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The basic region/leucine zipper (bZIP) transcription factors play important roles in plant development and responses to abiotic and biotic stresses. OsbZIP53 regulates resistance to Magnaporthe oryzae in rice by analyzing APIP5-RNAi transgenic plants. To further investigate the biological functions of OsbZIP53, we generated osbzip53 mutants using CRISPR/Cas9 editing and also constructed OsbZIP53 over-expression transgenic plants. Comprehensive analysis of phenotypical, physiological, and transcriptional data showed that knocking-out OsbZIP53 not only improved disease resistance by inducing a hypersensitivity response in plants, but also regulated the immune response through the salicylic acid pathway. Specifically, disrupting OsbZIP53 increased H2O2 accumulation by promoting reactive oxygen species generation through up-regulation of several respiratory burst oxidase homologs (Osrboh genes) and weakened H2O2 degradation by directly targeting OsMYBS1. In addition, the growth of osbzip53 mutants was seriously impaired, while OsbZIP53 over-expression lines displayed a similar phenotype to the wild type, suggesting that OsbZIP53 has a balancing effect on rice immune response and growth.

The basic region/leucine zipper (bZIP) transcription factors play important roles in plant development and responses to abiotic and biotic stresses. OsbZIP53 regulates resistance to Magnaporthe oryzae in rice by analyzing APIP5 -RNAi transgenic plants. To further investigate the biological functions of OsbZIP53 , we generated osbzip53 mutants using CRISPR/Cas9 editing and also constructed OsbZIP53 over-expression transgenic plants. Comprehensive analysis of phenotypical, physiological, and transcriptional data showed that knocking-out OsbZIP53 not only improved disease resistance by inducing a hypersensitivity response in plants, but also regulated the immune response through the salicylic acid pathway. Specifically, disrupting OsbZIP53 increased H 2 O 2 accumulation by promoting reactive oxygen species generation through up-regulation of several respiratory burst oxidase homologs (Osrboh genes) and weakened H 2 O 2 degradation by directly targeting OsMYBS1. In addition, the growth of osbzip53 mutants was seriously impaired, while OsbZIP53 over-expression lines displayed a similar phenotype to the wild type, suggesting that OsbZIP53 has a balancing effect on rice immune response and growth. [ABSTRACT FROM AUTHOR]

In order to explore the effect of controlled atmosphere (CA) storage on alleviating chilling injury (CI) in peach fruit and the possible underlying mechanism, the effect of CA treatment (5% O2 + 10% CO2) on internal browning index (IB), firmness, ethylene release rate, reactive oxygen species (ROS) content, malondialdehyde (MDA) content, compounds and key enzyme activities related to the ascorbic acid-glutathione (AsA-GSH) cycle and volatile contents in yellow-fleshed peach fruit (cv. Jinxiu) during low temperature ((0 ± 2) ℃) storage and shelf (20 ℃, 3 d) was investigated. The results showed that CA alleviated CI significantly relative to the control group; on the third day of the shelf life after 30-day cold storage (30dS3), IB was lower than 10%, fruit firmness decreased to below 10 N, and ethylene release rate was 1.7-fold as high as in the control. During the late period of cold storage, the contents of total ROS, MDA, and hydrogen peroxide (H2O2) were significantly lower and scavenging capacities against 1,1-diphenyl-lpicrylhydrazyl (DPPH) and 2,2’-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical cation free radicals were significantly higher in the CA-treated fruit than the control group (P < 0.05 or P < 0.01). Meanwhile, in the CA-treated peach fruit, the activity of superoxide dismutase (SOD) was increased by 36% on 30dS3, while the activities of AsA-GSH cycle-related key enzymes such as ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR), glutathione reductase (GR) and monodehydroascorbate reductase (MDHAR) were enhanced, and the conversion of reduced ascorbic acid to dehydroascorbic acid was significantly inhibited. Moreover, CA treatment accumulated higher amounts of C6 alcohols, esters, and lactones compared with the control group at the end of the shelf life; on 30dS3, the contents of γ-hexalactone, γ-decalactone, and δ-decalactone were increased by 3.0, 2.6 and 5.0 folds compared with the control group, respectively. In addition, higher contents of sucrose and sorbitol and lower contents of glucose and fructose were observed in the CA-treated fruit. Therefore, CA treatment (5% O2 + 10% CO2) can alleviate CI and maintain aroma quality by activating the AsA-GSH cycle and SOD, and enhancing ROS scavenging capacity in peach fruit.

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The alleviating effect and mechanism of cold shock pretreatment (−2 ℃ cold air for 3 h) on flesh browning in fresh-cut pitaya fruit was explored by evaluating its effect on the phenylpropanoid pathway and antioxidant system during storage. Results revealed that cold shock pretreatment efficiently inhibited the increase in electrical conductivity and malondialdehyde (MDA) content compared with the control. Cold shock pretreatment promoted the gene expression and activities of key enzymes (phenylalanine ammonia lyase, cinnamic acid 4-hydroxylase, and 4-coumarate-CoA ligase) related to phenylpropane biosynthesis, and improved the accumulation of total phenolics and flavonoids, as well as most individual phenolic compounds, which led to enhanced antioxidant capacity. The activities of superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) were increased by cold shock pretreatment. In addition, cold shock pretreatment accelerated the production of superoxide anion and H2O2 at the early stage of storage, but had no effect on their peaks and led to lower levels of superoxide anion and H2O2 afterwards, alleviating flesh browning in fresh-cut pitaya fruit. These results indicated that cold shock pretreatment can effectively alleviate wound-induced oxidative stress by modulating the phenylpropanoid pathway and reactive oxygen species (ROS) metabolism, thus inhibiting flesh browning in fresh-cut pitaya fruit.

Abscisic acid (ABA) plays a vital role in the induction of low temperature tolerance in plants. To understand the molecular basis of this phenomenon, we performed a proteomic analysis on an ABA-deficit mutant barley (Az34) and its wild type (cv Steptoe) under control conditions (25/18 °C) and after exposure to 0 °C for 24 h. Most of the differentially abundant proteins were involved in the processes of photosynthesis and metabolisms of starch, sucrose, carbon, and glutathione. The chloroplasts in Az34 leaves were more severely damaged, and the decrease in Fv/Fm was larger in Az34 plants compared with WT under low temperature. Under low temperature, Az34 plants possessed significantly higher activities of ADP-glucose pyrophosphorylase, fructokinase, monodehydroascorbate reductase, and three invertases, but lower UDP-glucose pyrophosphorylase activity than WT. In addition, concentrations of proline and soluble protein were lower, while concentration of H2O2 was higher in Az34 plants compared to WT under low temperature. Collectively, the results indicated that ABA deficiency induced modifications in starch and sucrose biosynthesis and sucrolytic pathway and overaccumulation of reactive oxygen species were the main reason for depressed low temperature tolerance in barley, which provide novel insights to the response of barley to low temperature under future climate change. [ABSTRACT FROM AUTHOR]

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The key factors for resistance to chilling injury in apricot fruits were obtained by analyzing the low-temperature storage characteristics of 21 varieties of apricot fruits in the main producing areas of China. Twenty-one varieties of apricots from different production areas in China were stored at 0 °C for 50 d and then shelved at 25 °C. The storage quality, chilling injury, reactive oxygen species (ROS), antioxidant ability, and contents of bioactive substances of the apricots were measured and analyzed. The results showed that the 21 varieties of apricot fruits could be divided into two categories according to tolerance during low-temperature storage, where there was chilling tolerance and lack of chilling tolerance. Eleven varieties of apricots, of which Xiangbai and Yunbai are representative, suffered from severe chilling injury after cold storage and shelf life. After 50 d of storage at 0 °C, the levels of superoxide anions and hydrogen peroxide accumulated in the 11 varieties of apricots with a lack of chilling tolerance during storage were significantly higher than those in the remaining 10 varieties of apricots with chilling tolerance. In addition, the activities of ROS scavenging enzymes, represented by superoxide dismutase, catalase and peroxidase, were significantly decreased in 11 varieties of apricots with a lack of chilling tolerance during storage. The contents of bioactive substances with ROS scavenging ability, represented by ascorbic acid, total phenols, carotenoids, and total flavonoids, also significantly decreased. The 10 varieties of apricots, of which Akeximixi and Suanmao are representative, were less affected by chilling injury because the production and removal of ROS were maintained at normal levels, avoiding the damaging effects of ROS accumulation in the fruit. In addition, the 10 apricot varieties with chilling tolerance during storage had higher sugar and acid contents after harvest. This could supply energy for physiological metabolism during cold storage and provide carbon skeletons for secondary metabolism, thus enhancing the chilling tolerance of the fruits. Based on the results of cluster analysis combined with the geographical distribution of the 21 fruit varieties, it was found that apricot varieties with chilling tolerance during storage were all from the northwestern region of China where diurnal temperature differences and rapid climate changes occur. In conclusion, maintaining the balance of ROS production and removal in apricots during cold storage is a key factor to enhance the storage tolerance of apricots. Moreover, apricots with higher initial glycolic acid and bioactive substance contents are less susceptible to chilling injury. [ABSTRACT FROM AUTHOR]

Red grapes (Vitis vinifera L.) have a high sugar content, thin skins, and relatively short shelf‐life after harvesting. We developed polylactic acid/polybutylene succinate film, prepared by extrusion of polylactic acid and polybutylene succinate, that significantly prolonged the shelf‐life of red grapes from 8 to 12 days by delaying the loss of weight, loss of hardness, and reduction in soluble solid content after harvesting. Further mechanistic study showed that this modified atmosphere film delayed the senescence of harvested red grape, the phenomenon that was highly related to the lower active oxygen species production and higher antioxidant enzyme activity compared to the non‐packaged grape. The proposed continuous and dynamic microenvironment regulation system is a promising method to study the mechanisms of respiratory metabolism in fruit and extends food shelf‐life while reducing food waste. Practical Application: In this study, we designed a means to microenvironmental regulatory packaging that directly creates a continuous, dynamic, and monitorable microenvironment. To ensure that the fruit inside the package underwent coordinated aerobic and anaerobic respiration, we melt‐extruded polylactic acid (PLA) and polybutylene succinate (PBS) to form a homogeneous biodegradable film. We demonstrated that the best preservation results were achieved with a film comprising an 80/20 PLA‐to‐PBS ratio. This film can prolong the shelf‐life of fruits by regulating respiratory metabolism. [ABSTRACT FROM AUTHOR]

The vigorous metabolism of reactive oxygen species (ROS) in postharvest ‘Kyoho’ grapes shortens the storage period, and reduce the commercial value. In this study, different concentrations (0, 10, 30, 50 and 70 mg/L) of diethyl aminoethyl hexanoate (DA-6) were sprayed on table grapes at veraison to investigate the effects of DA-6 treatment on postharvest fruit quality and ROS metabolism in ‘Kyoho’ grapes. By measuring the physiological indexes related to fruit quality, it was found that DA-6 treatment significantly reduced fruit mass loss, and delayed the decrease in fruit firmness and total soluble solid content, and this effect was most significant at a concentration of 50 mg/L. More importantly, 50 mg/L DA-6 treatment significantly increased the activity of superoxide dismutase, ascorbate peroxidase, catalase, glutathione reductase, 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging capacity and total reducing capacity, and suppressed the decrease in reduced ascorbic acid and glutathione contents and the accumulation of superoxide anion radical and malondialdehyde. In conclusion, pre-harvest spray of DA-6 maintained the stability of the ROS scavenging system in postharvest table grapes, kept ROS metabolism in a relatively balanced state, reduced oxidative damage, delayed fruit senescence, and prolonged the shelf life of ‘Kyoho’ grapes.

Aluminum is the most abundant metal element in the crust. Soil acidification will cause great increase of the aluminum solubility to produce a large number of Al3+, which is toxic to plants. The activated aluminum will inhibit root growth, affect nutrient absorption and many physiological and biochemical metabolism processes, and further reduce crop yield. Aluminum toxicity has been the most important limiting factor for crop growth in acid soils which account for about 40% of cultivated land in the world. Phytohormones are the key endogenous factors that regulate plant responses to various environmental stresses, and are crucial to the improvement of plant resistance and plant survival under various stresses. It is well known that abscisic acid, auxin, ethylene, cytokinin, jasmonic acid and other major plant hormones play an important role in regulating plant responses to aluminum toxicity stress. A large number of studies have shown that plant hormones can also improve the adaptability of plants to aluminum stress by regulating the activities of cell wall-modifying enzymes, reactive oxygen species metabolism and organic acid secretion. In addition, there are complex interactions between different plant hormone signals, which jointly mediate and regulate the adaptive response of plants to aluminum stress. In order to have a more comprehensive and in-depth understanding of the mechanism of plant hormones in aluminum toxicity response, and to provide new ideas for molecular genetic improvement of plants tolerance to aluminum toxicity, in the study, the signal transduction and regulation of plant hormone signals in the process of plant response to aluminum toxicity stress are reviewed, and the future research direction of plant hormones under aluminum toxicity stress is prospected.

Xinjiang 'Saimaiti' apricot fruit were used as the material to study the inhibitory effects of postharvest treatment with melatonin on black spot and its influence on reactive oxygen species metabolism. Fruit were vacuum impregnated into different concentrations of melatonin (50, 100, 200 μmol/L) under pressure of 0.05 MPa for 2 min, then atmospheric pressure was restored, and the fruit was maintained in the same solution for 8 min. The distilled water treatment was used as blank control. After naturally drying, the fruit were refrigerated (0±1℃, RH 90%~95%) for 48 h. After that, apricot fruits were inoculated with Alternaria alternata and stored at the same conditions.The lesion diameter and disease incidence of apricot fruit inoculated with A.alternata, the activities of superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), and superoxide anion radical (O2−·) production rate, cell membrane permeability, hydrogen peroxide (H2O2) and malondialdehyde (MDA) contents were measured regularly. Results showed that compared with the control group, different concentrations of exogenous melatonin treatment significantly delayed the increase of apricot fruit morbidity and inhibited the increase of apricot fruit the lesion diameter. At the end of storage, the spot diameters of apricot fruit were significantly lower in the 50, 100, and 200 μmol/L melatonin-treated groups by 11.92%, 28.49%, and 19.67% (P

In this study, “Xiahui 8” honey peach fruit was used as a test material to investigate the synergistic preservation effect of 1-methylcyclopropene (1-MCP) and laser microporous film (LMF). The peach fruits were fumigated with 2 μL/L 1-MCP for 24 h, then packed in LMF. The results showed that 1-MCP+LMF significantly reduced the respiratory intensity and weight loss of peach during cold storage (P

Fulvic acid (FA) can significantly alleviate cadmium (Cd) stress, but the specific metabolic response of FA to Cd toxicity is still not clarified. In the present study, we used untargeted metabolomic [gas chromatography–mass spectrometry (GC–MS) and liquid chromatography–mass spectrometry (LC–MS)] analysis to profile cucumber metabolism in response to Cd stress after spray application of FA. Our results showed that 331 differentially enriched metabolites (DEMs) were identified in leaf materials. These DEMs were enriched in 21 shared pathways in comparative groups of "Cd treatment vs. the control treatment" and "FA + Cd treatment vs. the Cd treatment." Specifically, treatment with FA significantly enhanced the organic acid content (citric acid, isocitric acid, 2-oxoglutaric acid, fumaric acid, and malic acid), which would contribute to provide sufficient substrates for the tricarboxylic acid (TCA) cycle and amino acid biosynthesis, thereby ensuring the normal production of energy and amino acid. At the same time, FA significantly increased the amino acid content (aspartate, citrulline, histidine, leucine, and phenylalanine). The accumulation of organic acid and amino acid can act as chelating agents for heavy metal ions and as scavengers of reactive oxygen species (ROS), thereby reducing intracellular oxidative damage. Furthermore, the application of FA improves antioxidant enzymes and accelerates ROS clearance. The improved contents of organic acid and amino acid, and the increased activity of antioxidant enzymes both played a central role in the reduction of malondialdehyde (MDA, 14.08%), hydrogen peroxide (H2O2, 61.70%) contents, and superoxide anion radical (O2−, 30.41%) production rate in plants under Cd stress. Taken together, the present study demonstrates the effects of FA on the antioxidant capacity and carbohydrate and amino acid metabolism of cucumber seedlings exposed to Cd stress, which provides comprehensive insights into the regulation of plants' response to Cd toxicity with FA was applied in cucumber. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aluminum is the most abundant metal element in the crust. Soil acidification will cause great increase of the aluminum solubility to produce a large number of Al3+, which is toxic to plants. The activated aluminum will inhibit root growth, affect nutrient absorption and many physiological and biochemical metabolism processes, and further reduce crop yield. Aluminum toxicity has been the most important limiting factor for crop growth in acid soils which account for about 40% of cultivated land in the world. Phytohormones are the key endogenous factors that regulate plant responses to various environmental stresses, and are crucial to the improvement of plant resistance and plant survival under various stresses. It is well known that abscisic acid, auxin, ethylene, cytokinin, jasmonic acid and other major plant hormones play an important role in regulating plant responses to aluminum toxicity stress. A large number of studies have shown that plant hormones can also improve the adaptability of plants to aluminum stress by regulating the activities of cell wall-modifying enzymes, reactive oxygen species metabolism and organic acid secretion. In addition, there are complex interactions between different plant hormone signals, which jointly mediate and regulate the adaptive response of plants to aluminum stress. In order to have a more comprehensive and in-depth understanding of the mechanism of plant hormones in aluminum toxicity response, and to provide new ideas for molecular genetic improvement of plants tolerance to aluminum toxicity, in the study, the signal transduction and regulation of plant hormone signals in the process of plant response to aluminum toxicity stress are reviewed, and the future research direction of plant hormones under aluminum toxicity stress is prospected. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In the present study, the fresh-cut water chestnuts of Guiti NO.3 were used as experimental materials and soaked with 6-benzylaminopurine (6-BA) of 100 mg/L, 200 mg/L, 400 mg/L for 3 minutes, and then the contents variations of total phenols, flavonoids, quinones, malondialdehyde (MDA), hydrogen peroxide (H2O2) and activities of polyphenol oxidase (PPO), peroxidase (POD), phenylalanine ammonium-lyase (PAL), catalase (CAT), superoxide dismutase (SOD) were evaluated using pure water treatment as control (CK), aiming to investigate the effects of 6-BA treatments with different concentrations on the browning and reactive oxygen species metabolism. Results showed that 6-BA treatments reduced the accumulation of total phenolics, flavonoids and quinone etc. and decreased PPO, POD and PAL activities compared with the control, resulting in effectively inhibiting browning of fresh-cut water chestnuts and maintaining the color during storage. Moreover, 6-BA treatments also suppressed the contents of MDA and H2O2, while increased CAT and SOD activities, thus improving the qualities of fresh-cut water chestnuts during storage. The 6-BA treatment of 400 mg/L presented superior effects on inhibiting browning and reactive oxygen species metabolism of fresh-cut water chestnuts. [ABSTRACT FROM AUTHOR]

The effects of γ-aminobutyric (GABA) on enzymatic browning, storage quality, membrane and reactive oxygen species (ROS) metabolism in fresh-cut stem lettuce were investigated. The results illustrated that GABA treatment delayed browning degree, polyphenol oxidase (PPO) activity and the expression of LsPPO. Meanwhile, higher chlorophyll and ascorbic acid contents were exhibited in GABA-treated stem lettuce, as well as the slower microbial propagation. Further investigation revealed that exogenous GABA application declined malondialdehyde content, electrolyte leakage and the enzyme activities of membrane metabolism, and the expression levels of related genes were also downregulated. In addition, GABA treatment scavenged ROS and strengthened the enzyme activities of ROS metabolism, as well as the expression levels of corresponding genes. Taken together, these findings implied that the repressed enzymatic browning and microbial propagation in GABA-treated stem lettuce were due to the inhibition of ROS accumulation, enhancement of membrane stability and increased resistance to oxidation. • Exogenous GABA inhibited the enzymatic browning of fresh-cut stem lettuce. • GABA treatment maintained the quality in fresh-cut stem lettuce. • GABA application inhibited the microbial propagation in fresh-cut stem lettuce. • GABA treated-fresh-cut stem lettuce exhibited higher membrane stability. • GABA treatment enhanced the antioxidant capacity in fresh-cut stem lettuce. [ABSTRACT FROM AUTHOR]

• Exogenous sucrose treatment was more effective than other treatments in mitigating LRT stress injury. • New insights into the regulation of sucrose in the roots of Malus baccata Borkh. in response to LRT. • Sucrose alleviated LRT stress by regulating the antioxidant system, α-linolenic acid metabolism, carbohydrate metabolism, phenylpropane biosynthesis, and flavonoid biosynthesis pathways in the roots. The root, a key organ for sensing the soil environment, is easily damaged by environmental stresses such as low soil temperature. Although the exact mechanism is unknown, exogenous sucrose can mitigate the oxidative damage to the root caused by low temperatures in the root zone. In this study, we examined how exogenous sucrose affected the transcriptome and physiology of Malus baccata Borkh. seedling roots at sub-low root-zone temperature (LRT). The exogenous sucrose treatment was more effective than other treatments in mitigating LRT stress injury. This was achieved by decreasing reactive oxygen species (O 2 .- and H 2 O 2) and malondialdehyde content, increasing the activities of antioxidant enzymes (SOD, POD, CAT, APX, GR, and MDHAR), increasing AsA and GSH content, and increasing soluble sugar content. Transcriptome analysis revealed that α-linolenic acid metabolism, fatty acid biosynthesis, phenylpropane biosynthesis, and glycolysis/gluconeogenesis were the primary areas of enrichment for the differentially expressed genes identified under the LRT treatment. Exogenous sucrose may enhance the tolerance of Malus baccata Borkh. to LRT by regulating the expression of differentially expressed genes (GST, LOX, SS, PFK, ADH , and 4CL) related to the antioxidant system, carbohydrate metabolism, α-linolenic acid metabolism, and phenylpropane biosynthesis pathways. These results offer a foundation for additional investigation into the molecular mechanism underlying the modulation of the root response to low temperature by exogenous sucrose. [ABSTRACT FROM AUTHOR]

Chromosome damage combined with defective recombinase activity renders cells inviable, owing to deficient double-strand break repair. Despite this, recA polA cells grow well under either DNA damage response (SOS) conditions or catalase medium supplementation. Catalase treatments reduce intracellular reactive oxygen species (ROS) levels, suggesting that recA polA cells are susceptible to not only chronic chromosome damage but also ROS. In this study, we used a reducing agent, vitamin C, to confirm whether cell growth could be improved. Vitamin C reduced ROS levels and rescued colony formation in recAts polA cells under restrictive temperatures in the presence of hslO, the gene encoding a redox molecular chaperone. Subsequently, we investigated the role of hslO in the cell growth failure of recAts polA cells. The effects of vitamin C were observed in hslO+ cells; simultaneously, cells converged along several ploidies likely through a completion of replication, with the addition of vitamin C at restrictive temperatures. These results suggest that HslO could manage oxidative stress to an acceptable level, allowing for cell division as well as rescuing cell growth. Overall, ROS may regulate several processes, from damage response to cell division. Our results provide a basis for understanding the unsolved regulatory interplay of cellular processes. [ABSTRACT FROM AUTHOR]

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Breast cancer patients have high serum reactive oxygen species (ROS) levels, which exert toxicity on the ovary. However, it is still unclear whether tumor-derived ROS play a role in endometrial development and function in breast cancer. Breast cancer patients and healthy controls were recruited and endometrial thickness was measured by transvaginal ultrasound (TVUS). Xenograft tumors of the breast cancer cell line MDA-MB-231 in a female BALB/c nude mice model were established, and the therapeutic mechanism of vitamin C (VC) was investigated on uterine pathology in vivo and the contribution of co-culture of breast cancer cell and endometrial epithelial cell on this process was examined in vitro. Median thickness in endometria was lower in breast cancer patients and tumor-bearing mice compared to controls. A gene signature of uteri in tumor-bearing mice demonstrated differential expression of genes (DEGs) regulating extracellular matrix (ECM) and epithelial-mesenchymal transition (EMT), and activation of TGF-β and MAPK signaling pathways. In addition, ROS, EMT- and ECM-related protein levels were enhanced in uteri in tumor-bearing mice, as well as in Ishikawa cells which were co-cultured with MDA-MB-231 cells compared to controls. Supplementation with VC reduced endometrial damage, inhibited the EMT process and collagen deposition, and maintained better histologic architecture of uteri in tumor-bearing mice via inactivation of the TGF-β1/p38MAPK pathway. In women with breast cancer oxidative stress in the endometrium results in a fibrotic response as a consequence of EMT. VC could alleviate endometrial fibrosis via TGF-β1/p38MAPK pathway and provide new predictive and therapeutic targets for fertility preservation in younger breast cancer patients., (© 2024 Federation of American Societies for Experimental Biology.)

Obesity plays a crucial role in the development and progression of type 2 diabetes mellitus (T2DM) by causing excessive release of free fatty acid from adipose tissue, which in turn leads to systemic infiltration of macrophages. In individuals with T2DM, the infiltration of macrophages into pancreatic islets results in islet inflammation that impairs beta cell function, as evidenced by increased apoptosis and decreased glucose-stimulated insulin secretion. The present study aimed to investigate the effects of non-lethal sonodynamic therapy (NL-SDT) on bone marrow-derived macrophages (BMDMs) exposed to high glucose and palmitic acid (HG/PA). These findings indicate that NL-SDT facilitates the expression of DRP1 through the transient production of mitochondrial ROS, which subsequently promotes mitophagy. This mitophagy was shown to limit the activation of the NLRP3 inflammasome and the secretion of IL-1β in BMDMs exposed to HG/PA. In co-culture experiments, beta cells exhibited significant dysfunction when interacting with HG/PA-treated BMDMs. However, this dysfunction was markedly alleviated when the BMDMs had undergone NL-SDT treatment. Moreover, NL-SDT was found to lower blood glucose levels and elevate serum insulin concentrations in db/db mice. Furthermore, NL-SDT effectively reduced the infiltration of F4/80-positive macrophages and the expression of CASP1 within islets. These findings provide fundamental insights into the mechanisms through which NL-SDT may serve as a promising approach for the treatment of T2DM., (© 2024 Federation of American Societies for Experimental Biology.)

The increase of coarse particulate matter (PM 10 ) due to industrialization and urban sprawl has been identified as a significant contributor to air pollution and a threat to human skin health and premature aging. The objective was to analyze the antioxidant effect of phenolic-enriched extracts (PHE) obtained from black bean (BB) and pinto bean (PB) varieties (Phaseolus vulgaris L.) and pure phenolic compounds (rutin, catechin, and gallic acid) in two human dermal fibroblasts cell lines exposed to PM 10 . Petunidin-3-O-glucoside was the most abundant anthocyanin, with 57 ± 0.9 mg/g dry extract (DE) in PHE-BB. Gallic acid was the prevalent phenolic acid with 8.2 ± 2.8 mg/g DE in PHE-BB (p < 0.05). Hs27 and Hs68 cell lines were exposed to PM 10 (100 μg/mL) to induce oxidative stress; PHE-BB reduced it by 69% ± 12 and PHE-PB by 80% ± 5 relative to PM 10 treatment (p < 0.05). Delphinidin-3-O-glucoside showed the highest binding affinity in adenosine monophosphate-activated protein kinase (AMPK) with -9.0 kcal/mol and quercetin-3-D-galactoside with -6.9 kcal/mol in sirtuin 1 (Sirt1). Rutin increased the expression of Sirt1 by 30% (p < 0.05) in the Hs27 cell line treated with PM 10 . Common bean extracts can potentially reduce oxidative stress induced by PM 10 in human dermal fibroblasts., 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.)

Research conducted previously has demonstrated that apoptosis significantly influences the chicken quality. While ROS are acknowledged as significant activators of apoptosis, the precise mechanism by which they influence muscle cell apoptosis in the post-mortem remains unclear. In this study, chicken samples were treated with rosemarinic acid and H 2 O 2 to induce varying ROS levels, and the ROS-triggered apoptosis mechanism in chicken muscle cells in post-mortem was analyzed. The TUNEL results revealed that elevated ROS levels in chicken were associated with a greater degree of muscle cell apoptosis. Western-blot results suggested that sarcoplasmic ROS could initiate apoptosis through the mitochondrial pathway by activating the MAPK-JNK signaling pathway. Moreover, TEM and shear force results demonstrated that muscle cell apoptosis initiates myofiber fragmentation and structural damage to sarcomeres, ultimately reducing chicken tenderness. This study enhances our understanding of post-mortem muscle cell apoptosis, providing valuable insights for regulating chicken quality., 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.)

Early-onset pre-eclampsia is believed to arise from defective placentation in the first trimester, leading to placental ischaemia/reperfusion (I/R) and oxidative stress. However, our current understanding of the effects of I/R and oxidative stress on trophoblast function is ambiguous in part due to studies exposing trophoblasts to hypoxia instead of I/R, and which report conflicting results. Here, we present a model of simulated ischaemia/reperfusion (SI/R) to recapitulate the pathophysiological events of early-onset pre-eclampsia (PE), by exposing first trimester cytotrophoblast HTR-8/SVneo cells to a simulated ischaemia buffer followed by reperfusion. We examined different ischaemia and reperfusion times and observed that 1 h ischaemia and 24 h reperfusion induced an increase in reactive oxygen species (ROS) production (P<0.0001) and oxygen consumption rate (P<0.01). SI/R-exposed trophoblast cells exhibited deficits in migration, proliferation, and invasion (P<0.01). While the deficits in migration and proliferation were rescued by antioxidants, suggesting an ROS-dependent mechanism, the loss of invasion was not affected by antioxidants, which suggests a divergent ROS-independent pathway. In line with this, we observed a decrease in MMP-9, the key regulatory enzyme necessary for trophoblast invasion (P<0.01), which was similarly unaffected by antioxidants, and pharmacological inhibition of MMP-9 replicated the phenotype of deficient invasion (P<0.01). Collectively, these data demonstrate that I/R impairs trophoblast migration and proliferation via a ROS-dependent mechanism, and invasion via an ROS-independent loss of MMP-9, disambiguating the role of oxidative stress and providing insights into the response of trophoblasts to I/R in the context of early-onset PE., (© 2024 The Author(s).)

Previous studies have demonstrated that combination therapy involving radiotherapy and aspirin decreases the survival rate of cancer cells. However, the mechanism by which aspirin exerts its radiation sensitization effect at the in vivo level remains largely unclear. In this study, we employed Caenorhabditis elegans (C. elegans) as a model organism to investigate the effect of aspirin combined with radio/chemo-therapy on tumors at the individual level. Here, we illustrate that high-dose aspirin increases the expression of genes involved in core apoptosis pathways (egl-1, ced-9, ced-4 and ced-3) and induces germ cell apoptosis in C. elegans through mitochondrial outer membrane permeabilization (MOMP) and elevation of reactive oxygen species (ROS) levels. Crucially, aspirin-induces ROS upregulates the expression of genes critical for DNA damage response (hus-1, clk-2 and cep-1) and genes involved in MAPK pathways (lin-45, mek-2, mpk-1, sek-1 and pmk-1), thereby mediating the enhanced sensitivity of radio/chemo-therapy by aspirin. Notably, aspirin fails to induce germ cell apoptosis and enhance radio/chemo-therapy in C. elegans lacking the expression of each of those genes. Furthermore, in a C. elegans tumor-like symptom model, aspirin enhances radio/chemo-therapy sensitivity through ROS induction. However, low-dose aspirin can diminish the apoptotic signal of reproductive cells in C. elegans and exert anti-inflammatory effects. Our research results suggest that the tumor-suppressive and radio/chemo-therapy sensitizing effects of aspirin provide robust experimental evidence for improving the clinical efficacy of tumor radio/chemo-therapy and deepening our understanding of aspirin's mechanism of action in cancer., 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.)

Celastrol, a pentacyclic triterpenoid found in Chinese herb Tripterygium wilfordii, is considered as one of the top-five natural medicinal compounds with high antioxidant property. However, celastrol has poor aqueous solubility and thereby low bioavailability, restricting its clinical application as drug. To overcome this problem, we nanonized celastrol by entrapping it within hydrophilic nanocarrier - calcium phosphate nanoparticle. The synthesized calcium phosphate celastrol nanoparticle (CPCN) had average size of 35 nm, spherical shape, significant stability with (-) 37 mV zeta potential, celastrol entrapment efficiency around 75 % and low celastrol release kinetics spanning over 7 days, as measured by different techniques like FESEM, AFM, DLS, and spectrophotometry. Studies on the antioxidant potency of CPCN by flow cytometry and fluorescence microscopy depicted that the toxicity developed in human neuroblastoma cells SH-SY5Y by treatment with the selective neurotoxin MPP + iodide (N-Methyl-4-phenylpyridinium iodide) got reduced by pretreatment of the cells with CPCN. Determination of cellular ROS content, depolarization level of mitochondrial membrane potential, cell cycle analysis and nuclear damage in MPP + -exposed cells demonstrated that CPCN had about 65 % more antioxidant efficacy over that of bulk celastrol. Thus, the nanonization process transformed hydrophobic celastrol into hydrophilic CPCN, having high potentiality to be developed as an effective antioxidant drug., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Prof. Tarakdas Basu has patent A PROCESS FOR SYNTHESIS OF CELASTROL-LOADED CALCIUM PHOSPHATE NANOPARTICLE AS A POTENT ANTIOXIDANT pending to UNIVERSITY OF KALYANI. If there are other authors, they 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.)

Domoic acid (DA) is a compound generated as a secondary metabolite during harmful algal blooms, has historically received attention as the potent neurotoxicity in marine environment. However, the aerobic degradation mechanism of DA and the DA-degrader remain largely unknown. Here, we revealed the mechanism of aerobic degradation of DA by a ubiquitous marine Pseudoalteromonas sp., and more importantly, we confirmed that the degradation of DA is mediated by biogenic reactive oxygen species (ROS), rather than direct enzyme-mediated as traditionally conceived. Results indicated that DA degradation was caused by biogenic O 2 - and OH, where DA underwent reactions of decarboxylation, hydroxylation, and oxidation to yield the detoxification terminal product. Besides, whole genome sequencing and RT-qPCR analysis revealed that the genes conferring to encoding leucine dehydrogenase (ldh) and Na+-translocated NADH-quinone oxidoreductase (nqrA, nqrF) are responsible for biogenic ROS production. Finally, we found through comparative proteomic analysis that biogenic ROS mediated the DA degradation may be prevalent in the environment. Overall, this work not only reveals aerobic biotransformation mechanism of DA, but also identifies a novel mechanism of DA degradation, which provides new perspective into the environmental fate of DA and the artificial bioremediation of DA., 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.)

Fluoride (F) and cadmium (Cd) as well known environmental pollutants can cause nephrotoxicity to damage human health, while the joint toxicity of F and Cd to the renal tubular epithelial cells remains still elusive. The interactive influence between F and Cd in oxidative stress, apoptosis, and mitochondrial autophagy of renal tubular epithelial cells was explored. Cells were submitted to varying concentrations with of NaF (1, 5, 10, and 15 μg/mL) combined with CdCl 2 ·2.5H 2 O (1 μg/mL) for 12 h. Following this, the combined cytotoxicity was assessed. Our results show that different doses of F had varying effects on Cd-mediated nephrotoxicity, with a synergistic effect observed in the high F (15 μg/mL) co-treated with Cd. In response to the Cd induction, the high F treatment resulted in the formation of multiple autophagosomes and notably increased the levels of LDH, ROS, and MMP. It also elevated the MDA contents while decreasing the activities of SOD, GSH-Px, and CAT. Additionally, it yielded a higher Bax/Bcl-2 ratio, which further promotes the apoptotic process. The treatment also disturbed energy metabolism, resulting in a reduction of both ATP and ADP. Furthermore, autophagy-related genes and proteins, including PINK1, Parkin, LC3A, LC3B, and SQSTM1, were significantly improved. In brief, high F of 15 μg/mL aggravated Cd-mediated nephrotoxicity of renal tubular epithelial cells via the ROS-PINK1/Parkin pathway., 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 extensive use of plastic products has exacerbated micro/nanoplastic (MPs/NPs) pollution in the atmosphere, increasing the incidence of respiratory diseases and lung cancer. This study investigates the uptake and cytotoxicity mechanisms of polystyrene (PS) NPs in human lung epithelial cells. Transcriptional analysis revealed significant changes in cell adhesion pathways following PS-NPs exposure. Integrin α5β1-mediated endocytosis was identified as a key promoter of PS-NPs entry into lung epithelial cells. Overexpression of integrin α5β1 enhanced PS-NPs internalization, exacerbating mitochondrial Ca2+ dysfunction and depolarization, which induced reactive oxygen species (ROS) production. Mitochondrial dysfunction triggered by PS-NPs led to oxidative damage, inflammation, DNA damage, and necrosis, contributing to lung diseases. This study elucidates the molecular mechanism by which integrin α5β1 facilitates PS-NPs internalization and enhances its cytotoxicity, offering new insights into potential therapeutic targets for microplastic-induced lung diseases., Competing Interests: Declaration of competing interest The authors declared 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. Published by Elsevier B.V.)

GUARD CELL HYDROGEN PEROXIDE-RESISTANT1 (GHR1), a leucine-rich repeat receptor-like kinase, is involved in abscisic acid (ABA)-induced stomatal closure. We investigated the role of GHR1 in reactive oxygen species (ROS) signaling for ABA-induced stomatal closure. ABA induced ROS production in wild type (WT) and the ghr1 of Arabidopsis thaliana. Hydrogen peroxide induced stomatal closure, accompanying the generation of acrolein in guard cells. The reactive carbonyl species (RCS) scavengers inhibited the ABA- and H2O2-induced stomatal closure in WT. In the ghr1, H2O2 failed to induce acrolein production and stomatal closure while RCS induced stomatal closure. Thus, GHR1 functions downstream of ROS and is required for the generation of RCS in guard-cell ABA signaling. In the ghr1, Ca2+ induced stomatal closure but RCS did not activate ICa channels. The GHR1 may be also involved in a Ca2+-independent pathway for ABA-induced stomatal closure., (© The Author(s) 2024. Published by Oxford University Press on behalf of Japan Society for Bioscience, Biotechnology, and Agrochemistry.)

Oxidative stress is a major pathological factor that impedes the diabetic wound healing process. Procyanidins (PC) form nanoparticle-vesicles (PPNs) through hydrogen bonding and exhibit good drug delivery capability; however, their application in diabetic wounds is unsatisfactory. To meet the antioxidant needs for treating, high-throughput screening in the natural product library (NPL) under in vitro oxidative stress conditions was conducted to enhance the antioxidant activity of PPNs. HUVECs treated with tert-Butyl Hydroperoxide (TBHP) were established as screening model in vitro. Baicalein (BAI) was identified from over 600  products in the library as the most effective one to combat oxidative stress. Further study showed that PC and BAI may react in equal proportions to synthesize new vesicles, named BAI-PC Polyphenolic nanovesicles (BPPNs), which possess reactive oxygen species (ROS) responsive and antioxidant effects. Network pharmacology indicated that in diabetic wounds, the target genes of PC are mainly enriched in the vascular endothelial growth factor (VEGF)-related pathways, while BAI primarily regulates tyrosine phosphorylation. The complementarity between the two has been validated in both in vitro and in vivo experiments. In summary, the antioxidant drug BAI, identified through high-throughput screening of NPL, could optimize the biological function of PPNs; the newly-synthesized BPPNs may accelerate diabetic wound healing through dual mechanisms of promoting angiogenesis and combating oxidative stress., Competing Interests: Declarations. Ethics approval and consent to participate: All animal experiments were approved by the Institutional Ethical Committee of Wenzhou Medical University (wydw2023-0243). Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Bacterial biofilms are one of the major contributors to the refractoriness of septic arthritis. Although nitric oxide (NO)-enhanced photodynamic (PDT) therapy has been involved in biofilm eradication, the anti-biofilm efficacy is usually hindered by the short half-life and limited diffusion distance of active molecules. Herein, we report a three-arm structure using the photosensitive core chlorin e6 to integrate three α-cyclodextrin (α-CD) polyrotaxane chains as the supramolecular nanocarrier of NO-enhanced PDT therapy, in which NO was loaded on the cationic rings (α-CDs). Beneficial from the enhanced permeability of the nanocarrier due to the collective act on biofilms by the molecular motions (slide and rotation of rings) of three chains in different directions, NO capable of inducing biofilm dispersal and reactive oxygen species were efficiently delivered deep inside biofilms under 660 nm laser irradiation, and reactive nitrogen species with stronger bactericidal ability was produced in-situ, further accomplishing bacteria elimination inside biofilms. In-vivo therapeutic performance of this platform was demonstrated in a rat septic arthritis model by eliminating the methicillin-resistant Staphylococcus aureus infection, and potentiating the immune microenvironment regulation and bone loss inhibition, also providing a promising strategy to numerous obstinate clinical infections caused by biofilms., Competing Interests: Declarations. Ethics approval and consent to participate: Protocols of animal experiments included in this study were approved by the Experimental Animal Ethics Committee of Jinan University. Consent for publication: All authors confirmed that this work has not been published before, and was not under consideration for publication elsewhere. All authors have approved the submission of this manuscript to Journal of Nanobiotechnology. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Background: Trichoderma reesei is renowned for its cellulase-producing ability and is used for biofuel production from lignocellulose. In plants and fungi, cellulase production is induced by cellulose and suppressed by glucose; however, whether metformin can enhance cellulase production and mitochondrial function in T. reesei remains unclear. Metformin reduces blood glucose levels by inhibiting hepatic gluconeogenesis; therefore, it is worth investigating whether metformin transmission modulates cellulase biosynthesis in T. reesei., Results: Metformin increased cellulase production and the transcription of cellulase-related genes. It also enhanced the concentrations of Ca 2+ in the cytosol and mitochondria and regulated the transcription levels of cellulase-related genes by modulating calcium homeostasis in T. reesei QM6a. In addition, metformin was identified as an antioxidant that can enhance cellulase activity by reducing reactive oxygen species (ROS). Our results demonstrated that metformin influences the state of mitochondria by enhancing mitochondrial activity and membrane potential to promote cellulase production., Conclusion: Collectively, these results indicate that metformin enhances cellulase production, scavenges ROS, and protects mitochondrial activity in T. reesei., Competing Interests: Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Background: Hyperoside (quercetin-3-O-β-D-galactopyranoside) is a flavonol glycoside compound derived from plants in the Hypericum and Crataegus genera that reportedly exhibits an array of anti-inflammatory, antioxidant, and antitumor properties such that it has been used to treat various diseases. Whether it can serve as an effective treatment for chronic myeloid leukemia (CML) cells, however, has yet to be established. The present study was thus devised to assess the therapeutic effects of hyperoside on CML cells and to clarify the underlying mechanism of action., Methods: Cellular viability, proliferative activity, migration, and apoptotic death were respectively analyzed through CCK-8, EDU, transwell, and flow cytometry assays. RNA-seq and bioinformatics approaches were further employed to evaluate the mechanisms through which hyperoside influences CML cells, while analyses of reactive oxygen species (ROS) and free iron were detected with commercial kits. Transmission electron microscopy was used to assess mitochondrial morphology. Molecular docking, cellular thermal shift assay (CETSA), and drug affinity responsive target stability (DARTS) approaches were also used to explore the ability of hyperoside to target NRF2., Results: From a mechanistic perspective, hyperoside was able to inhibit SLC7A11/GPX4 signaling in a manner that was abrogated by the ferroptosis inhibitor ferrostatin-1. NRF2 was also closely associated with the inactivation of the SLC7A11/GPX4 axis mediated by hyperoside such that overexpressing NRF2 ablated the benefits associated with hyperoside treatment., Conclusions: The present analyses indicate that hyperoside can target the NRF2/SLC7A11/GPX4 axis to induce ferroptotic CML cell death., Competing Interests: Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Cholinergic treatments with an emphasis on M1 muscarinic acetylcholine receptor (mAChR) agonists as potential modulating agents are a new approach in Alzheimer's disease (AD) therapy. In previous research, we designed and characterized novel thiazolidine-2,4-dione (TZD)-derived compounds that possess anti-AD properties and enhance the expression of mAChRM1 in rats. This study evaluated a novel orthosteric agonist of mAChRM1 from related pathways that has shown promising anti-Alzheimer's disease activity. PC12 cells were exposed to various concentrations of TZ4M before they were exposed to scopolamine (3 µM). Immunocytochemistry and western blot analyses revealed that TZ4M increased the expression of mAChRM1 in differentiated cells induced by scopolamine-treated PC12 cells. The results showed that TZ4M (3 and 5 µM) markedly upregulated PKC and ChAT protein expression, and the cells were significantly protected against increased ROS levels followed by neuronal cell loss, as evidenced by the MTT assay. TUNEL staining indicated that TZ4M impeded the shaping of apoptotic bodies. Analysis of the amino acid sequences of the ligand-protein binding site indicated that TZ4M is bound to the orthosteric site (acetylcholine site). This study revealed that TZ4M, a derivative of TZD, effectively protects against scopolamine-induced damage. TZ4M, a novel mACRM1 orthosteric agonist, is promising for treating AD., Competing Interests: Declarations. Competing interests: The authors declare no competing interests. Ethical approval: All methods were carried out in accordance with relevant guidelines and regulations., (© 2024. The Author(s).)

Purpose: Pharmacological inhibition of ferroptosis, a specific form of regulated cell death, has emerged as a promising therapeutic strategy for alleviating symptoms and enhancing endoscopic outcomes in patients suffering from ulcerative colitis. Rhoifolin, a prominent bioactive constituent abundant in the widely consumed fruit Citrus grandis (grapefruit), has garnered attention for its ability to diminish the levels of reactive oxygen species (ROS), which are key inducers of ferroptosis across diverse cellular contexts. In this study, we aimed to investigate whether rhoifolin exerts its beneficial effects on colitis by modulating the process of epithelial ferroptosis., Methods: Colitis model was successfully established in C57BL/6 mice through the administration of 2.5% dextran sulfate sodium (DSS) solution for a duration of 9 days, which was freely accessible for drinking. RNA sequencing was conducted to delve into the mechanisms underlying the rhoifolin-mediated effects on colitis. To evaluate the impact of rhoifolin on ferroptosis in epithelial cells, several key indicators were measured, including mitochondrial morphology, colonic glutathione (GSH) levels, lipid peroxidation product contents, and ROS levels., Results: The results indicated that rhoifolin exhibited profound anti-colitis properties and effectively curbs ferroptosis in epithelial cells of mice subjected to DSS treatment. The RNA sequencing analysis further revealed that rhoifolin stimulated a remarkable upregulation of colonic cell migration-inducing protein (CEMIP) expression by approximately 2.4-fold in colitis-affected mice. Notably, depletion of CEMIP significantly blocked the rhoifolin-induced increase in the cystine transporter solute carrier family 7 member 11 (SLC7A11, from 1.9-fold to approximately 1.1-fold), as well as the elevation of cystine uptake (from 1.72-fold to 1.2-fold) and glutathione (GSH) biosynthesis (from 2.1-fold to 1.2-fold), and the suppression of epithelial ferroptosis (from 0.51-fold to 0.94-fold) in mice with colitis. Molecular docking investigations have pinpointed crucial amino acid residues within CEMIP, specifically His267, His289, and Phe265, as the primary interaction sites (docking score: -7.8 kcal/mol), facilitating the engagement of rhoifolin via hydrogen bonding interactions., Conclusion: Rhoifolin significantly mitigated DSS-induced colitis primarily through inhibiting epithelial ferroptosis. The activation of CEMIP by citrus-derived rhoifolin led to a notable upregulation of SLC7A11 expression, thereby enhanced cystine uptake and facilitated GSH biosynthesis, ultimately suppressed the occurrence of ferroptosis in epithelial cells., Competing Interests: Declarations. Conflict of interest: The authors declare no conflicts of interest. Ethical approval: The study was conducted following the guidelines of the National Institute of Health Guide for Care and Use of Laboratory Animals (Publication no. 85–23, revised 1985), and was approved by the Dalian Medical University Animal Care and Ethics Committee (No: AEE20047)., (© 2024. Springer-Verlag GmbH Germany, part of Springer Nature.)

Reactive oxygen species (ROS) are essential modulators of epigenetic modifications under abiotic stress. However, the mutual regulation mechanism of the two under cadmium (Cd) stress is unclear. In this work, we investigated this issue using Cd-stressed pakchoi seedlings treated with six epi-modification inhibitors (5-AC, RG108, TSA, CUDC101, AT13148, and H89) as experimental materials. The experimental data showed that Cd stress caused ROS accumulation and chromatin decondensation. Addition of low concentrations of epi-modification inhibitors increased histone acetylation modification levels, and effectively attenuated cell cycle arrest and DNA damage caused by Cd-induced ROS accumulation, where histone acetylation modification levels were co-regulated by histone acetyltransferase and deacetyltransferase gene transcription. Moreover, the addition of the antioxidant Thi enhanced this mitigating effect. Also, TSA addition at high concentrations could also increase Cd-induced ROS accumulation. Based on this, we propose that the ROS molecular pathway may be related to epigenetic regulation, and chromatin modification may affect ROS accumulation by regulating gene expression, providing a new perspective for studying the regulatory mechanism of epigenetic modification under abiotic stress., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Cao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Heat-resistant fungal conidia are a common source of contamination and can cause significant difficulties in producing spawns. Through the use of PCR method, Aspergillus tubingensis and Aspergillus flavus as common microbial contaminants found in wheat grain spawn were identified that had been sterilized at 120 ºc for 2 h. Since these conidia are highly resistant to standard sterilization techniques, alternative methods were used to treat them with NaOCl and cold plasma and evaluate their effectiveness in reducing contamination. Optical emission spectroscopy (OES) analysis of the plasma showed dominant emissions from the N 2 second positive system and N 2 + first negative system, while reactive oxygen species (ROS) spectral lines were undetected due to collision-induced quenching effects. Field Emission Scanning Electron Microscopy (FESEM) and Energy Dispersive X-ray Spectroscopy (EDXS) analyses revealed notable alterations in the elemental makeup of conidia surfaces, as evidenced by a marked rise in levels of Na, O, Cl (in the case of NaOCl treatment) and N (in the case of plasma treatment). The conidia size was reduced at lower levels of NaOCl, but with increased concentrations and plasma treatment, the conidia underwent rupture and, in some cases, pulverization. The research suggests that utilizing a combined approach can be highly effective in eliminating heat-resistant fungal conidia and drastically cutting down the sterilization time for producing wheat spawn to only 30 s., Competing Interests: Declarations. Competing interests: The authors declare no competing interests. Research involving plants: All authors comply with the IUCN Policy Statement on Research Involving Species at Risk of Extinction., (© 2024. The Author(s).)

The critical-sized bone defect resulting from trauma, tumor resection, and congenital deformity fails to undergo spontaneous healing due to its substantial size, while the ensuing inflammatory process and hypoxic environment further impede the regenerative process. Therefore, it has consistently presented a significant clinical challenge. In the present study, we incorporate a glycyrrhizic acid (GA)-functionalized hydrogel onto the surface of a Hydroxyapatite (Hap)-modified Polycaprolactone (PCL) scaffold to fabricate a composite scaffold. The composed scaffold showed favorable anti-inflammatory and antioxidative capabilities by modulating macrophage polarization and scavenging reactive oxygen species (ROS); the modification of Hap enhanced its osteogenic ability. An in vivo rat skull defect model confirmed that the composed scaffold efficiently promotes bone regeneration. In general, the composed scaffold with the ability of osteoimmune microenvironment regulation can effectively repair critical-sized bone defects. This strategy provides a promising method for the reconstruction of large segmental bone defects.

Photodynamic therapy has been developed as a promising treatment for malignant tumors, which inspires research into photosensitizers. However, the therapeutic efficacy of individual photosensitizers is often hampered by the physiological environment. The assembly of biological materials with synthetic molecules offers a strategy to enhance functionality while improving tolerance to varying physiological conditions. Herein, we present a biohybrid system for enhanced phototherapy efficacy through a simple two-step assembly process. Photoactive lipid nanoparticles were assembled based on synthesized conjugated molecules and lipophilic prodrugs, which were then modularly assembled with red blood cells (RBCs). Driven by hydrophobic and electrostatic interactions, hydrophobic conjugated molecules were efficiently incorporated into the RBCs, while lipophilic prodrugs were simultaneously inserted into the cell membranes. The engineered RBCs harnessed the natural oxygen transport capability, enabling the internal conjugated molecules to effectively produce reactive oxygen species (ROSs) even under oxygen-poor conditions. Meanwhile, the use of ROS-cleavable linkers in prodrugs enhanced drug release for chemotherapy, which is a perfect complement to photodynamic therapy. In vitro and in vivo experiments proved the improved phototherapy efficacy of the biohybrid system. Furthermore, the changes in aggregation directed Förster resonance energy transfer between conjugated molecules and fluorescent drugs provided a mechanism to track drug release from engineered RBCs. Therefore, the modular assembly of biohybrid systems can offer multiple functionalities required for phototherapy, on-demand drug release, and imaging.

Spinal cord injury (SCI) is a serious neurological disease that can result in paralysis. After SCI occurs, the blood-spinal cord barrier (BSCB) is disrupted, and permeability is transiently elevated. However, the permeability of the BSCB returns to normal over time, which prevents many drugs from being used in subsequent treatments. In this study, we designed a borneol-functionalized macrophage membrane encapsulating mesoporous selenium nanoparticles loaded with resveratrol (MSe-Res-BMMs) for SCI treatment. In vivo animal experiments and in vitro cell experiments demonstrated that MSe-Res-BMMs were able to protect neurons from ferroptosis by reducing ROS levels and increasing glutathione peroxidase-4 (GP x -4) activity. In addition, this treatment also reduced ROS-induced inflammation and apoptosis by decreasing the expression of inflammatory factor IL-1β and apoptotic factor Cleaved Caspase-3 at the site of injury. Therefore, MSe-Res-BMMs are expected to provide new therapeutic options for SCI treatment.

Exploring the interaction between black phosphorus (BP)-based hybrid systems and target proteins is of great significance for understanding the biological effects of 2D nanomaterials at the molecular level. Density functional theory (DFT) calculations revealed that different terminal groups of the azobenzene (AB) motif in BP@AB hybrids can affect the extent of interfacial charge transfer between the BP sheet and AB-derivatives, which determines the electrostatic interaction with proteins and hence biofunctions of BP@AB hybrids. With the advantage of AB modification, BP@AB hybrids displayed antitumor effects and induced production of cellular reactive oxygen species and apoptosis in cancer cells. Through the proteomics profiling, cellular ribosome and lipid metabolic processes were screened out as the target pathways of the BP@AB-NH 2 in HeLa cells, while the BP@AB-S-S-AB system mainly targets the ERBB and PPAR signaling pathways. Molecular docking simulations revealed that due to the positive charge, ribosomal pathway proteins enriched in negatively charged amino acids such as lysine and arginine are preferentially adsorbed and bound by BP@AB-NH 2 hybrids. Whereas for BP@AB-S-S-AB, receptors containing narrow and long pocket domains are more likely to bind with BP@AB-S-S-AB by van der Waals forces for the rod-like hybrids. Different biomolecule targeting and action modes of BP@AB hybrids have been rationalized by different electrostatic environments and matching of geometric configurations, shedding insight for designing efficient and targeted modification of a 2D nanomaterial-based strategy for cancer therapy.

Choroidal neovascularization (CNV) represents a hallmark of neovascular fundus diseases, including age-related macular degeneration and diabetic retinopathy. Traditional eyedrops have encountered formidable challenges in treating CNV, primarily due to their extremely poor intraocular bioavailability and potential adverse off-target effects. Herein, an ocular-permeable supramolecular prodrug eyedrop (Di-DAS/P-PCD) has been developed for the on-demand delivery of antiangiogenic agents in the oxidative microenvironment of CNV. The eyedrop nanoformulation is composed of cell-penetrating peptide-modified PEGylated cyclodextrin (P-PCD) and reactive oxygen species (ROS)-sensitive antiangiogenic dasatinib prodrug Di-DAS. In a laser-induced CNV mouse model, daily instillation of Di-DAS/P-PCD has achieved remarkable penetration into the choroid and significantly suppressed CNV growth while exhibiting a good biocompatibility profile. Our results highlight the potential of the supramolecular prodrug eyedrops as a versatile approach for the targeted treatment of CNV and other neovascular eye disorders.

Despite the use of surgical resection and chemotherapy in the clinical treatment of oral squamous cell carcinoma (OSCC), the 5-year survival rates of advanced patients are low. Therefore, more efficient strategies are urgently needed. Herein, a chemo/ferroptosis synergistic therapeutic system-DMEFe nanoparticles (NPs) is established for the treatment of OSCC. To create this system, the chemotherapeutic agent doxorubicin (DOX) was loaded into mesoporous silica nanoparticles and further coated with a pH-sensitive metal polyphenol (iron ion and epigallocatechin gallate). These nanoparticles displayed excellent pH-sensitive drug-control release properties, and the release ratio of DOX at pH 5.5 was twice as high than that at pH 7.4. Additionally, DMEF NPs were effectively taken up by the OSCC cell line SSC-25, which greatly impeded the proliferation of these cells. Notably, these nanoparticles increased the intracellular level of reactive oxygen species and effectively exhibited cytotoxity effects. The mechanistic results proved that DMEFe NPs regulated the expression of ferroptosis-related genes to induce ferroptosis of SSC-25 cells. Eventually, this chemo/ferroptosis therapeutic system exhibited remarkable antitumor effects and provided a novel strategy for the treatment of OSCC.

Stimuli-responsive nanoscale polymer-drug conjugates are one of the most promising alternatives in the realm of advanced therapeutics, rendering several characteristics such as spatio-temporal control over drug release, reduced off-target toxicity, enhanced bioavailability, and longer blood circulation time of the drug. Fostered by the aforementioned conceptualization, our quest to develop an ideal polymer-drug conjugate has originated the present investigation of developing a reactive oxygen species (ROS) and esterase-responsive self-assembled polymer-drug (chlorambucil, CBL) conjugate with biotin pendants (DP2) for cancer cell targeting, surrogating another antineoplastic drug, doxorubicin (DOX) via physical encapsulation (DP2@DOX). The ROS and esterase trigger not only released the covalently stitched CBL but also resulted in DOX release by dismantling the amphiphilic balance of the nanoaggregates. Biotinylation-mediated enhancement of cellular uptake of DP2@DOX was reflected in the synergistic anticancer activity of both the drugs (CBL and DOX) in HeLa cells (biotin receptor-positive cells) compared to HEK 293T cells (biotin receptor-negative cells). Furthermore, the selective internalization of the fluorophore-tagged DOX-loaded polymer (DP4@DOX) in HeLa cells compared to HEK 293T cells was confirmed by confocal microscopy and flow cytometry. In summary, the present investigation demonstrates a state-of-the-art self-assembled polymer-drug conjugate as a next-generation dual stimuli-responsive drug delivery vehicle.

There is an association between noise exposure and cognitive impairment, and noise may have a more severe impact on patients with Alzheimer's disease (AD) and mild cognitive impairment; however, the mechanisms need further investigation. This study used the classic AD animal model APP/PS1 mice to simulate the AD population, and C57BL/6J mice to simulate the normal population. We compared their cognitive abilities after noise exposure, analyzed changes in Cluster of Differentiation (CD) between the two types of mice using transcriptomics, identified the differential CD molecule: CD36 in APP/PS1 after noise exposure, and used its pharmacological inhibitor to intervene to explore the mechanism by which CD36 affects APP/PS1 cognitive abilities. Our study shows that noise exposure has a more severe impact on the cognitive abilities of APP/PS1 mice, and that the expression trends of differentiation cluster molecules differ significantly between C57BL/6J and APP/PS1 mice. Transcriptomic analysis showed that the expression of CD36 in the hippocampus of APP/PS1 mice increased by 2.45-fold after noise exposure (p < 0.001). Meanwhile, Western Blot results from the hippocampus and entorhinal cortex indicated that CD36 protein levels increased by approximately 1.5-fold (p < 0.001) and 1.3-fold (p < 0.05) respectively, after noise exposure in APP/PS1 mice. The changes in CD36 expression elevated oxidative stress levels in the hippocampus and entorhinal cortex, leading to a decrease in PI3K/AKT phosphorylation, which in turn increased M1-type microglia and A1-type astrocytes while reducing the numbers of M2-type microglia and A2-type astrocytes. This increased neuroinflammation in the hippocampus and entorhinal cortex, causing synaptic and neuronal damage in APP/PS1 mice, ultimately exacerbating cognitive impairment. These findings may provide new insights into the relationship between noise exposure and cognitive impairment, especially given the different expression trends of CD molecules in the two types of mice, which warrants further research., 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.)