Search Results (138)

Powdery mildew (PM), caused by Sphaerotheca phaseoli, severely threatens mungbean (Vigna radiata) productivity and quality, yet the molecular basis of resistance remains poorly defined. This study employed transcriptome profiling to compare defense responses in a resistant genotype, SUPER5, and a susceptible variety, CN84-1, following pathogen infection. A total of 1755 differentially expressed genes (DEGs) were identified, with SUPER5 exhibiting strong upregulation of genes encoding pathogenesis-related (PR) proteins, disease resistance proteins, and key transcription factors. Notably, genes involved in phenylpropanoid and flavonoid biosynthesis, pathways associated with antimicrobial compound and lignin production, were markedly induced in SUPER5. In contrast, CN84-1 showed limited activation of defense genes and downregulation of essential regulators such as MYB14. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses highlighted the involvement of plant–pathogen interaction pathways, MAPK signaling, and reactive oxygen species (ROS) detoxification in the resistant response. Quantitative real-time PCR validated 11 candidate genes, including PAL3, PR2, GSO1, MLO12, and P21, which function in pathogen recognition, signaling, the biosynthesis of antimicrobial metabolites, the production of defense proteins, defense regulation, and the reinforcement of the cell wall. Co-expression network analysis revealed three major gene modules linked to flavonoid metabolism, chitinase activity, and responses to both abiotic and biotic stresses. These findings offer valuable molecular insights for breeding PM-resistant mungbean varieties. Full article

Bardoxolone methyl, also known as CDDO-Me or RTA 402, is a synthetic oleanane triterpenoid that has garnered significant attention as a potent pharmacological activator of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Nrf2 is a master regulator of cellular redox homeostasis, controlling the expression of genes involved in antioxidant defense, detoxification, and mitochondrial function. By inducing Nrf2 and promoting the transcription of downstream antioxidant response element (ARE)-driven genes, bardoxolone methyl enhances cellular resilience to oxidative stress and inflammation. This mechanism is central not only to its cytoprotective effects but also to its emerging role in oncology. A number of studies investigated the effects of bardoxolone methyl in several malignancies including breast cancer, lung cancer, pancreatic ductal adenocarcinoma, prostate cancer, colorectal cancer, oral and esophageal squamous cell carcinoma, ovarian cancer and glioblastoma. Studies in the literature indicate that bardoxolone methyl exhibits anticancer activity through several mechanisms, including the suppression of cell proliferation, induction of cell cycle arrest and apoptosis, inhibition of epithelial–mesenchymal transition (EMT), and impairment of cancer cell stemness. Additionally, bardoxolone methyl modulates mitochondrial function, reduces glycolytic and oxidative phosphorylation capacities, and induces reactive oxygen species (ROS)-mediated stress responses. In this review, we summarize the available literature regarding the studies which investigated the effects of bardoxolone methyl as anticancer agent. Full article

Paraquat is one of the most widely used nonselective herbicides globally. Although the emergence of weed resistance to paraquat has progressed relatively slowly since the first reported case in Japan in 1980, it has been steadily increasing. Resistance in weedy plants is predominantly associated with non-target-site resistance (NTSR), particularly via reduced uptake and translocation to target sites (i.e., chloroplasts) and/or enhanced sequestration; increased antioxidant capacity is also a common mechanism by which plants cope with various stresses, including reactive oxygen species (ROS). However, direct evidence for paraquat transport mediated by membrane transporters in weeds has not been established. Over the past decade, research, especially in model plants such as Arabidopsis thaliana, has advanced our understanding of the mechanisms underlying plant resistance to paraquat. This brief review summarized recent studies on paraquat resistance, with a particular focus on uptake, translocation, and sequestration mechanisms. For instance, three L-amino acid transporter (LAT) proteins (LAT1/3/4) and one (PDR11) belonging to the PDR (pleiotropic drug resistance) subfamily within the ABC (ATP-binding cassette) transporter family were confirmed to exhibit paraquat transporter activity; furthermore, transporters such as DTX6 (detoxification efflux carrier) can export/sequestrate paraquat inside the cell to the vacuole and apoplast, which confers stronger paraquat resistance to nearly commercial doses. In addition, the evolving perspectives in paraquat resistance research integrating big data and artificial intelligence, development of paraquat-tolerant crops, and a proposal of ryegrass (Lolium. spp.) and/or goosegrass (Eleusine indica) as a model weed species for paraquat resistance studies were also briefly discussed. Further advances in elucidating the molecular mechanisms of paraquat resistance in plants, including weeds, are anticipated. Full article

Salt stress severely constrains global crop productivity. However, most sweet corn cultivars exhibit weak tolerance to salt stress. In this study, two sweet corn CSSLs, salt-tolerant line D55 and salt-sensitive line D96, were selected as materials. We conducted comparative phenotyping and physiological profiling of seedlings under salinity treatment, and transcriptome analysis was carried out by sampling root tissues at 0 h, 4 h, 12 h, and 72 h post-treatment. The results indicated that D55 exhibited enhanced seedling height, root length, fresh weight, relative chlorophyll content, and antioxidant enzyme activities, while showing reduced malondialdehyde accumulation in comparison to D96. Pairwise comparisons across time points (0 h, 4 h, 12 h, 72 h) identified 6317 and 6828 differentially expressed genes (DEGs) in D55 and D96. A total of 49 shared DEGs across four time points were identified in D55 and D96, which were enriched in 12 significant Gene Ontology (GO) terms. Only eight DEGs were shared between genotypes across all comparisons. Transcriptomic analysis revealed 1281, 1946, and 1717 DEGs in genotypes D55 and D96 at 4 h, 12 h, and 72 h post-salt treatment, respectively. Genes associated with reactive oxygen species (ROS) homeostasis, phenylpropanoid metabolism, cutin, suberin and wax biosynthesis, and benzoxazinoid synthesis exhibit enhanced sensitivity in the salt-tolerant genotype D55. This leads to an enhanced ROS scavenging capacity and the establishment of a multi-layered defense mechanism. Additionally, brassinosteroid (BR), gibberellin (GA), and abscisic acid (ABA) and auxin-related genes exhibited different responses to salt stress in sweet corn. A hypothetical model, which established a multi-layered salt adaptation strategy, by integrating ROS detoxification, osmotic balance, and phytohormone signaling, was put forward. By integrating transcriptome and differential chromosomal fragment data, our findings identify 14 candidate genes for salt tolerance, providing potential ideal target genes in breeding to improve salt tolerance in sweet corn. Full article

Physiological oxidative stress plays a pivotal role in supporting proper growth and development. While moderate oxidative stress is essential for activating key metabolic pathways and maintaining normal cellular signaling, excessive production of reactive oxygen species (ROSs) can overwhelm the immature antioxidant systems of newborns, potentially leading to cellular damage and impaired physiological function. This vulnerability is particularly pronounced in the central nervous system, where limited detoxification capacity exacerbates the risk of oxidative damage, following hypoxic–ischemic events. Antioxidants agents—such as melatonin, erythropoietin, allopurinol, N-acetylcisteine, selenium, iminobiotin, taurine, and acetyl-L-carnitine—have demonstrated significant neuroprotective effects in preclinical experimental studies, reducing markers of oxidative injury and improving neurological outcomes. These neuroprotective agents have also been evaluated in clinical trials, demonstrating antioxidant effects. A major issue lies in the complexity of neurological damage, which is not associated with a single pathological pathway. Additionally, the inability of these agents to reach effective concentrations within the central nervous system, along with inconsistencies across clinical trials in terms of dosage and administration methods, hinders the ability to obtain robust results. Future efforts should therefore focus on the development of delivery systems capable of crossing the blood–brain barrier and on establishing standardized clinical trial protocols and study designs. This educational review aims to provide a comprehensive overview of emerging protective strategies, including antioxidant bioactive agents and nutritional interventions. It also explores the underlying mechanisms of oxidative stress and its impact on neonatal brain injury. Full article

Acrylamide (ACR), utilized as a precursor for producing polyacrylamide for water purification, has demonstrated neurotoxic properties. However, the mechanisms underlying its neurotoxicity remain inadequately understood. In this investigation, Caenorhabditis elegans were exposed to ACR at concentrations ranging from 250 to 1000 μg/mL and then their locomotor behavior, neuronal development, neurotransmitter concentrations, and gene expression profiles were assessed. Exposure to 250–1000 μg/mL ACR resulted in observable behaviors such as head swiveling and body bending, accompanied by a significant reduction in body size. Furthermore, ACR exposure caused damage to serotonergic, cholinergic, dopaminergic, and glutamatergic neuronal structures. In this context, elevated levels of serotonin, dopamine, acetylcholine, and glutamate were detected, along with notable upregulation of the expression of genes associated with neurotransmitters, including tph-1, cat-4, mod-1, mod-5, cat-1, ser-1, dat-1, dop-1, dop-3, unc-17, cho-1, eat-4, and glr-2. Moreover, ACR exposure elevated reactive oxygen species (ROS), O₂, and H₂O₂ levels while concurrently depleting glutathione (GSH), thereby compromising the antioxidant defense system. This led to a significant upsurge in the expression of genes involved in the nematode ACR detoxification pathway, specifically daf-16, skn-1, mlt-1, sod-3, gst-4, gcs-1, hsf-1, and hsp-16.2. Additionally, Spearman correlation analysis revealed a significant inverse relationship between certain neurotransmitter and antioxidant genes and locomotor activities, highlighting the role of these genes in mediating ACR-induced neurotoxicity in C. elegans. Collectively, this research enhances the understanding of the mechanisms related to ACR neurotoxicity. Full article

High concentrations of ammonia nitrogen could result in the death of aquatic animals and cause a huge economic loss in the aquaculture industry. However, the metabolic responses to acute ammonia nitrogen stress remain largely unknown in Penaeus monodon. In this study, we first investigated the histological change in tissues in Penaeus monodon under 96 h acute ammonia nitrogen stress. The result of the paraffin section showed that acute ammonia nitrogen stress induced severe epithelial detachment and lumen dilatation of the hepatopancreas, swollen and hemocyte infiltration of the gills, and mucosa exfoliation and shortened villi of the intestine in Penaeus monodon, suggesting the impairment of the normal physiological function in these tissues. We next examined the change in the metabolic product in the plasma and the enzyme activity in the hepatopancreas after ammonia nitrogen stress. Upon ammonia stress, both the concentration of ammonia and urea nitrogen significantly increased, while there was no significant increase in the concentration of uric acid, which is consistent with the results that the enzyme activity of glutamine synthetase (GS), glutamate dehydrogenase (GDH), and aspartate transaminase (GOT) became significantly elevated and the enzyme activity of adenosine deaminase (ADA) in the purine metabolism pathway significantly decreased after ammonia stress, suggesting that shrimp could convert excessive ammonia to urea for ammonia detoxification through the ammonia–nitrogen metabolism pathways. Interestingly, we also observed a significant increase in superoxide dismutase (SOD) activity, suggesting a potential role of this antioxidant enzyme in the clearance of reactive oxygen species (ROS) induced via ammonia stress. Moreover, we found that acute ammonia nitrogen stress inhibited the enzyme activity of caspase 3 and caspase 8, suggesting an important role of apoptosis in protecting Penaeus monodon against acute ammonia stress. Overall, our findings revealed that Penaeus monodon may employ metabolic and purine pathways and undergo oxidative stress and apoptosis for ammonia detoxification under ammonia nitrogen stress, thus providing new insight into the metabolic response of shrimp to acute ammonia stress. Full article

Plants face various abiotic stresses in their natural environments that trigger the production of reactive oxygen species (ROS), leading to oxidative stress and potential cellular damage. This comprehensive review examines the interplay between plant antioxidant defense systems and ROS under abiotic stress conditions. We discuss the major enzymatic antioxidants, including superoxide dismutase, catalase, reductases, and peroxidases, as well as non-enzymatic antioxidants, such as ascorbic acid, glutathione, polyphenols, and flavonoids, which play crucial roles in ROS detoxification. This review elaborates on different types of ROS, their production sites within plant cells, and their dual role as both damaging oxidants and key signaling molecules. We discuss how various abiotic stresses—including heat, cold, drought, flooding, salinity, and heavy metal toxicity—induce oxidative stress and trigger specific antioxidant responses in plants. Additionally, the mechanisms of ROS generation under these abiotic stress conditions and the corresponding activation of enzymatic and non-enzymatic scavenging systems are discussed in detail. This review also discusses recent advances in understanding ROS signaling networks and their integration with other stress-response pathways. This knowledge provides valuable insights into plant stress-tolerance mechanisms and suggests potential strategies for developing stress-resistant crops by enhancing antioxidant defense systems. Moreover, the strategic ROS modulation through priming, exogenous antioxidants, nanoparticles, or genetic tools can enhance plant resilience. Integrating these methods with agronomic practices (e.g., irrigation management) offers a sustainable path to climate-smart agriculture. Our review reveals that ROS accumulation can be detrimental; however, the coordinated action of various antioxidant systems helps plants maintain redox homeostasis and adapt to environmental stress. Full article

Background: Sucralose and benzo(a)pyrene (B[a]P) are widespread foodborne substances known to harm human health. However, the effects of their combined exposure on kidney function remain unclear. This study aimed to investigate the mechanisms by which sucralose and B[a]P induce kidney injury through P-glycoprotein (PGP/ABCB1), a crucial protein involved in cellular detoxification. Methods: C57BL/6N mice were co-treated with sucralose and B[a]P for 90 days to evaluate their impact on kidney histopathology and function. In vitro experiments assessed cell viability, reactive oxygen species (ROS) levels, and B[a]P accumulation by flow cytometry. Molecular docking and cellular thermal shift assay (CETSA) were used to determine the binding affinity of sucralose to PGP. Furthermore, PCR, Western blotting, and immunohistochemistry were performed to analyze the expression of PGP and its upstream transcription factors. Results: Ninety days of co-exposure to sucralose and B[a]P significantly exacerbated renal dysfunction in mice, as evidenced by the elevated level of serum creatinine and urea nitrogen, which could be reverted by ROS scavenger N-acetyl cysteine (NAC). In vitro, sucralose promoted cellular accumulation of B[a]P, consequently enhancing B[a]P-induced cell growth inhibition and ROS production. Consistently, B[a]P accumulation was enhanced by PGP knockdown in both HK2 and HEK-293 cells. Mechanistically, sucralose can directly bind to PGP, competitively inhibiting its efflux capacity and increasing intracellular B[a]P retention. Prolonged co-exposure further downregulated PGP expression, possibly through the reductions of its transcriptional regulators (PXR, NRF2, and NF-κB). Conclusions: Co-exposure to sucralose and B[a]P exacerbates renal injury by impairing PGP function. Mechanistically, sucralose inhibits PGP activity, resulting in the accumulation of B[a]P within renal cells. This accumulation triggers oxidative stress and inhibits cell growth, which demonstrates that sucralose potentiates B[a]P-induced nephrotoxicity by directly inhibiting PGP-mediated detoxification pathways, thus underscoring the critical need to evaluate toxicity risks associated with combined exposure to these compounds. Full article

Gaseous chlorine dioxide (ClO₂) is a potent antimicrobial agent used to control microbial contamination in food and water. This study evaluates the bactericidal activity of gaseous ClO₂ released from a sodium chlorite (NaClO₂) pad against Campylobacter jejuni. Exposure to a low concentration (0.4 mg/L) of dissolved ClO₂ for 2 h resulted in a >93% reduction of C. jejuni, highlighting the bacterium’s extreme sensitivity to gaseous ClO₂. To elucidate the molecular mechanism of ClO₂-induced bactericidal action, transcriptomic analysis was conducted using RNA sequencing (RNA-seq). The results indicate that C. jejuni responds to ClO₂-induced oxidative stress by upregulating genes involved in reactive oxygen species (ROS) detoxification (sodB, ahpC, katA, msrP, and trxB), iron transport (ceuBCD, cfbpABC, and chuBCD), phosphate transport (pstSCAB), and DNA repair (rdgB and mutY). Reverse transcription-quantitative PCR (RT-qPCR) validated the increased expression of oxidative stress response genes but not general stress response genes (spoT, dnaK, and groES). These findings provide insights into the antimicrobial mechanism of ClO₂, demonstrating that oxidative damage to essential cellular components results in bacterial cell death. Full article

PM2.5, a fine particulate matter, poses considerable health risks. When inhaled, PM2.5 can deeply penetrate the lungs, triggering respiratory issues such as pneumonia and bronchitis, aggravating heart and lung conditions, increasing the risk of lung cancer, causing cardiovascular problems, and affecting the nervous, immune, and reproductive systems. This study investigated the protective effects of the combination extract (CRGE) of Thunbergia laurifolia Lindl. (Rang Chuet) water extract (RWE), and Zingiber officinale (ginger) ethanol extract (GEE) against PM2.5-induced oxidative stress in A549 and HepG2 cells. CRGE exhibited superior cytoprotective effects compared to the single extracts (RWE and GEE) by significantly reducing PM2.5-induced cytotoxicity and reactive oxygen species production while enhancing antioxidant enzyme activity. To investigate the effects of PM2.5 exposure on cellular responses, gene expression analysis was conducted on a panel of antioxidant enzymes (heme oxygenase 1, superoxide dismutase, catalase, and glutathione peroxidase), the phase II detoxification enzyme NQO1, and the inflammatory markers interleukin (IL)-6 and IL-8 using the A549 and HepG2 cell lines. CRGE treatment effectively reversed the PM2.5-mediated changes in gene expression in both cell lines, suggesting that it may help restore cellular antioxidant defense mechanisms and mitigate PM2.5-induced oxidative stress. This study showed that CRGE holds promise as a natural antioxidant and cytoprotective agent against PM2.5-induced oxidative stress. Further studies are required to investigate the underlying mechanisms and confirm the efficacy of CRGE in vivo. Full article

Zearalenone (ZEA) is one of the common mycotoxins in feeds. ZEA and its metabolites have estrogen-like activity and can competitively bind to estrogen receptors, causing reproductive dysfunction and damage to reproductive organs. The toxicity mechanism of ZEA mainly inhibits the antioxidant pathway and antioxidant enzyme activity, induces cell cycle arrest and DNA damage, and blocks the process of cellular autophagy to produce toxic effects. In animal husbandry practice, when animals ingest ZEA-contaminated feed, it is likely to lead to abortion in females, abnormal sperm viability in males with inflammatory reactions in various organs, and cancerous changes in the reproductive organs of humans when they ingest contaminated animal products. In this paper, we reviewed in detail how ZEA induces oxidative damage by inducing the generation of reactive oxygen species (ROS) and regulating the expression of genes related to oxidative pathways, induces germ cell apoptosis through the mitochondrial and death receptor pathways, and activates the expression of genes related to autophagy in order to induce cellular autophagy. In addition, the molecular detoxification mechanism of ZEA is also explored in this paper, aiming to provide a new direction and theoretical basis for the development of new ZEA detoxification methods to better reduce the global pollution and harm caused by ZEA. Full article

Over-accumulation of reactive oxygen species (ROS) causes hepatocyte dysfunction and apoptosis that might lead to the progression of liver damage. Sirtuin-3 (SIRT3), the main NAD+-dependent deacetylase located in mitochondria, has a critical role in regulation of mitochondrial function and ROS production as well as in the mitochondrial antioxidant mechanism. This study explores the roles of astragaloside IV (AST-IV) and formononetin (FMR) in connection with SIRT3 for potential antioxidative effects. It was shown that the condition of combined pre- and post-treatment with AST-IV or FMR at all concentrations statistically increased and rescued cell proliferation. ROS levels were not affected by pre-or post-treatment individually with AST-IV or pre-treatment with FMR; however, post-treatment with FMR resulted in significant increases in ROS in all groups. Significant decreases in ROS levels were seen when pre- and post-treatment with AST-IV were combined at 5 and 10 μM, or FMR at 5 and 20 μM. In the condition of combined pre- and post-treatment with 10 μM AST-IV, there was a significant increase in SOD activity, and the transcriptional levels of Sod2, Cat, and GPX1 in all treatment groups, which is indicative of reactive oxygen species detoxification. Furthermore, AST-IV and FMR activated PGC-1α and AMPK as well as SIRT3 expression in AML12 hepatocytes exposed to t-BHP-induced oxidative stress, especially at high concentrations of FMR. This study presents a novel mechanism whereby AST-IV and FMR yield an antioxidant effect through induction of SIRT3 protein expression and activation of an antioxidant mechanism as well as mitochondrial biogenesis and mitochondrial content and potential. The findings suggest these agents can be used as SIRT3 modulators in treating oxidative-injury hepatocytes. Full article

Alkaline environments such as alkaline lands, lakes, and industrial wastewater are not conducive to the growth of plants and microorganisms due to high pH and salinity. ChbZIP1 is a bZIP family transcription factor isolated from an alkaliphilic microalgae (Chlorella sp. BLD). Previous studies have demonstrated its ability to enhance alkaline tolerance in Arabidopsis thaliana. However, the potential of ChbZIP1 to confer similar alkaline tolerance in other microalgae remains unclear, and the specific mechanisms are not fully understood. The analysis of cellular physiological and biochemical indicators revealed that the ChbZIP1 transformants exhibited enhanced photosynthetic activity, increased lipid accumulation, and reduced fatty acid unsaturation. Genes associated with cellular reactive oxygen species (ROS) detoxification were found to be upregulated, and a corresponding increase in antioxidant enzyme activity was detected. In addition, the relative abundance of intracellular ROS and malondialdehyde (MDA) was significantly lower in the transformants. In summary, our research indicates that ChbZIP1 enhances the tolerance of Chlamydomonas reinhardtii to alkaline environments through several mechanisms, including the repair of damaged photosynthesis, increased lipid accumulation, improved fatty acid unsaturation, and enhanced antioxidant enzyme activity. This study aims to contribute to a more comprehensive understanding of the mechanisms underlying alkalinity tolerance in microalgae and offers new insights and theoretical foundations for the utilization of microalgae in alkaline environments. Full article

Phascolosoma esculenta is a unique aquatic invertebrate native to China, whose habitat is highly susceptible to environmental pollution, making it an ideal model for studying aquatic toxicology. Mitochondrial thioredoxin (Trx2), a key component of the Trx system, plays an essential role in scavenging reactive oxygen species (ROS), regulating mitochondrial membrane potential, and preventing ROS-induced oxidative stress and apoptosis. This study investigated the toxicity of cadmium (Cd) on P. esculenta and the role of P. esculenta Trx2 (PeTrx2) in Cd detoxification. The results showed that Cd stress altered the activities of T-SOD and CAT, as well as the contents of GSH and MDA in the intestine. After 96 h of exposure, histological damages such as vacuolization, cell necrosis, and mitophagy were observed. Suggesting that Cd stress caused oxidative damage in P. esculenta. Furthermore, with the prolongation of stress time, the expression level of intestinal PeTrx2 mRNA initially increased and then decreased. The recombinant PeTrx2 (rPeTrx2) protein displayed dose-dependent redox activity and antioxidant capacity and enhanced Cd tolerance of Escherichia coli. After RNA interference (RNAi) with PeTrx2, significant changes in the expression of apoptosis-related genes (Caspase-3, Bax, Bcl-2, and Bcl-XL) were observed. Proving that PeTrx2 rapidly responded to Cd stress and played a vital role in mitigating Cd-induced oxidative stress and apoptosis. Our study demonstrated that PeTrx2 is a key factor for P. esculenta to endure the toxicity of Cd, providing foundational data for further exploration of the molecular mechanisms underlying heavy metal resistance in P. esculenta. Full article