoxicity, we chose to administer melatonin through intraperitoneal injection in rats following an intrahippocampal injection of Ni into the left hippocampus. This approach allows us a targeted investigation into the influence of melatonin on the neurotoxic effects of Ni, particularly within the crucial context of the hippocampus. In the present study, we demonstrated that melatonin efficiency reduced lactate dehydrogenase level, and preserved antioxidant enzyme activities in Ni-exposed hippocampal tissue. It also mitigated the decline in superoxide dismutase and catalase activities. On the other hand, melatonin could act directly by reducing reactive oxygen species Ni-induced overproduction. Taking to gather these two potential mechanisms of action could be responsible for the adverse effect of Ni on the behavioral alteration observed in our study. This study provides significant insights into the potential of melatonin to mitigate the detrimental effects of Ni on the brain, particularly into the hippocampal region, suggesting its possible implications for the treatment of neurological disorders related to Ni exposure., Competing Interests: Declarations. Competing interests: The authors have no relevant financial or non-financial interests to disclose. Ethical approval: All animal experiments were carried out under the National Institutes of Health Guide for the Care and Use of Laboratory Animals and approved by the Animal Ethics Committee (Local Institutional Research Committee)., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

Tannic acid (TA) is a metal chelating polyphenol that plays a crucial role in metal detoxification, but its modulatory role in co-exposure of these heavy metals' exposure needs to be explored. Cadmium (Cd) and nickel (Ni) are inorganic hazardous chemicals in the environment. Humans are prone to be exposed to the co-exposure of Cd and Ni, but the toxicological interactions of these metals are poorly defined. Present study was undertaken to study the preventive role of TA in Cd-Ni co-exposure-evoked hepato-renal toxicity in BALB/c mice. In the current investigation, increased oxidative stress in metal intoxicated groups was confirmed by elevated peroxidation of the lipids and significant lowering of endogenous antioxidant enzymes. Altered hepato-renal serum markers, DNA fragmentation, and histological alterations were also detected in the metal-treated groups. Present study revealed that Cd is a stronger toxicant than Ni and when co-exposure was administered, additive, sub-additive, and detrimental effects were observed. Prophylactic treatment with TA significantly reinstated the levels of lipid peroxidation (LPO), non-enzymatic, and enzymatic antioxidants. Moreover, it also restored the serum biomarker levels, DNA damage, and histoarchitecture of the given tissues. TA due to its metal chelating and anti-oxidative properties exhibited cyto- and genoprotective potential against Cd-Ni co-exposure-induced hepatic and renal injury., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Nickel (Ni) is a common metal with a nephrotoxic effect, damaging the kidneys. This study investigated the mechanism by which gallic acid (GA) protects mice kidneys against renal damage induced by Nickel oxide nanoparticles (NiO-NPs). Forty male Swiss albino mice were randomly assigned into four groups, each consisting of ten mice ( n  = 10/group): Group I the control group, received no treatment; Group II, the GA group, was administrated GA at a dosage of 110 mg/kg/day body weight; Group III, the NiO-NPs group, received injection of NiO-NPs at a concentration of 20 mg/kg body weight for 10 consecutive days; Group IV, the GA + NiO-NPs group, underwent treatment with both GA and NiO-NPs. The results showed a significant increase in serum biochemical markers and a reduction in antioxidant activities. Moreover, levels of 8-hydroxy-2'-deoxyguanosine (8-OH-dG), phosphorylated nuclear factor kappa B (p65), and protein carbonyl (PC) were significantly elevated in group III compared with group I. Furthermore, the western blot analysis revealed significant high NF-κB p65 expression, immunohistochemistry of the NF-κB and caspase-1 expression levels were significantly increased in group III compared to group I. Additionally, the histopathological inspection of the kidney in group III exhibited a substantial increase in extensive necrosis features compared with group I. In contrast, the concomitant coadministration of GA and NiO-NPs in group IV showed significant biochemical, antioxidant activities, immunohistochemical and histopathological improvements compared with group III. Gallic acid has a protective role against kidney dysfunction and renal damage in Ni-nanoparticle toxicity.

Objective: The results of epidemiological studies on the association between nickel exposure and diabetes remain controversial. Therefore, an update meta-analysis was conducted to examine the association between urinary nickel levels and diabetes risk, and to focus on whether there is an association between blood nickel levels and diabetes risk., Methods: Relevant studies were comprehensively searched from PubMed, Web of Science, and Wanfang databases from their inception to July 2024. The random-effects model was utilized to determine pooled Standard Mean Difference (SMD) and 95% confidence intervals (CIs), with stratified and sensitivity analyses also performed. Heterogeneity between studies was assessed using I 2 statistic, while publication bias was evaluated using Egger's and Begg's tests. The quality of the included studies was assessed using the Newcastle-Ottawa Scale., Results: A total of 19 studies involving 46,071 participants were included in this meta-analysis. The random-effects model indicated that the pooled SMD for nickel exposure levels in diabetic patients and non-diabetic controls were 0.16 (95% CI 0.07-0.2) for urine and 0.03 (95% CI -0.20 to 0.27) for blood, respectively., Conclusion: It was discovered that diabetes risk was positively correlated with urinary nickel levels, whereas there was no significant correlation with blood nickel levels. Furthermore, it appeared that the association between nickel exposure and diabetes risk differ in individuals with diabetes compared to those with pre-diabetes, and that the direction of the correlation may even be reversed. In conclusion, more high-quality prospective studies are needed in order to validate these findings in future research endeavors., Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO, registration number: CRD42024534139., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Lu, Shi, Han, Liu and Jiang.)

Present investigations were undertaken to record the vulnerability of testis to nickel oxide nano and microparticles in Wistar rat with special reference to their preferred bioaccumulation, consequent generation of reactive species, reciprocal influence on testosterone synthesis, DNA damage in spermatids and histopathological changes. Suitable numbers of rats were gavaged NiONPs or NiOMPs (5 mg/kg b.w.each) for 15 and 30 days. Testes en bloc were removed and processed for the estimation of selected parameters. Results showed that rat testes could accumulate nickel in an exposure time dependent manner. Generation of malondialdehyde, a denominator of ROS, increased significantly in the testes of NiONPs treated rats. Moreover, serum testosterone values also increased in NiONPs treated rats. Higher DNA damage in sperms was also recorded. Nano and microparticles of nickel, both could induce specific dose and time dependent lesions in the testis of rat. Histopathological results revealed degeneration of germinal epithelium and spermatocytes; hypertrophy of seminiferous tubules and necrosis. SEM results also indicated specific morphological changes in cellular components of tubules. This study suggests that testis is also vulnerable to the adverse effects of NiONPs alike liver and kidney. Both micro and nanoparticles of nickel elicited differential effects in a dose and exposure time dependent manner. However, NiONPs induced greater overall toxicity than NiOMPs. The results are expected to be helpful in determining the human reproductive health risks, associated with environmental/ occupational exposure to nanoparticles of nickel., (© 2024. The Author(s), under exclusive licence to Society for Reproductive Investigation.)

Zinc oxide (ZnO) and nickel oxide (NiO) nanoparticles (NPs) are widely used in various industries due to their distinctive physico-chemical and biological properties. However, concerns have been raised about their potential toxicity in humans. While many studies have reviewed their effects on visceral organs upon ingestion, inhalation, or skin contact, limited reviews are available regarding their adverse consequences on the liver and kidneys resulting from intraperitoneal administration in rats. Hence, this systematic review is the first to uniquely address this issue. A systematic search was performed on PubMed and Google scholar to identify articles that explored the toxic effects of ZnO-NPs and NiO-NPs in rats following intraperitoneal injection. The quality of the articles was assessed using SYCLE's risk of bias tool, leading to the selection of 16 articles; 14 for ZnO-NPs, 1 for NiO-NPs and 1 for both NPs. This review revealed that ZnO-NPs induces an acute toxicity in liver and kidney that is dose dependent. The impairments were marked by changes in organs functional markers, lipid and glucose levels and antioxidant deficiencies and lipid peroxidation. NiO-NPs also showed considerable toxicity, despite the limited studies. Further, variability of physico-chemical properties among studies complicated the toxicity assessment. To conclude, this study provides a novel contribution by summarizing the literature findings that suggest potential adverse intraperitoneal hepatorenal toxic outcomes associated with ZnO-NPs and NiO-NPs. Future research should focus on long-term effects and standardizing protocols to ensure the safe use of ZnO-NPs and NiO-NPs in industrial and clinical practices.

The intensifying production and release into the environment as well as the increasing potential in agricultural applications make the relationship between plants and nickel nanoparticles (Ni NPs) a relevant and timely topic. The aim of this review is to give an overview and discuss the latest findings about the relationship of Ni NPs and plants. Ni NPs can be synthesized using phytochemicals derived from plant parts in an environmentally friendly manner. There are several ways for these nanoparticles to enter plant cells and tissues. This can be demonstrated through various imaging and chemical mapping approaches (e.g., transmission electron microscopy, X-ray fluorescence spectroscopy etc.). NiO NPs affect plants at multiple levels, including subcellular, cellular, tissue, organ, and whole-plant levels. However, the effects of Ni NPs on plants' ecological partners (e.g., rhizobiome, pollinators) remain largely unknown despite their ecotoxicological significance. The main cause of the Ni NPs-triggered damages is the reactive oxygen species imbalance as a consequence of the modulation of antioxidants. In non-tolerant plants, the toxicity of NiO NPs can be mitigated by exogenous treatments such as the application of silicon, salicylic acid, or jasmonic acid, which induce defense mechanisms whereas Ni-hypertolerant plant species possess endogenous defense systems, such as cell wall modifications and nitrosative signaling against NiO NP stress. Research highlights the role of Ni NPs in managing fungal diseases, showcasing their antifungal properties against specific pathogens. Due to the essentiality of Ni, the application of Ni NPs as nanofertilizers might be promising and has recently started to come into view., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Effect assessments of metals are mostly based on single-metal, single-species tests, thereby ignoring metal-mixture effects and indirect effects through species interactions. We tested the combined effects of metal and species interactions in two-trophic algal-daphnid microcosms. Metal-mixture effects on daphnid communities may propagate from effects on the generally more sensitive algal communities. Four different algal communities (three species each), with and without addition of the same daphnid community (three species) were exposed to single metals and one metal mixture (17:17:51 µg/L Ni:Cu:Zn). Daphnid densities were negatively affected by metals in the two-trophic test, the magnitude of which depended on the algal community composition. Algal densities were overall positively affected by the metals in the two-trophic test but negatively in the single-trophic test, illustrating an indirect positive effect in the two-trophic system due to a reduced grazing pressure. Metal effects on daphnid communities in the two-trophic test (day 21) were correlated with metal effects on the single-trophic-level algal communities during exponential growth (R 2  = 0.55, p = 0.0011). This finding suggests that metal effects propagate across trophic levels due to a reduced food quantity. However, the indirect positive effects on algal densities, resulting in abundant food quantity, suggests that metal effects can also propagate to daphnids due to a reduced food quality (not measured directly). Metal-mixture interactions on daphnid densities varied during exposure, but were additive or antagonistic relative to independent action when final daphnid densities were considered (day 56). This suggests stronger indirect effects of the mixture compared with the single metals. Overall, our study highlights the dynamic aspect of community-level effects, which empirical reference models such as independent action or concentration addition cannot predict. Environ Toxicol Chem 2024;43:2350-2364. © 2024 SETAC., (© 2024 SETAC.)

Nickel phytotoxicity has been attributed, among others, to oxidative stress. However, little is known about Ni-induced phospholipid modifications, including the oxidative ones. Accumulation of reactive oxygen species (ROS), antioxidative enzyme activities, malondialdehyde and the early lipid oxidation products contents, membrane permeability, phospholipid profile as well as phospholipid unsaturation degree were studied in the 1st and the 2nd leaves of hydroponically grown cucumber seedlings subjected to Ni stress. Compared to the 2nd leaf the 1st one showed stronger visual Ni toxicity symptoms, higher Ni, O 2 .- and H 2 O 2 accumulation as well as greater enhancement in membrane permeability. Enzyme activities were differently influenced by Ni stress, however most pronounced changes were generally found in the 1st leaf. Ni treatment resulted in oxidation of leaf lipids, which was evidenced by appearance of increased contents of MDA and the early produced oxylipins. Among the latter 9-hydroxyoctadecatrienoic acid (9-HOTrE) and 13-hydroxyoctadecatrienoic acid (13-HOTrE) contents showed the most pronounced increase in response to Ni treatment. Exposure to the metal led to the changes in the leaf phospholipid profile and increased degree of phospholipid unsaturation. The obtained results have been discussed in relation to the difference in Ni stress severity between the 1st and the 2nd leaves., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Heavy metal pollution causes severe abiotic stress in cereal crops around the world. This study investigated the effects of different concentrations (0, 100, 200, and 300 mg·kg -1 ) of nickel, lead, and copper stress on the growth and biochemical responses of Aegilops tauschii seedlings, to provide a reference for research on the mechanism of invasion and screening potential sources of wheat tolerance genes. The results showed that nickel, lead, and copper stress caused a significant decrease in the contents of chlorophyll a, chlorophyll b, and chlorophyll (a + b) in A. tauschii, thereby inhibiting photosynthesis to different degrees and hindering seedling growth, which was reflected in significant reductions in plant height and root length, with the most notable effect observed under stress by 300 mg·kg -1 lead. As the concentration of heavy metals increased, the activities of antioxidant enzymes (SOD, POD, and APX), non-enzymatic antioxidants (GSH and AsA), and the contents of osmotic regulatory substances (proline and soluble proteins) in A. tauschii significantly increased. Additionally, heavy metal stress increased H 2 O 2 and TBARS levels. However, when the nickel, lead, and copper concentrations reached 300 mg·kg -1 , no significant differences were found in H 2 O 2 or TBARS levels compared to those in the CK group. To summarize, A. tauschii can mitigate the accumulation of ROS and membrane lipid peroxidation caused by heavy metal stress through self-regulation, thus exhibiting a certain degree of tolerance to stress caused by different concentrations of nickel, lead, and copper. Finally, the evaluation using the membership function method revealed that among the three heavy metals, A. tauschii exhibited the strongest adaptation to Cu, followed by Ni and Pb., (© 2024. The Author(s).)

The problem of potentially toxic metal pollution is increasingly acute with the development of human society. In this study, we investigated the remediation of nickel (Ni) and cadmium (Cd) co-contamination through inoculating rice with three new-isolated Ni- and Cd-resistant plant growth-promoting rhizobacteria (PGPR) Y3, Y4, and Y5. These three strains possessed growth-promoting properties, including 1-aminocyclopropane-1-carboxylic acid (ACC) deaminase activity, the ability of indoleacetic acid (IAA) production, phosphate solubilization, siderophores production, and exopolysaccharide (EPS) development. According to 16S rDNA sequence homology, strains Y3, Y4, and Y5 were identified as Pseudomonas sp., Chryseobacterium sp., and Enterobacter sp., respectively. Based on the results of rice germination experiments conducted under combined toxicity, we set the contamination concentrations for Ni 2+ at 20 μg mL -1 and Cd 2+ at 40 μg mL -1 . Then we conducted potting experiments at these concentration levels to study the effects of strains Y3, Y4, and Y5 on rice growth under synergistic Ni and Cd stress. The results indicated that the inoculated strains Y3, Y4, and Y5 were effective in promoting the growth of rice seedlings under the combined stress of Ni and Cd, and conferring tolerance to Ni and Cd by increasing the antioxidant enzyme activities of the seedlings. Among them, strain Y3 exhibited stronger ACC deaminase activity, IAA production capacity, and EPS production capacity, showing the most pronounced growth-promoting effect on rice. It was demonstrated that after inoculation with strain Y3, the germination rate of rice seeds increased by 43 %, the fresh weight of stems improved by 35 %, and the chlorophyll content enhanced by 70 % and other growth-promoting phenomena. Additionally, under Ni and Cd stress, strain Y5 performed better than strain Y4 in terms of IAA production capacity and its influence on rice root growth, suggesting that IAA production might play a specifically essential role in root growth under Ni and Cd stress., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper, (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Nickel ferrite nanoparticles (NiF NPs) have growing applications in biomedical and nanomedicine fields. However, knowledge concerning their ecotoxicity during the early developmental stages of invertebrates, such as gastropods, remains scarce. Thus, the current study aimed to evaluate whether NiF NPs and nickel chloride (NiCl 2 ) induce toxic effects on embryos and newly hatched snails of freshwater species Biomphalaria glabrata (Say, 1818). NiF NPs were synthesized and characterized by multiple techniques, and their ecotoxicity was assessed by Biomphalaria embryotoxicity test (BET) during 144 h of exposure and an acute toxicity test (96 h) using newly hatched snails. NiF NPs induced mortality, developmental delay, reduced hatching rate, and promoted morphological changes in B. glabrata. Also, NiF NPs induced higher toxicity in embryos than in newly hatched B. glabrata. Overall, results showed that the early developmental stages of gastropods are a target group for nanoparticle toxicity in freshwater ecosystems., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Research in understanding the role of genetics and epigenetics in plant adaptations to environmental stressors such as metals is still in its infancy. The objective of the present study is to assess the effect of nickel on DNA methylation level and distribution in white birch ( Betula papyrifera Marshall) using reduced representation bisulfite sequencing (RRBS). The distribution of methylated C sites of each sample revealed that the level of methylation was much higher in CG context varying between 54% and 65%, followed by CHG (24%-31.5%), and then CHH with the methylation rate between 3.3% and 5.2%. The analysis of differentially methylated regions (DMR) revealed that nickel induced both hypermethylation and hypomethylation when compared to water. Detailed analysis showed for the first time that nickel induced a higher level of hypermethylation compared to controls, while potassium triggers a higher level of hypomethylation compared to nickel. Surprisingly, the analysis of the distribution of DMRs revealed that 38%-42% were located in gene bodies, 20%-24% in exon, 19%-20% in intron, 16%-17% in promoters, and 0.03%-0.04% in transcription start site. RRBS was successful in detecting and mapping DMR in plants exposed to nickel., Competing Interests: The authors declare there are no competing interests.

This study focuses on FSMPs for oncologic patients, specifically analyzing the toxicological profiles of nickel (Ni), chromium (Cr), and selenium (Se) within these products available in Polish pharmacies. The presence of these elements was quantified using inductively coupled plasma mass spectrometry (ICP-MS). Results indicated variations in the concentrations of Ni, Cr, and Se across different FSMP samples, with some products exceeding the acceptable limits set by regulatory guidelines. The study highlights the potential health risks associated with nickel exposure, including dermatitis and carcinogenesis, and the complex roles of chromium and selenium, which can be both beneficial and harmful depending on their levels. Our findings reveal significant variability in the elemental content across different FSMP products, i.e.: Ni: 0.155-25.488 μg/portion, Cr: 0.076-28.726 μg/portion and Se: 0.083-20.304 μg/portion). Notably, selenium levels in FSMPs showed considerable discrepancies compared to manufacturers' declarations, averaging only about 20% of the stated values. Regulatory assessments based on the Acceptable Daily Intake (ADI) and Permitted Daily Exposure (PDE) descriptors indicated that the estimated weekly intake of Ni, Cr, and Se from these FSMPs did not exceed the provisional tolerable weekly intake (PTWI) values. However, the highest Ni content was 30.58% of the PTWI, raising concerns about potential health risks, including dermatitis and carcinogenesis. The results for Cr underscored the necessity for careful monitoring due to its potential toxic effects. Selenium, despite its essential role, showed levels inadequate to meet the Recommended Dietary Allowance (RDA), potentially impacting its intended health benefits., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Background: Commensal bacteria colonizing oral mucosa and skin play an essential role in maintaining host-microbiome homeostasis. It is unknown whether cytotoxicity resulting from metal ions leaching from medical devices may be influenced by commensal microbes., Objective: Determine whether the extent of apoptosis triggered by nickel or titanium ions is influenced by Streptococcus mitis and whether apoptosis occurs via the intrinsic or extrinsic apoptosis pathway., Methods: Reconstructed Human Gingiva (RHG) and Skin (RHS) were topically exposed to titanium or nickel salts in the presence or absence of S. mitis. Cytotoxicity and apoptosis were assessed by histology, immunohistochemistry, TUNEL assay, and Western Blot., Results: S. mitis alone resulted in negligible cytotoxicity. After metal exposure, localized apoptosis was observed in the epithelium and fibroblasts within the lamina propria hydrogel of both RHG and RHS. S. mitis enhanced metal-mediated apoptosis in gingiva but not in skin. Apoptosis was mediated via the extrinsic pathway caspase 8. Activation of the execution phase of apoptosis occurred via caspases 3 and 7, and PARP-1., Conclusion: Our study supports the finding that metals have irritant, cytotoxic properties resulting in apoptosis when leaching into skin or gingiva. Particularly for gingiva, commensal microbes exaggerate this detrimental effect., Competing Interests: Declaration of competing interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Although the production and use of nickel oxide nanoparticles (NiONP) are widespread, environmental and public health problems are associated with it. The kidney is the primary organ in excretion and is among the target organs in nanoparticle toxicity. This study aimed to compare the renal toxicity of nickel oxide (NiO) microparticles and nickel oxide nanoparticles by different routes of administration, such as oral, intraperitoneal (IP), and intravenous (IV). Seven groups were formed, with 42 male rats and six animals in each group. NiO oral (150 mg/kg), NiO IP (20 mg/kg), NiO IV (1 mg/kg), NiONP oral (150 mg/kg), NiONP IP (20 mg/kg), and NiONP IV (1 mg/kg) was administered for 21 days. After NiO and NiONP administration, a decrease in antioxidant activities and an increase in lipid peroxidation occurred in the kidney tissue of rats. Increased kidney urea, uric acid, and creatinine levels were observed. Inhibition of acetylcholinesterase activity and an increase in interleukin 1 beta were detected. Apoptotic markers, Bax, caspase-3, and p53 up-regulation and Bcl-2 down-regulation were observed. In addition, histopathological changes occurred in the kidney tissue. In general, it was observed that nickel oxide microparticles and nickel oxide nanoparticles cause inflammation by causing oxidative stress in the kidney tissue, and NiONP IV administration is more effective in renal toxicity., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

Nickel is toxic to humans. Its compounds are carcinogenic. Furthermore, nickel allergy is a severe health problem that affects approximately 10–20% of humans. The mechanism by which these conditions develop remains unclear, but it may involve the cleavage of specific proteins by nickel ions. Ni(II) ions cleave the peptide bond preceding the Ser/Thr-Xaa-His sequence. Such sequences are present in all four enzymes of the melatonin biosynthesis pathway, i.e., tryptophan 5-hydroxylase 1, aromatic-l-amino-acid decarboxylase, serotonin N-acetyltransferase, and acetylserotonin O-methyltransferase. Moreover, fragments prone to Ni(II) are exposed on surfaces of these proteins. Our results indicate that all four studied fragments undergo cleavage within tens of hours at pH 8.2 and 37 °C, corresponding with the conditions in the mitochondrial matrix. Since melatonin, a potent antioxidant and anti-inflammatory agent, is synthesized within the mitochondria of virtually all human cells, depleting its supply may be detrimental, e.g., by raising the oxidative stress level. Intriguingly, Ni(II) ions have been shown to mimic hypoxia through the stabilization of HIF-1α protein, but melatonin prevents the action of HIF-1α. Considering all this, the enzymes of the melatonin biosynthesis pathway seem to be a toxicological target for Ni(II) ions. [ABSTRACT FROM AUTHOR]

Globally, heavy metal pollution of soil has remained a problem for food security and human health, having a significant impact on crop productivity. In agricultural environments, nickel (Ni) is becoming a hazardous element. The present study was performed to characterize the toxicity symptoms of Ni in pepper seedlings exposed to different concentrations of Ni. Four-week-old pepper seedlings were grown under hydroponic conditions using seven Ni concentrations (0, 10, 20, 30, 50, 75, and 100 mg L−1 NiCl2. 6H2O). The Ni toxicity showed symptoms, such as chlorosis of young leaves. Excess Ni reduced growth and biomass production, root morphology, gas exchange elements, pigment molecules, and photosystem function. The growth tolerance index (GTI) was reduced by 88-, 75-, 60-, 45-, 30-, and 19% in plants against 10, 20, 30, 50, 75, and 100 mg L−1 Ni, respectively. Higher Ni concentrations enhanced antioxidant enzyme activity, ROS accumulation, membrane integrity [malondialdehyde (MDA) and electrolyte leakage (EL)], and metabolites (proline, soluble sugars, total phenols, and flavonoids) in pepper leaves. Furthermore, increased Ni supply enhanced the Ni content in pepper’s leaves and roots, but declined nitrogen (N), potassium (K), and phosphorus (P) levels dramatically. The translocation of Ni from root to shoot increased from 0.339 to 0.715 after being treated with 10–100 mg L−1 Ni. The uptake of Ni in roots was reported to be higher than that in shoots. Generally, all Ni levels had a detrimental impact on enzyme activity and led to cell death in pepper seedlings. However, the present investigation revealed that Ni ≥ 30 mg L−1 lead to a deleterious impact on pepper seedlings. In the future, research is needed to further explore the mechanism and gene expression involved in cell death caused by Ni toxicity in pepper plants. [ABSTRACT FROM AUTHOR]

In this study, nickel tolerance (NiSO4.7H2O) of some Turkish national barley (Hordeum vulgare L.) genotypes (Bülbül-89, Kalaycı-97, Karatay-94, Larende, Tarm-92, Tokak-157/37, Yesevi-93 and Zeynel Ağa) was investigated. Barley genotypes were exposed to different nickel concentrations [0 mM (control), 250, 500, 1000, 1500, and 2000 ppm]. Nickel toxicity significantly inhibited root and coleoptile growth in all barley genotypes in a concentration-dependent manner. However, root growth was much more inhibited by nickel applications in comparison with coleoptile growth, probably due to a higher level of sensitivity of root meristems against nickel toxicity or direct contact of roots with nickel ions in the growth medium. Root growth in the genotype Karatay-94 and coleoptile growth in the genotype Yesevi-93 was more remarkably reduced by nickel toxicity. Root and coleoptile growth in the genotypes Larende and Kalaycı-97 were less affected under nickel toxicity, respectively. In addition, nickel toxicity disturbed water relations in barley genotypes dependent on the organ type, as demonstrated by more severe inhibition in root fresh weight as compared to coleoptile fresh weight. These results could show that nickel toxicity reduced water uptake from growth medium in barley genotypes used in this study. Changes in dry weight of roots and coleoptiles indicated that nickel toxicity more severely decreased biomass accumulation in roots of barley genotypes. The calculated tolerance indices demonstrated that the genotype Kalaycı-97 is the most tolerant to nickel toxicity, while the genotype Karatay-94 is the most susceptible one.

Globally, heavy metal pollution of soil has remained a problem for food security and human health, having a significant impact on crop productivity. In agricultural environments, nickel (Ni) is becoming a hazardous element. The present study was performed to characterize the toxicity symptoms of Ni in pepper seedlings exposed to different concentrations of Ni. Four-week-old pepper seedlings were grown under hydroponic conditions using seven Ni concentrations (0, 10, 20, 30, 50, 75, and 100 mg L–1 NiCl2. 6H2O). The Ni toxicity showed symptoms, such as chlorosis of young leaves. Excess Ni reduced growth and biomass production, root morphology, gas exchange elements, pigment molecules, and photosystem function. The growth tolerance index (GTI) was reduced by 88-, 75-, 60-, 45-, 30-, and 19% in plants against 10, 20, 30, 50, 75, and 100 mg L–1 Ni, respectively. Higher Ni concentrations enhanced antioxidant enzyme activity, ROS accumulation, membrane integrity [malondialdehyde (MDA) and electrolyte leakage (EL)], and metabolites (proline, soluble sugars, total phenols, and flavonoids) in pepper leaves. Furthermore, increased Ni supply enhanced the Ni content in pepper’s leaves and roots, but declined nitrogen (N), potassium (K), and phosphorus (P) levels dramatically. The translocation of Ni from root to shoot increased from 0.339 to 0.715 after being treated with 10–100 mg L–1 Ni. The uptake of Ni in roots was reported to be higher than that in shoots. Generally, all Ni levels had a detrimental impact on enzyme activity and led to cell death in pepper seedlings. However, the present investigation revealed that Ni ≥ 30 mg L–1 lead to a deleterious impact on pepper seedlings. In the future, research is needed to further explore the mechanism and gene expression involved in cell death caused by Ni toxicity in pepper plants.