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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.

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.)

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 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.

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]

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 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.)

Copyright of Journal of Chinese Institute of Food Science & Technology 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.)

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]

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]

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.)

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.

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.)

Heart failure (HF) is a clinical syndrome resulting from left ventricular systolic and diastolic dysfunction, leading to significant morbidity and mortality worldwide. Despite improvements in medical treatment, the prognosis of HF patients remains unsatisfactory, with high rehospitalization rates and substantial economic burdens. The heart, a high-energy-consuming organ, relies heavily on ATP production through oxidative phosphorylation in mitochondria. Mitochondrial dysfunction, characterized by impaired energy production, oxidative stress, and disrupted calcium homeostasis, plays a crucial role in HF pathogenesis. Additionally, inflammation contributes significantly to HF progression, with elevated levels of circulating inflammatory cytokines observed in patients. The interplay between mitochondrial dysfunction and inflammation involves shared risk factors, signaling pathways, and potential therapeutic targets. This review comprehensively explores the mechanisms linking mitochondrial dysfunction and inflammation in HF, including the roles of mitochondrial reactive oxygen species (ROS), calcium dysregulation, and mitochondrial DNA (mtDNA) release in triggering inflammatory responses. Understanding these complex interactions offers insights into novel therapeutic approaches for improving mitochondrial function and relieving oxidative stress and inflammation. Targeted interventions that address the mitochondria-inflammation axis hold promise for enhancing cardiac function and outcomes in HF patients., 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. Published by Elsevier B.V.)

Hexabromocyclododecane (HBCD) has been detected in animals and humans blood. As an environment contamination, HBCD damages tissues and organs in animals and humans and produces cytotoxicity. In current study, we explored the effect of HBCD on premature testicular aging in vivo and in vitro. In vivo, C57 mice (8-week-old) were used as model to estimate the effect of HBCD on premature testicular aging. The results showed that testes were premature aging through measuring several aging-related markers (such as p16 INK4a , hereafter p16; p21 CIP , hereafter p21) in response to HBCD exposure for 20 weeks. In addition, HBCD exposure can cause oxidative stress and inflammation. Further, mouse spermatogonial cells (GC-1spg cells) were premature senescence after HBCD exposure by the evaluation of cellular senescence marker molecules. Hence, GC-1spg cell line was applied for cell model to investigate the molecule mechanism by which HBCD cause premature testicular aging., Through eliminating Fe 2+ in senescent GC-1spg cells, cellular senescence was greatly alleviated. Thus, Fe 2+ was identified as the key driver molecule in HBCD-induced premature cellular senescence. Next, we found that elevated iron levels in HBCD-triggered senescent GC-1spg cells were due to Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy. Furthermore, our results revealed that HBCD-induced senescence was caused by Fe 2+ mediated oxidative stress. In summary, HBCD-induced premature testicular aging is dependent on NCOA4/Fe 2+ /ROS signaling molecule. The current study lays the foundation for further exploration of the effects of HBCD on reproductive toxicology., 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. Published by Elsevier B.V.)

Chondrocytes, known for their metabolic adaptability in response to varying stimuli, play a significant role in osteoarthritis (OA) progression. Glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the pentose phosphate pathway, has recently been found to upregulate in OA chondrocyte. However, the exact role of G6PD in temporomandibular joint osteoarthritis (TMJOA) and its effect on chondrocyte function remains unclear. In present study, we induced OA-like conditions in the rat temporomandibular joint via occlusal disharmony (OD), noting a marked increase in G6PD expression in the condylar cartilage. Our data show that G6PD knockdown in mandibular condylar chondrocytes (MCCs) reduces the expression of catabolic enzymes (e.g., MMP3, MMP13) and inflammatory cytokines (e.g., IL6) induced by IL-1β. G6PD knockdown also mitigates IL-1β-induced upregulation of ERK, JNK, and p38 phosphorylation and reduces reactive oxygen species (ROS) levels by decreasing the nicotinamide adenine dinucleotide phosphate (NADPH) and NADPH oxidases 4 (NOX4) mRNA expression. In summary, G6PD appears to regulate the inflammatory state of condylar chondrocytes via the NOX-ROS-MAPK axis, highlighting its potential as a therapeutic target for TMJOA., 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. Published by Elsevier B.V.)

Ferroptosis is a novel iron-dependent form of cell death discovered in recent years, characterized by the accumulation of ferrous iron, the production of reactive oxygen species (ROS) through the Fenton reaction, and lipid peroxidation, ultimately leading to the disruption of the antioxidant system and cell membrane damage. Extensive research has found that ferroptosis plays a significant role in regulating tumor cell immune evasion, tumor development, and remodeling the tumor microenvironment. Small Extracellular vesicles (sEVs), carrying various bioactive molecules (ncRNA, DNA, proteins), are key nanoscale mediators of intercellular communication. Increasing evidence confirms that EVs can regulate the ferroptosis pathway in tumors, promoting tumor cell immune evasion and reshaping the tumor microenvironment. This article aims to comprehensively review the key mechanisms by which sEVs mediate ferroptosis in cancer and provide new insights into targeting tumor immunotherapy., 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.)

Cancer immunotherapies are ineffective in nonresponding patients due to absence of immune responses. Here, we identified that dihydroartemisinin (DHA) induced immunogenic cell death (ICD) in hepatocellular carcinoma (HCC), proved by release or surface expose of damage-associated molecular patterns and in vivo protective vaccine activity. Mechanistically, DHA can inhibit cyclin-dependent kinases (CDKs), leading to a buildup of intracellular reactive oxygen species (ROS), which induces immunogenic cell death. In both Hepa1-6 and H22 tumor bearing mice, DHA exerted anti-tumor activity through increasing tumor-infiltrating CD8 + T cells with expression of activation makers (CD25 and CD69), secretion of intracellular cytokines (IFN-γ and TNF-α) and activated dendritic cells expressing MHCⅡ, CD80 and CD86. In hepa1-6 tumor bearing mice, DHA decreased immunosuppressive myeloid-derived suppressor cells. Furthermore, DHA enhanced the anti-PD-1 antibody and chimeric antigen receptor (CAR) T cell-mediated tumor suppression through recruitment and activation of endogenous CD8 + T cells. Overall, we demonstrated that by inhibiting CDKs, DHA can remodel tumor micro-environment to amplify anti-tumor immune responses in HCC. These findings provide a promising therapy option for HCC patients., (Copyright © 2024. Published by Elsevier B.V.)

Platycodin D (PLD), a major bioactive component of triterpene saponins found in Platycodon grandiflora, is renowned for its anti-inflammatory and antioxidant properties. This study aims to explore the protective effects and regulatory mechanisms of PLD in an LPS-induced inflammation injury model of BEAS-2B cells. Initially, PLD was identified from Platycodon grandiflora extracts utilizing UPLC-Q-TOF-MS/MS technology. The effects of PLD on the viability, morphology, ROS levels, and inflammatory factors of LPS-induced BEAS-2B cells were then investigated. The results showed that PLD significantly alleviated LPS-induced oxidative stress and inflammatory injury. Further analysis revealed that PLD positively influenced apoptosis levels, mitochondrial morphology, and related gene expression, indicating its potential to mitigate LPS-induced apoptosis and alleviate mitochondrial dysfunction. Using molecular docking technology, we predicted the binding sites of PLD with mitochondrial autophagy protein. Gene expression levels of autophagy-related proteins were measured to determine the impact of PLD on mitochondrial autophagy. Additionally, the study examined whether the mitochondrial autophagy agonists rapamycin (RAPA) could modulate the upregulation of inflammasome-related factors NLRP3 and Caspase-1 in LPS-induced BEAS-2B cells. This was done to evaluate the regulator mechanisms of PLD in pulmonary inflammatory injury. Our findings suggest that PLD's mechanism of action involves the regulation of mitochondrial autophagy, which in turn modulates inflammatory responses., 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.)

Purpose: In developed countries, endometrial cancer (EC) is the most prevalent gynecological cancer and its occurrence is associated with chronic inflammation. ATP5F1D is a subunit of ATP synthase (complex V), as well as the important component of mitochondrial electron transport chain (ETC). ETC play compelling roles in carcinogenesis. To date, little is known about the role of ATP5F1D in EC., Methods: ATP5F1D expression was identified in EC tissues and EC cell lines. We evaluated the influence of ATP5F1D on clinical features and prognosis based on TCGA database. The effects of ATP5F1D in EC malignant progression by applying loss-of-function assays in KLE and Ishikawa cell lines were detected by EdU, CCK-8, wound healing, Transwell, and flow cytometry assays. Additionally, electron microscope, LDH release, ELISA, mitochondrial ROS measurement, and Immunofluorescence were performed to demonstrate ATP5F1D can affect the pyroptosis of EC. To observe the anti-tumor effect on ATP5F1D silencing, we established an in vivo human endometrial tumor model using nude mice., Results: ATP5F1D expression was significantly upregulated in EC and was associated with favorable prognosis. ATP5F1D knockdown inhibited the proliferation, invasion, and migration of EC cells. Similarly, in nude mice, ATP5F1D knockdown suppressed the growth EC cells. Knocking down ATP5F1D lead to decrease the production of mitochondrial ROS (mtROS) and inhibited pyroptosis of EC cells., Conclusion: Downregulation of ATP5F1D as a new therapeutic strategy that could mediate pyroptosis via suppressing mtROS/NLRP3/caspase-1/GSDMD pathway to inhibit EC progression., 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.)

PANoptosis is manifested with simultaneous activation of biomarkers for both pyroptotic, apoptotic and necroptotic signaling via the molecular platform PANoptosome and it is involved in pathologies of various inflammatory diseases including hemophagocytic lymphohistiocytosis (HLH). Scutellarin is a flavonoid isolated from herbal Erigeron breviscapus (Vant.) Hand.-Mazz. and has been shown to possess multiple pharmacological effects, but it is unknown whether scutellarin has any effects on PANoptosis and related inflammatory diseases. In this study, we found that scutellarin inhibited cell death in bone marrow-derived macrophages (BMDMs) and J774A.1 cells treated with TGF-β-activated kinase 1 (TAK1) inhibitor 5Z-7-oxozeaenol (OXO) plus lipopolysaccharide (LPS), which has been commonly used to induce PANoptosis. Western blotting showed that scutellarin dose-dependently inhibited the activation biomarkers for pyroptotic (Caspase-1p10 and GSDMD-NT), apoptotic (cleaved Casp3/8/9 and GSDME-NT), and necroptotic (phosphorylated MLKL) signaling. The inhibitory effect of scutellarin was unaffected by NLRP3 or Caspase-1 deletion. Interestingly, scutellarin blocked the assembly of PANoptosome that encompasses ASC, RIPK3, Caspase-8 and ZBP1, suggesting its action on upstream signaling. Consistent with this, scutellarin inhibited mitochondrial damage and mitochondrial reactive oxygen species (mtROS) generation in cells treated with OXO+LPS. Further, mito-TEMPO that can scavenge mtROS significantly inhibited OXO+LPS-induced PANoptotic cell death. In line with the in vitro results, scutellarin markedly alleviated systemic inflammation, multiple organ injury, and activation of PANoptotic biomarkers in mice with HLH. Collectively, our data suggest that scutellarin can inhibit PANoptosis by suppressing mitochondrial damage and mtROS generation and thereby mitigating multiple organ injury in mice with inflammatory disorders., 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. Published by Elsevier B.V.)

Innate immunity serves as the first line of host defense in the body against pathogenic infections or malignant diseases. Reactive oxygen species (ROS), as vital signaling mediators, can efficiently elicit innate immune responses to oxidative-related stress or damage. In the era of nanomedicine, various immunostimulatory nanosystems have been extensively designed and synthesized to elicit immune responses for the immunotherapy of cancer or infectious diseases. In this review, we emphasize that ROS derived from nanosystems regulates innate immune cells to potentiate immunotherapeutic efficacy, such as primarily dendritic cells, macrophages, or natural killer cells. Meanwhile, we also summarize the pathway of ROS generation triggered by exogenous nanosystems in innate immune cells of DCs, macrophages, and NK cells., 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.)

Invasion and adhesion of neutrophils into tissues and their concomitant secretion play an important role in the development of vascular pathologies, including abdominal aortic aneurysm (AAA). Chronic administration of angiotensin II is used to initiate AAA formation in mice. The role of aldosterone in this process is being studied. We conducted for the first time a complex comparative study of the effects of angiotensin II and aldosterone on the adhesion of human neutrophils to fibronectin and the concomitant secretion of proteins, free amino acids as well as reactive oxygen (ROS) and nitrogen (NO) species. Neither angiotensin II nor aldosterone affected the attachment of neutrophils to fibronectin and the concomitant production of ROS. We showed for the first time that aldosterone stimulated the release of amino acid hydroxylysine, a product of lysyl hydroxylase, the activity of which is positively correlated with cell invasiveness. Aldosterone also initiates the secretion of matrix metalloproteinase 9 (MMP-9) and cathepsin G, which may reorganize the extracellular matrix and stimulate the recruitment and adhesion of neutrophils to the aortic walls. Angiotensin II did not affect protein secretion. It may contribute to neutrophil-induced vascular injury by inhibiting the production of NO or by increasing the secretion of isoleucine. Our results suggest that it is aldosterone-induced neutrophil secretion that may play a significant role in neutrophil-induced vascular wall destruction in angiotensin II-induced AAA or other vascular complications., 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.)

Metabolomics significantly impacts drug discovery and precise disease management. This study meticulously assesses the metabolite profiles of cells treated with Crocin, Dexamethasone, and mesenchymal stem cells (MSCs) under oxidative stress induced by 2-chloroethyl ethyl sulfide (CEES). Gas chromatography/mass spectrometry (GC/MS) analysis unequivocally identified substantial changes in 37 metabolites across the treated groups. Notably, pronounced alterations were observed in pathways associated with aminoacyl-tRNA biosynthesis and the metabolism of aspartate, serine, proline, and glutamate. These findings demonstrate the potent capacity of the analyzed treatments to effectively reduce inflammation, mitigate reactive oxygen species production, and enhance cell survival rates. SIGNIFICANCE., Competing Interests: Declaration of competing interest The authors report no conflicts of interest., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Acetyl tripeptide-30 citrulline, a commercialized bio-active peptide, is widely used in anti-wrinkle formulations. Volunteer-based tests have demonstrated that topical application of products containing acetyl tripeptide-30 citrulline significantly reduces the visibility of stretch marks. However, there is still a lack of research dedicated to systematically and holistically evaluating its cosmetic properties and elucidating its mechanisms of action. In this study, we assessed the cosmetic potential of acetyl tripeptide-30 citrulline using human immortalized keratinocytes (HaCaT) and mouse embryonic fibroblasts (3T3). Our findings reveal that acetyl tripeptide-30 citrulline exhibits anti-inflammatory and antioxidant activities in skin cells, particularly effective against the inflammatory markers cyclooxygenase-2 (COX2), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), and the extent of inhibition of reactive oxygen species (ROS) production ranged from 95 % to 340 %. Moreover, acetyl tripeptide-30 citrulline specifically up-regulates Collagen IV and down-regulates matrix metalloproteinase-9 (MMP9), enhances the expression of skin barrier proteins transglutaminase 1 (TGM1) and filaggrin (FLG), thereby demonstrating its reparative capabilities. Additionally, acetyl tripeptide-30 citrulline increases the expression of the water channel protein aquaporin 3 (AQP3), thus improving skin hydration function. These results substantiate the previously proclaimed cosmetic attributes of acetyl tripeptide-30 citrulline and support its efficacy as an anti-aging agent in dermatological applications., 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 Author(s). Published by Elsevier B.V. All rights reserved.)

Minocycline, a broad-spectrum tetracycline antibiotic, has been shown to possess anti-inflammatory and antioxidative effects in various neurodegenerative diseases. However, its specific effects on retinitis pigmentosa (RP) have not been thoroughly investigated. Therefore, the objective of this study was to explore the potential role of minocycline in treating RP. In this investigation, we used rd1 to explore the antioxidant effect of minocycline in RP. Minocycline therapy effectively restored retinal function and structure in rd1 mice at 14 days postnatal. Additionally, minocycline inhibited the activation of microglia. Moreover, RNA sequencing analysis revealed a significant downregulation in the expression of mitochondrial genes within the retina of rd1 mice. Further KEGG and GO pathway analysis indicated impaired oxidative phosphorylation and electron transport chain processes. TEM confirmed the presence of damaged mitochondria in photoreceptors, while JC-1 staining demonstrated a decrease in mitochondrial membrane potential, accompanied by an increase in mitochondrial reactive oxygen species (ROS) levels. However, treatment with minocycline successfully reversed the abnormal expression of mitochondrial genes and reduced the levels of mitochondrial ROS, thereby providing protection against photoreceptor degeneration. Collectively, minocycline demonstrated the ability to rescue photoreceptor cells in RP by effectively modulating mitochondrial homeostasis and subsequently inflammation. These findings hold significant implications for the development of potential therapeutic strategies for RP., 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 random flap is one of the commonly used techniques for tissue defect repair in surgery and orthopaedics, however the risk of ischaemic necrosis at the distal end of the flap limits its size and clinical application. Metformin (Met) is a first-line medication in the treatment of type 2 diabetes, with additional effects such as anti-tumor, anti-aging, and neuroprotective properties. In this study, we aimed to investigate the biological effects and potential mechanisms of Met in improving the survival of random skin flaps. Twenty-four male Sprague-Dawley rats and 12 male C57BL/6J mice underwent McFarlane flap surgery and divided into control (Ctrl) and Met groups (100 mg/kg). The survival rate of the flap were evaluated on day 7. Angiography, Laser doppler blood flow imaging, and H&E staining were used to assess blood flow supply and the levels of microvascular density. Then, reactive oxygen species (ROS) and malondialdehyde (MDA) levels, and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured by test kits. Immunohistochemistry analysis was conducted to evaluate the expression of Vascular Endothelial Growth Factor A (VEGFA), Vascular endothelial cadherin (VE-cadherin) and CD31. Rats and mice in the Met group exhibited higher flap survival rate, microcirculatory flow, and higher expression levels of VEGFA and VE-cadherin compared with the Ctrl group. In addition, the level of oxidative stress was significantly lower in the met group. And then we demonstrated that the human umbilical vein endothelial cells (HUVECs) treated with Met can alleviate tert-butyl hydroperoxide (TBHP)-stimulated cellular dysfunction and oxidative stress injury. Mechanistically, Met markedly stimulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1), and promoted Nrf2 nuclear translocation. Silencing of Nrf2 partially abolished the antioxidant and therapeutic effects of Met. In summary, our data have confirmed that Met has a positive effect on flap survival and reduces necrosis. The mechanism of action involves the regulation of the Nrf2/HO-1 signaling pathway to combat oxidative stress and reduce damage., 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.)

Global warming has been shown to harmfully affect symbiosis between Symbiodiniaceae and other marine invertebrates. When symbiotic dinoflagellates (the genus Breviolum) were in vitro exposed to acute heat stress of +7 °C for a period of 5 days, the results revealed the negative impact on all physiological and other cellular parameters measured. Elevated temperatures resulted in a severe reduction in algal density of up to 9.5-fold, as well as pigment concentrations, indicating the status of the physiological stress and early signs of photo-bleaching. Reactive oxygen species (ROS) were increased in all heated dinoflagellate cells, while the antioxidant-reduced glutathione levels initially dropped on day one but increased under prolonged temperature stress. The cell viability parameters were reduced by 97 % over the heating period, with an increased proportion of apoptotic and necrotic cells. Autofluorescence (AF) for Cy5-PE 660-20 was reduced from 1.7-fold at day 1 to up to 50-fold drop at the end of heating time, indicating that the AF changes were highly sensitive to heat stress and that it could be an extremely sensitive tool for assessing the functionality of algal photosynthetic machinery. The addition of the drug 5-AZA-2'-deoxycytidine (5-AZA), which inhibits DNA methylation processes, was assessed in parallel and contributed to some alterations in algal cellular stress response. The presence of drug 5-AZA combined with the temperature stress had an additional impact on Symbiodiniaceae density and cell complexity, including the AF levels. These variations in cellular stress response under heat stress and compromised DNA methylation conditions may indicate the importance of this epigenetic mechanism for symbiotic dinoflagellate thermal tolerance adaptability over a longer period, which needs further exploration. Consequently, the increased ROS levels and changes in AF signals reported during ongoing heat stress in dinoflagellate cells could be used as early stress biomarkers in these microalgae and potentially other photosynthetic species., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Chromium (Cr) poses a high ecological risk, however the toxic mechanisms of Cr in different valence states to soil organisms at cellular and molecular levels are not exactly. In this study, the Eisenia fetida coelomocytes and Cu/Zn-superoxide dismutase (Cu/Zn-SOD) were chosen as the target subjects to investigate the effects and mechanisms of cellular toxicity induced by Cr(VI) and Cr(III). Results indicated that Cr(VI) and Cr(III) significantly reduced the coelomocytes viability. The level of reactive oxygen species (ROS) was markedly increased after Cr(VI) exposure, which finally reduced antioxidant defense abilities, and induced lipid peroxidation and cellular membrane damage in earthworm coelomocytes. However, Cr(III) induced lower levels of oxidative stress and cellular damage with respect to Cr(VI). From a molecular perspective, the binding of both Cr(VI) and Cr(III) with Cu/Zn-SOD resulted in protein backbone loosening and reduced β-Sheet content. The Cu/Zn-SOD showed fluorescence enhancement with Cr(III), whereas Cr(VI) had no obvious effect. The activity of Cu/Zn-SOD continued to decrease with the exposure of Cr. Molecular docking indicated that Cr(III) interacted more readily with the active center of Cu/Zn-SOD. Our results illustrate that oxidative stress induced by Cr(VI) and Cr(III) plays an important role in the cytotoxic differences of Eisenia fetida coelomocytes and the binding of Cr with Cu/Zn-SOD can also affect the normal structures and functions of antioxidant defense-associated protein., 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 DEAD-box family is the largest family of RNA helicases (RHs), playing crucial roles in RNA metabolism and plant stress resistance. In this study, we report that an RNA helicase, RH12, positively regulates plant salt tolerance, as rh12 knockout mutants exhibit heightened sensitivity to salt stress. Further analysis indicates that RH12 is involved in the abscisic acid (ABA) response, as rh12 knockout mutants show increased sensitivity to ABA. Examination of reactive oxygen species (ROS) revealed that RH12 helps inhibit ROS accumulation under salt stress during seed germination. Additionally, RH12 accelerates the degradation of specific germination-related transcripts. In conclusion, our results demonstrate that RH12 plays multiple roles in the salt stress response in Arabidopsis., Competing Interests: Declaration of competing interest All authors disclosed no relevant relationships., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Oxygen (O 2 ) metabolism plays a critical role in cornea wound healing, regeneration, and homeostasis; however, the underlying spatiotemporal mechanisms are poorly understood. Here we used an optical sensor to profile O 2 flux in intact and wounded corneas of mouse eyes. Intact corneas have unique centrifugal O 2 influx profiles, smallest flux at the cornea center, and highest at the limbus. Following cornea injury, the O 2 influx profile presents three distinct consecutive phases: a "decreasing" phase from 0 to 6 h, a "recovering" phase from 12 to 48 h, and a 'peak' phase from 48 to 72 h, congruent to previously described healing phases. Immediately after wounding, the O 2 influx drops at wound center and wound edge but does not change significantly at the wound side or limbus. Inhibition of reactive oxygen species (ROS) in the decreasing phase significantly reduces O 2 influx, decreases epithelial migration and consequently delays healing. The dynamics of O 2 influx show a positive correlation with cell proliferation at the wound side, with significantly increased proliferation at the peak phase of O 2 influx. This study elucidates the spatiotemporal O 2 dynamics in both intact and wounded rodent cornea and shows the crucial role of O 2 dynamics in regulating cell migration and proliferation through ROS metabolism, ultimately contributing to wound healing. These results demonstrate the usefulness of the micro-optrode in the characterization of spatiotemporal O 2 dynamics. Injury-induced changes in O 2 metabolism and ROS production modulate O 2 dynamics at wound and control cell migration and proliferation, both essential for proper wound healing., (© 2024 The Author(s). The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.)

Aflatoxin B1 (AFB1) is recognized as the most toxic mycotoxin, widely present in nature and known to specifically target the liver, leading to severe consequences to animal and human health. The mechanisms underlying AFB1-induced hepatotoxicity involve oxidative stress and apoptosis. Radix Bupleuri (RB) and its extracts (RBE), traditional Chinese herbs with a rich history spanning over 2000 years, have been reported to possess hepatoprotective properties. Nevertheless, the impact of RBE on AFB1-induced liver injury remains to be fully elucidated. The current study utilized Pekin ducks as experimental models to explore the effects of RBE on AFB1-induced liver injury both in vitro and in vivo. In vitro findings indicated that RBE mitigated AFB1-induced cytotoxicity, improved primary duck hepatocytes (PDHs) morphology, and reduced intracellular reactive oxygen species (ROS) levels. In vivo experiments demonstrated that: I) RBE alleviated the growth inhibitory caused by AFB1, as evidenced by improved final body weight and weight gain. II) AFB1 led to significant alterations in serum biochemical parameters (AST, ALT, TP, and ALB) and liver lesions attenuated by RBE supplementation at 2.5 g/kg. III) RBE significantly mitigated oxidative stress induced by AFB1. IV) AFB1-induced changes in mRNA and protein levels associated with oxidative stress and apoptosis were counteracted by RBE. In conclusion, our results suggest that RBE offers protection against AFB1-induced liver injury in ducks, primarily through its antioxidative and anti-apoptotic properties. These findings indicate the potential of RBE in preventing and treating AFB1 poisoning., 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.)

Famoxadone is a chiral fungicide frequently found in the environment and agricultural products. However, the health risks of famoxadone enantiomers are not well understood. This study investigated the stereoselective cytotoxicity and metabolic behavior of famoxadone enantiomers in mammals. Results showed that R-famoxadone was 1.5 times more toxic to HepG2 cells than S-famoxadone. R-famoxadone induced more pronounced ferroptosis compared to S-famoxadone. It caused greater upregulation of genes related to iron transport and lipid peroxidation, and greater downregulation of genes related to peroxide clearance. Furthermore, R-famoxadone induced more severe lipid peroxidation and reactive oxygen species (ROS) accumulation through ACSL4 activation and GPX4 inhibition. Additionally, the bioavailability of R-famoxadone in mice was six times higher than that of S-famoxadone. Liver microsome assays, cytochrome P450 (CYP450) inhibition assays, human recombinant CYP450 assays, and molecular docking suggested that the lower binding affinities of CYP2C8, CYP2C19, and CYP2E1 for R-famoxadone caused its preferential accumulation. Overall, R-famoxadone poses a higher risk than S-famoxadone due to its greater cytotoxicity and persistence. This study provides the first evidence of ferroptosis-induced stereoselective toxicity, offering insights for the comprehensive health risk assessment of chiral famoxadone and valuable references for the application of high-efficiency, low-risk pesticide enantiomers., 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.)

Reactive oxygen species (ROS) are widely considered to the effective therapeutics for fighting bacterial infections especially those associated with biofilm. However, biofilm microenvironments including hypoxia, limited H 2 O 2 , and high glutathione (GSH) level seriously limit the therapeutic efficacy of ROS-based strategies. Herein, we have developed an acidic biofilm microenvironment-responsive antibacterial nanoplatform consisting of copper-dopped bovine serum albumin (CBSA) loaded with copper peroxide (CuO 2 ) synthesized in situ and indocyanine green (ICG). The three-in-one nanotherapeutics (CuO 2 /ICG@CBSA) are capable of releasing Cu 2+ and H 2 O 2 in a slightly acidic environment, where Cu 2+ catalyzes the conversion of H 2 O 2 into hydroxyl radical (•OH) and consumes the highly expressed GSH to disrupt the redox homeostasis. With the assistance of an 808 nm laser, the loaded ICG not only triggers the production of singlet oxygen ( 1 O 2 ) by a photodynamic process, but also provides photonic hyperpyrexia that further promotes the Fenton-like reaction for enhancing •OH production and induces thermal decomposition of CuO 2 for the O 2 -self-supplying 1 O 2 generation. The CuO 2 /ICG@CBSA with laser irradiation demonstrates photothermal-augmented multi-mode synergistic bactericidal effect and is capable of inhibiting biofilm formation and eradicating the biofilm bacteria. Further in vivo experiments suggest that the CuO 2 /ICG@CBSA can effectively eliminate wound infections and accelerate wound healing. The proposed three-in-one nanotherapeutics with O 2 /H 2 O 2 -self-supplied ROS generating capability show great potential in treating biofilm-associated bacterial infections. STATEMENT OF SIGNIFICANCE: Here, we have developed an acidic biofilm microenvironment-responsive nanoplatform consisting of copper-dopped bovine serum albumin (CBSA) loaded with copper peroxide (CuO 2 ) synthesized in situ and indocyanine green (ICG). The nanotherapeutics (CuO 2 /ICG@CBSA) are capable of releasing Cu 2+ and H 2 O 2 in an acidic environment, where Cu 2+ catalyzes the conversion of H 2 O 2 into •OH and consumes the overexpressed GSH to improve oxidative stress. With the aid of an 808 nm laser, ICG provides photonic hyperpyrexia for enhancing •OH production, and triggers O 2 -self-supplying 1 O 2 generation. CuO 2 /ICG@CBSA with laser irradiation displays photothermal-augmented multi-mode antibacterial and antibiofilm effect. Further in vivo experiments prove that CuO 2 /ICG@CBSA effectively eliminates wound infection and promotes wound healing. The proposed three-in-one nanotherapeutics show great potential in treating biofilm-associated bacterial infections., 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 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.)

Immunotherapy can enhance primary tumor efficacy, restrict distant growth, and combat lung metastasis. Unfortunately, it remains challenging to effectively activate the immune response. Here, tertiary butyl, methoxy, and triphenylamine (TPA) were utilized as electron donors to develop multifunctional photosensitizers (PSs). CNTPA-TPA, featuring TPA as the donor (D) and cyano as the acceptor (A), excelled in reactive oxygen species (ROS) generation due to its smaller singlet-triplet energy gap (ΔE S-T ) and larger spin-orbit coupling constant (SOC). Additionally, cyano groups reacted with glutamate (Glu) and glutathione (GSH), reducing intracellular GSH levels. This not only enhanced PDT efficacy but also triggered redox dyshomeostasis-mediated ferroptosis. The positive effects of photodynamic therapy (PDT) and ferroptosis promoted immunogenic cell death (ICD) and immune activation. By further combining anti-programmed cell death protein ligand-1 (anti-PD-L1) antibody, the powerful treatments of ferroptosis-assisted photodynamic immunotherapy significantly eradicated the primary tumors, inhibited the growth of distant tumors, and suppressed lung metastasis. In this study, a three-pronged approach was realized by single-component CNTPA-TPA, which simultaneously served as metal-free ferroptosis inducers, type-I photosensitizers, and immunologic adjuvants for near-infrared fluorescence imaging (NIR FLI)-guided multimodal phototheranostics of tumor. STATEMENT OF SIGNIFICANCE: (1) CNTPA-TPA shared the smallest singlet-triplet energy gap and the largest spin-orbit coupling constant, which boosted intersystem crossing for efficient type-I photodynamic therapy (PDT); (2) Special reactions between cyano groups with glutamate and glutathione in mild conditions restricted the biosynthesis of intracellular GSH. GSH-depletion efficiently induced glutathione peroxidase 4 inactivation and lipid peroxide, resulting in ferroptosis of tumor cells; (3) The combination treatments of ferroptosis-assisted photodynamic immunotherapy induced by single-component CNTPA-TPA with the participation of anti-PD-L1 antibody resulted in increased T-cell infiltration and profound suppression of both primary and distant tumor growth, as well as lung metastasis., 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 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.)

Exploring highly efficient ultrasound-triggered catalysts is pivotal for various areas. Herein, we presented that Ba 2+ doped brookite TiO 2 nanorod (TiO 2 : Ba) with polarization-induced charge separation is a candidate. The replacement of Ba 2+ for Ti 4+ not only induced significant lattice distortion to induce polarization but also created oxygen vacancy defects for facilitating the charge separation, leading to high-efficiency reactive oxygen species (ROS) evolution in the piezo-catalytic processes. Furthermore, the piezocatalytic ability to degrade dye wastewater demonstrates a rate constant of 0.172 min -1 and achieves a 100 % antibacterial rate at a low dose for eliminating E. coli. This study advances that doping can induce piezoelectricity and reveals that lattice distortion-induced polarization and vacancy defects engineering can improve ROS production, which might impact applications such as water disinfection and sonodynamic therapy., 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.)

Ethnopharmacological Relevance: Various components of Lonicera japonica Thunb. (LJT) exhibit pharmacological activities, including anti-inflammatory and antioxidant effects. Nevertheless, the relationship between LJT and ferroptosis remains largely unexplored., Aim of the Study: The purpose of this research was to look into the role of LJT in regulating LPS-induced ferroptosis in ALI and to compare the effects of different parts of LJT., Materials and Methods: We established a mice ALI model by treating with LPS. Administered mice with different doses of Lonicerae Japonicae Flos (LJF), Lonicera Japonica Leaves (LJL) and Lonicerae Caulis (LRC) extracts, respectively. The levels of IL-6, IL-1β, TNF-α, IL-4, IL-10, and PGE2 in bronchoalveolar lavage fluid (BALF) were measured using enzyme-linked immunosorbent assay. Furthermore, the concentrations of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS), and total ferrous ions (Fe 2+ ) in lung tissues were evaluated. Hematoxylin and eosin staining was conducted to examine the morphological structure of lung tissues. Transmission electron microscopy was used to investigate the ultrastructural morphology of mitochondria. Furthermore, the effects of LJT were evaluated via immunohistochemical staining, western blotting, and quantitative real-time polymerase chain reaction analyses. Finally, employing molecular docking and molecular dynamics research techniques, we aimed to identify crucial components in LJT that might inhibit ferroptosis by targeting nuclear factor erythroid 2-related factor 2 (Nrf2) and glutathione peroxidase 4 (GPX4)., Results: We observed that pretreatment with LJT significantly mitigated LPS-induced lung injury and suppressed ferroptosis. This was supported by reduced accumulation of pro-inflammatory cytokines, ROS, MDA, and Fe 2+ , along with increased levels of anti-inflammatory cytokines, SOD, GSH, Nrf2, and GPX4 in the lung tissues of ALI mice. Luteolin-7-O-rutinoside, apigenin-7-O-rutinoside, and amentoflavone in LJT exhibit excellent docking effects with key targets of ferroptosis, Nrf2 and GPX4., Conclusions: Pretreatment with LJT may alleviate LPS-induced ALI, possibly by suppressing ferroptosis. Our initial results indicate that LJT activates the Nrf2/GPX4 axis, providing protection against ferroptosis in ALI. This finding offers a promising therapeutic candidate for ALI treatment., 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.)

Organophosphate flame retardants 2-ethylhexyldiphenyl phosphate (EHDPP) and cadmium (Cd) are ubiquitous in environmental matrices, and dermal absorption is a major human exposure pathway. However, their detrimental effects on the human epidermis remain largely unknown. In this study, human keratinocytes (HaCaT cells) were employed to examine the toxicity and underlying mechanisms of co-exposure to EHDPP and Cd. Their influence on cell morphology and viability, oxidative damage, apoptosis, and tight junction were determined. The results showed that co-exposure decreased cell viability by >40 %, induced a higher level of oxidative damage by increasing the generation of reactive oxygen species (1.3 folds) and inhibited CAT (79 %) and GPX (90 %) activities. Moreover, Cd exacerbated EHDPP-induced mitochondrial disorder and cellular apoptosis, which was evidenced by a reduction in mitochondrial membrane potential and an elevation of cyt-c and Caspase-3 mRNA expression. In addition, greater loss of ZO-1 immunoreactivity at cellular boundaries was observed after co-exposure, indicating skin epithelial barrier function disruption, which may increase the human bioavailability of contaminants via the dermal absorption pathway. Taken together, oxidative damage, cell apoptosis, and tight junction disruption played a crucial role in EHDPP + Cd triggered cytotoxicity in HaCaT cells. The detrimental effects of EHDPP + Cd co-exposure were greater than individual exposure, suggesting the current health risk assessment or adverse effects evaluation of individual exposure may underestimate their perniciousness. Our data imply the importance of considering the combined exposure to accurately assess their health implication., 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.)

Organophosphate esters (OPEs) are one of the emerging environmental threats, causing the hazard to ecosystem safety and human health. Yet, the toxic effects and metabolic response mechanism after Escherichia coli (E.coli) exposed to TDCIPP and TEHP is inconclusive. Herein, the levels of SOD and CAT were elevated in a concentration-dependent manner, accompanied with the increase of MDA contents, signifying the activation of antioxidant response and occurrence of lipid peroxidation. Oxidative damage mediated by excessive accumulation of ROS decreased membrane potential and inhibited membrane protein synthesis, causing membrane protein dysfunction. Integrative analyses of GC-MS and LC-MS based metabolomics evinced that significant perturbation to the carbohydrate metabolism, nucleotide metabolism, lipids metabolism, amino acid metabolism, organic acids metabolism were induced following exposure to TDCIPP and TEHP in E.coli, resulting in metabolic reprogramming. Additionally, metabolites including PE(16:1(5Z)/15:0), PA(17:0/15:1(9Z)), PC(20:2(11Z,14Z)/12:0), LysoPC(18:3(6Z,9Z,12Z)/0:0) were significantly upregulated, manifesting that cell membrane protective molecule was afforded by these differential metabolites to improve permeability and fluidity. Overall, current findings generate new insights into the molecular toxicity mechanism by which E.coli respond to TDCIPP and TEHP stress and supply valuable information for potential ecological risks of OPEs on aquatic ecosystems., 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.)

Nanomedicines that combine reactive oxygen species (ROS)-responsive polyprodrug and photodynamic therapy have shown great potential for improving treatment efficacy. However, the consumption of ROS by overexpressed glutathione in tumor cells is a major obstacle for achieving effective ROS amplification and prodrug activation. Herein, we report a polyprodrug-based nanoparticle that can realize ROS amplification and cascaded drug release. The nanoparticle can respond to the high level of hydrogen peroxide in tumor microenvironment, achieving self-destruction and release of quinone methide. The quinone methide depletes intracellular glutathione and thus decreases the antioxidant capacity of cancer cells. Under laser irradiation, a large amount of ROS will be generated to induce cell damage and prodrug activation. Therefore, the glutathione-depleting polyprodrug nanoparticles can efficiently inhibit tumor growth by enhanced photodynamic therapy and cascaded locoregional chemotherapy., 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.)