Search Results (292)

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive motor neuron degeneration and chronic neuroinflammation in the brain and spinal cord, involving complex interactions between neurons and immune cells. Carnosine (β-alanyl-L-histidine) has pathophysiological relevance due to its ability to detoxify reactive carbonyl species, including α,β-unsaturated aldehydes, scavenge free radicals, and chelate zinc, and has also been proposed to function in the central nervous system as a histidine reservoir for histamine synthesis. Here, we investigated the effects of carnosine supplementation on the cerebellar proteome of SOD1^G93A ALS rats using quantitative proteomics. Carnosine treatment extensively remodeled mitochondrial, antioxidant, and synaptic vesicle-trafficking protein networks and increased the abundance of glutamatergic and GABAergic receptor subunits relative to untreated ALS animals, with several of these changes exceeding wild-type levels. Pathway enrichment analyses identified significant up-regulation of Rab-mediated vesicle trafficking, synaptic vesicle cycling, and neurotransmitter transport/secretion pathways, alongside a partial reduction in RNA splicing and proteasomal subunits that were elevated in untreated ALS animals. Cross-comparison with the ALS-associated proteomic signature revealed that most carnosine-responsive proteins followed, rather than reversed, the direction of disease-associated change, indicating that carnosine predominantly potentiates an endogenous compensatory program rather than restoring a wild-type-like proteome. Collectively, these findings show that carnosine drives systems-level remodeling of mitochondrial and synaptic networks in the ALS cerebellum, identifying candidate compensatory pathways and supporting further functional validation of carnosine as a component of multimodal therapeutic strategies in ALS. Full article

Oxidative stress is a major constraint limiting animal health and productive performance by disrupting redox homeostasis, mitochondrial function, intestinal integrity, and mineral metabolism. Agronomic biofortification of forage with essential trace minerals represents a promising nutritional strategy; however, its physiological and molecular mechanisms remain poorly understood. This study evaluated the effects of dietary zinc–iron (Zn–Fe) biofortified alfalfa on oxidative stress, antioxidant defense, mineral transport, mitochondrial bioenergetics, intestinal barrier integrity, inflammatory responses, tissue mineral deposition, and growth performance in guinea pigs. Forty-eight male guinea pigs were allocated to six experimental groups according to dietary treatment (control, Zn-biofortified alfalfa, or Zn–Fe biofortified alfalfa) and oxidative stress status. Oxidative biomarkers, antioxidant enzyme activities, inflammatory mediators, mineral concentrations, targeted RT–qPCR, mitochondrial function, intestinal histomorphology, and multivariate physiological analyses were performed. Zn–Fe biofortified alfalfa markedly reduced reactive oxygen species, malondialdehyde, protein carbonyls, 8-hydroxy-2′-deoxyguanosine, advanced oxidation protein products, and the oxidative stress index while significantly increasing superoxide dismutase, catalase, glutathione peroxidase, total antioxidant capacity, and the glutathione redox ratio. Targeted gene-expression analysis demonstrated coordinated upregulation of intestinal mineral transporters (ZIP4, DMT1, and MT1), activation of the Nrf2 antioxidant pathway, increased expression of mitochondrial regulatory genes, and suppression of inflammatory mediators. These molecular responses were accompanied by improved ATP production, mitochondrial membrane potential, respiratory-chain activity, preservation of intestinal villus architecture, enhanced expression of tight-junction proteins, increased tissue Zn and Fe deposition, superior feed efficiency, and greater body weight gain. Integrated physiological analyses consistently identified the Zn–Fe biofortified treatment as the highest-performing physiological phenotype, indicating coordinated adaptation across multiple biological systems. These findings demonstrate that Zn–Fe biofortified alfalfa enhances oxidative stress resilience through simultaneous regulation of mineral transport, antioxidant defense, mitochondrial bioenergetics, intestinal barrier integrity, and systemic physiological performance. Agronomic biofortification of forage therefore represents a promising nutritional strategy for improving animal health, mineral utilization, and productive efficiency under oxidative stress. Full article

Background: Oxidative stress is an important contributor to brain abnormalities in Down syndrome (DS), but the status of the nuclear factor erythroid 2-related factor 2 (NRF2) antioxidant pathway during early postnatal development remains poorly understood. The current study aimed to investigate whether an impairment of the NRF2 pathway is already present in the Ts65Dn mouse model of trisomy 21 at neonatal life stages and whether early treatment with astaxanthin-loaded stealth solid lipid nanoparticles (AST-SSLNs) positively impacts NRF2 signaling and reduces oxidative stress. Methods: Hippocampal NRF2 pathway components and oxidative stress markers were analyzed in neonate Ts65Dn and euploid mice. From postnatal day (P)3 to P15, mice received daily subcutaneous injections of AST-SSLNs or unloaded nanoparticles. NRF2 pathway activation, reactive oxygen species (ROS), lipid peroxidation, protein carbonylation, and safety parameters were evaluated. Results: Untreated Ts65Dn mice exhibited early impairment of the NRF2 pathway, characterized by increased BACH1, reduced NRF2 activation, and decreased HO-1 expression. Neonatal AST-SSLN treatment enhanced NRF2 activation, improved HO-1 levels, and normalized ROS accumulation, lipid peroxidation, and protein carbonylation in the hippocampus, a brain region critically impaired in DS. Treatment had no adverse effects on survival, body weight, or brain weight. Conclusions: These findings demonstrate that NRF2 pathway dysfunction is an early event in trisomy 21 and identify the neonatal period as a potential therapeutic window to counteract oxidative stress. AST-SSLNs represent a promising nanomedicine-based strategy to activate the impaired NRF2 pathway and reduce early hippocampal oxidative damage in DS. Full article

Objective: This study investigated the effects of three chronic stress exposure models (permanent elimination, forced swimming, and food and water deprivation) on bone oxidative stress, structure, and metabolism in vivo. Methods: Adult rats were exposed to different stress conditions, while control animals were maintained under standard laboratory conditions. Bone morphological and histological parameters, oxidative stress biomarkers, antioxidant defense system, and mineral concentrations were assessed. Results: Stress exposure resulted in significant reductions in body weight, femur weight, and femur length compared to controls. A marked increase in oxidative stress biomarkers was observed in bone tissue, including lipid peroxidation, reactive oxygen species, hydroperoxides, hydrogen peroxide, protein carbonyls, and advanced oxidation protein products. In contrast, antioxidant defenses, including enzymatic activities and levels of glutathione, non-protein thiols, and vitamin C, was significantly decreased. Bone calcium and phosphorus levels were reduced, whereas their plasma concentrations were increased following stress exposure. Histological analysis confirmed the biochemical alterations, suggesting that chronic stress can disrupt bone integrity via oxidative mechanisms. Conclusions: These findings highlight the need for strategies to control and reduce stress-related disorders to maintain skeletal health under various chronic stress conditions. Full article

Methylglyoxal (MG), a reactive carbonyl species, is now recognized as a novel signaling molecule regulating abiotic stress tolerance and plant growth. Using tolerant (BHL-25 and BHL-27) and susceptible (BARI Barley-6 and BHL-26) genotypes, the study aimed to reveal the detailed mechanisms of MG-priming-induced salt stress tolerance in barley (Hordeum vulgare L.). Seeds were primed with MG, and seven-day-old seedlings were transferred to hydroponic solution. After one week of seedling growth in hydroponic solutions, the salinity stress was imposed. The five treatments were as follows: control (0 salt + 0 mM MG), salt (16 dS m⁻¹) + 0 mM MG, salt + 0.25 mM MG, salt + 0.5 mM MG, and salt + 1 mM MG. Significant genotype-dependent changes were observed in response to salt stress based on morphological, physiological and biochemical traits. Salt stress significantly impaired shoot length, shoot dry weight, root volume, root dry weight, relative water content, leaf Na⁺ content and K⁺/Na⁺ ratio. Salinity stress caused a significant increase in oxidative indices in all genotypes; however, the tolerant genotypes showed a lower increase. Importantly, in plants grown from MG-primed seeds, the negative effects of salt stress were reversed by modulating the K⁺/Na⁺ ratio, the activities of antioxidative and glyoxalase pathway enzymes as well as the redox state of ascorbate and glutathione. In conclusion, MG-mediated salt tolerance was linked to a reduction in reactive oxygen species (ROS) and activation of ROS and MG detoxification processes as well as favorable regulation of the K⁺/Na⁺ ratio, glutathione and ascorbate redox state that improved the growth of the barley plants under salinity. Full article

The influence of natural and synthetic blue food colorants on the human body, including the cardiovascular system, is a complex and not fully understood topic. Considering that various papers have demonstrated that oxidative stress is a crucial step in the development of cardiovascular diseases (CVDs), our experiments on the pro- or antioxidant action of three blue food colorants (one natural colorant—genipin—and two synthetic colorants—brilliant blue FCF and patent blue V) focused on two aspects that are important for the development of CVDs: the level of biomarkers of oxidative stress induced by H₂O₂/Fe²⁺ (the donor of hydroxyl radicals—one of the most aggressive reactive oxygen species produced in humans) in human blood platelets and human plasma, as well as the arachidonic acid cascade in blood platelets stimulated by thrombin (in vitro). Our results demonstrated that two tested blue colorants—genipin and brilliant blue FCF (at four used concentrations: 2, 10, 20, and 200 µM)—reduced plasma lipid peroxidation induced by H₂O₂/Fe²⁺. Moreover, all tested blue colorants (genipin, brilliant blue FCF, and patent blue V; at the concentrations 2, 10, 20, and 200 µM) inhibited lipid peroxidation in blood platelets treated with H₂O₂/Fe²⁺. In contrast, only genipin (at the highest used concentration—200 µM) statistically significantly reduced plasma protein carbonylation induced by H₂O₂/Fe²⁺ (inhibition of this process: about 25%). However, all tested food colorants decreased blood platelet protein carbonylation stimulated by H₂O₂/Fe²⁺, but their action was not always statistically significant. In addition, we noted that all used blue food colorants (1–200 µM) have protector effects on the change in the level of thiol groups in plasma proteins stimulated by H₂O₂/Fe²⁺, but these tested colorants change the level of thiol groups in blood platelets treated with H₂O₂/Fe²⁺ only at the highest used concentration—200 µM. In conclusion, the present study provides the first data on the antioxidant potential of genipin, brilliant blue FCF, and patent blue V in selected elements of blood treated with H₂O₂/Fe²⁺. Earlier and current studies have indicated the promising potential of these blue food colorants, especially genipin (without cytotoxicity toward human blood platelets), which can modify the oxidative stress of platelets and plasma in vitro at concentrations (1–200 µM) which can be obtained in blood during its administration. However, the presented results have limitations, especially concerning the mechanistic clarity surrounding the antioxidant properties of the tested blue food colorants. Therefore, further in vivo experiments are needed to provide a better understanding of their antioxidant potential. Full article

Asthma is a heterogeneous chronic airway disease in which oxidative stress (OS) plays a central mechanistic role beyond classical immune-mediated inflammation. Reactive oxygen and nitrogen species (ROS/RNS), generated by recruited inflammatory cells and activated airway structural cells, drive epithelial injury, mucus hypersecretion, airway remodeling, and modulate key transcription factors including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. This review synthesizes current evidence on the multilevel redox-based determinants of asthma severity, spanning from genetic polymorphisms to circulating biomarkers. We examine serum antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), peroxiredoxins (PRDXs), and the thioredoxin (Trx) system as dynamic indicators of systemic redox status and disease severity, alongside oxidative enzymes including NADPH oxidases and dual oxidases (NOX/DUOX), xanthine oxidase (XO), and myeloperoxidase (MPO) that serve as upstream sources of airway oxidant burden. Functional genetic polymorphisms in antioxidant genes (SOD2, CAT, glutathione S-transferase mu 1/glutathione S-transferase theta 1 (GSTM1/GSTT1), heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1 (Nrf2/KEAP1)) and oxidative enzyme genes including nitric oxide synthase 1/2/3 (NOS1/2/3), MPO, cytochrome b-245 alpha chain (CYBA), and xanthine dehydrogenase (XDH) are reviewed as modulators of individual redox capacity and asthma susceptibility, with particular attention to gene–environment interactions. We further discuss oxidative damage biomarkers, including malondialdehyde (MDA), 8-isoprostanes, 4-hydroxynonenal, 8-oxo-7, 8-dihydro-2′-deoxyguanosine, protein carbonyls, 3-nitrotyrosine, and advanced oxidation protein products as indicators of lipid, DNA, and protein oxidation that correlate with disease activity and control. The roles of micronutrient cofactors in modulating antioxidant enzyme function and their potential as contextual biomarkers are also addressed. Additionally, emerging evidence on microRNAs (miRNAs) linked to OS biology in asthma is presented. Finally, we critically evaluate the challenges limiting clinical translation, including biomarker non-specificity, analytical variability, gene–environment complexity, and the absence of standardized reference ranges. This integrated framework supports the development of multilevel redox prognostic panels combining genetic, enzymatic, and oxidative damage readouts for improved asthma phenotyping, severity stratification, and personalized therapeutic approaches. Full article

Fluorinated carboxylate ester solvents are promising electrolyte components for lithium metal batteries because they can improve oxidative stability and promote LiF-rich solid electrolyte interphase (SEI) formation. However, how fluorination position and degree regulate their intrinsic decomposition behavior on lithium metal remains unclear. Herein, density functional theory (DFT) calculations and ab initio molecular dynamics (AIMD) simulations were employed to systematically investigate six pure fluorinated ethyl acetate solvents on the Li(001) surface, including α-fluorinated ethyl fluoroacetate (EFA), ethyl difluoroacetate (EDFA), and ethyl trifluoroacetate (ETFA), as well as β-fluorinated 2-fluoroethyl acetate (FEA), 2,2-difluoroethyl acetate (DFEA), and 2,2,2-trifluoroethyl acetate (TFEA). Electronic-structure analysis shows that although the lowest unoccupied molecular orbitals (LUMOs) of all six solvents are mainly distributed around the carbonyl and adjacent regions, the dominant electron-accepting center strongly depends on the fluorination position. In α-fluorinated solvents, the LUMO is highly localized on the α-C atom directly bonded to fluorine, whereas in β-fluorinated solvents, it remains concentrated around the carbonyl C atom. Real-time Bader charge and bond-evolution analyses reveal that fluorination position is the primary factor governing the initial decomposition pathway. The α-fluorinated series preferentially undergoes C-F bond cleavage, and increasing fluorination degree induces deeper cascade decomposition; fully fluorinated ETFA even exhibits C=O double bond cleavage. In contrast, β-fluorinated solvents preferentially undergo carbonyl-side C-O bond cleavage, while C-F bond cleavage occurs only in subsequent steps or is completely suppressed. Notably, β-fluorinated solvents retain high chemical stability even with α-H atoms because the LUMO electron density on α-H is negligible. Meanwhile, limited deep decomposition can still provide F⁻ species for SEI formation. These findings establish an atomic-level structure–reactivity relationship for fluorinated carboxylate ester solvents and provide theoretical guidance for designing stable electrolyte solvents for lithium metal batteries. Full article

Oxidative stress (OS) is elevated in patients with end-stage kidney disease undergoing maintenance dialysis and contributes to increased cardiovascular risk. While kidney dysfunction and dialysis can generate OS, the acute effects of a single dialysis session remain unclear due to variability in study design and the biomarkers used. In this observational study, blood samples from 68 hemodialysis patients were collected before and after a single session. Plasma levels of the reactive oxygen species marker superoxide (O₂^•−) and OS-damage marker lipid hydroperoxides (LOOHs), protein-bound malondialdehyde (PrMDA), protein-bound thiobarbituric acid reactive substances (PrTBARSs), and protein carbonyls (PrCOs) were measured. LOOHs increased significantly by 50% post-dialysis, whereas PrMDA and PrTBARSs decreased modestly by ~10%. No significant changes were observed in O₂^•− or PrCOs. Dialysis vintage correlated positively with LOOHs, PrMDA, and PrTBARSs, but not with O₂^•− or PrCOs. No significant associations were found between OS markers and comorbidities, medication or sex. The post-dialysis rise in LOOHs, an early-formed and least accumulating lipid peroxidation marker, may reflect acute changes in OS during a single HD session. The rising association of PrMDA and PrTBARSs with dialysis vintage may suggest cumulative OS over time. Full article

Endometriosis is associated with oxidative stress and debilitating symptoms, yet its pathophysiology remains incompletely understood, and current treatments are still limited. In this study, oxidative stress responses were compared in 2D and 3D cultures of 12Z and Ishikawa cells using hydrogen peroxide (H₂O₂) as a pro-oxidant and N-acetylcysteine (NAC) as an antioxidant. We evaluated H₂O₂ sensitivity, Reactive Oxygen Species (ROS) production, glutathione redox homeostasis, and biomolecular damage. The results showed that 12Z cells display greater vulnerability to oxidative stress than Ishikawa cells, with higher basal ROS levels (p < 0.01) and increased sensitivity to H₂O₂. In 3D culture, 12Z cells exhibited a 72% depletion of total glutathione under oxidative stress, a response not observed in 2D cultures, which instead showed a compensatory pattern. This vulnerability was further supported by increased lipid peroxidation and protein carbonylation. Although NAC restored cell viability and protected lipids and proteins, it did not prevent DNA damage. Together, these findings demonstrate marked differences in antioxidant responses between the two cell models and reinforce the value of 3D systems for investigating oxidative stress-related mechanisms. These results provide mechanistic insights relevant to endometriosis-associated redox imbalance and support further investigation of glutathione dysregulation and ROS-mediated damage in disease-related contexts. Full article

Reactive oxygen species (ROS) are integral components of plant signaling networks that mediate interactions between plants and their environment, thereby regulating diverse physiological and biochemical processes. While controlled ROS production is essential for stress perception and signal transduction, excessive ROS accumulation induces oxidative damage. ROS-mediated lipid peroxidation of polyunsaturated fatty acids leads to the formation of highly electrophilic α,β-unsaturated carbonyl compounds collectively referred to as reactive carbonyl species (RCS). Under severe abiotic stress conditions, excessive RCS accumulation exerts cytotoxic effects and causes widespread cellular dysfunction. In contrast, at subtoxic levels, RCS function as important secondary messengers that modulate stress-responsive signaling pathways, including programmed cell death, stomatal regulation, and adaptive responses to abiotic stresses. This review critically synthesizes current advances in understanding the dual roles of ROS and RCS as both damaging agents and signaling molecules in plants. Particular emphasis is placed on the mechanistic basis of ROS-RCS crosstalk and their interactions in abiotic stress tolerance. Furthermore, this review highlights emerging research gaps and outlines future perspectives aimed at translating redox signaling insights into strategies for improving plant stress resilience under changing environmental conditions. Full article

Embryos being treated using assisted reproductive technology (ART) are unavoidably exposed to physical stressors, thus producing reactive oxygen species (ROS) which trigger mitophagy to support embryonic development. However, the mechanisms underlying the regulation of mitophagy in early embryonic development remain largely unexplored. Here, we found that Mucin 1 (MUC1) exhibited a uniform distribution in both mouse and human oocytes, and its expression peaked at the blastocyst stage. Further analysis revealed that Muc1 knockout impairs blastocyst formation in vitro. Correspondingly, Muc1 knockout led to the accumulation of mitochondrial reactive oxygen species (mtROS) and a reduction in phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1)/Parkinson protein 2 (PARK2/Parkin)-dependent mitophagy. Stimulation of mitophagy via low-dose carbonyl cyanide 3-chlorophenylhydrazone (CCCP) treatment rescued the blastocyst formation defect in Muc1-null embryos. Vitamin C supplementation effectively scavenged mtROS and restored developmental competence. Together, our findings establish that MUC1 safeguards early embryonic development by promoting mitophagy to decrease mtROS levels in vitro. Moreover, vitamin C could compensate for Muc1 deficiency by eliminating mtROS. This study not only identified a new function of MUC1 in protecting early embryonic development in vitro, but also revealed a novel mechanism of mitophagy regulation in early embryos, which has potential applications for ART. Full article

A polymer electrolyte is developed by integrating a poly(methyl methacrylate) (PMMA)/eutectic electrolyte (EE) phase into a porous polyethylene (PE) scaffold via a solution-casting strategy. In this rigid–flexible coupled architecture, the PMMA matrix serves as a solid host that coordinates with Li⁺ through its polar carbonyl groups, thereby promoting lithium salt dissociation and establishing a stable ion transport network. The incorporated EE, composed of ethylene carbonate and LiTFSI, effectively reduces the glassy rigidity of PMMA and provides continuous pathways for fast ionic conduction. Meanwhile, the porous PE scaffold reinforces mechanical strength and resists lithium dendrite penetration, enabling a thin electrolyte membrane with excellent flexibility. The resulting electrolyte achieves an ionic conductivity of 1.59 × 10⁻⁴ S cm⁻¹ at 30 °C, a lithium-ion transference number of 0.45, and an electrochemical stability window up to 4.75 V. In Li||LiFePO₄ cells, it delivers stable cycling at 3 C for 1000 cycles with 76.8% capacity retention and a Coulombic efficiency exceeding 99.9%. The monomer-free design eliminates residual reactive species that commonly compromise interfacial stability, offering a reliable pathway toward high-voltage solid-state lithium-metal batteries. Full article

Methotrexate (MTX) is widely used for its chemotherapeutic and immunosuppressive properties, but is limited by oxidative stress-mediated hepatotoxicity. Nanoantioxidant delivery systems can enhance the stability, solubility, and in vivo efficacy of natural antioxidants. This study investigated the hepatoprotective effects of myricetin (MYR), a flavonoid with potent antioxidant activity, and its liposomal nanoantioxidant formulation (MYR-loaded liposomal nanoparticles, MYR-LNPs) against MTX-induced liver injury in male albino Sprague Dawley rats. Sixty rats were randomly allocated to six groups: control, MTX, MYR, MYR-LNPs, and combinations of MTX with MYR-LNPs. MYR-LNPs were successfully formulated and physicochemically characterized, exhibiting a mean particle size of 95.6 nm, a zeta potential of −32 mV, and a narrow polydispersity index, collectively confirming their colloidal stability and suitability for hepatic delivery. MTX markedly disrupted liver function, increasing serum AST, ALT, ALP, and bilirubin and decreasing total protein, albumin, and globulin, whereas co-treatment with MYR-LNPs substantially restored these parameters and outperformed free MYR. MTX-induced oxidative stress, reflected by depleted hepatic GSH and antioxidant enzymes (GPx, SOD, CAT, GST), elevated reactive oxygen species (ROS), malondialdehyde (MDA), and protein carbonyls and downregulated NRF2/HO-1, was significantly counteracted by MYR-LNPs. In addition, MYR-LNPs mitigated MTX-evoked inflammation and nitrosative stress by reducing NF-κB, TNF-α, IL-1β, nitric oxide, and iNOS expression. They corrected apoptotic imbalance by lowering Bax and caspase 3 while increasing Bcl-2. Histopathological and ultrastructural assessments confirmed that MYR-LNPs preserved hepatic architecture and mitochondrial integrity. These findings indicate that MYR-loaded liposomal nanoantioxidants provide superior protection against MTX-induced hepatotoxicity by modulating oxidative stress, inflammation, and apoptosis, supporting their potential as an advanced nanodrug delivery strategy for antioxidant therapy. Full article

Arsenic induces apoptosis in both cancerous and non-cancerous cells. The mechanism of arsenic-induced apoptosis is complex. We previously demonstrated that the antioxidant acetyl L-carnitine prevented sodium arsenite-induced apoptosis in zebrafish embryos. To gain more insight into the mechanism of arsenic-induced apoptosis, we explored the effect of another antioxidant, N-acetylcysteine (NAC). Co-treatment of sodium arsenite with 1 or 2 mM NAC had no effect on zebrafish development. There was a significant but partial reduction in apoptosis in the embryos co-treated with sodium arsenite and 1 mM NAC, while embryos treated with 1 mM NAC alone showed the loss of normal apoptosis that was observed in the control embryos. Complete abolition of apoptosis occurred in embryos co-treated with sodium arsenite and 2 mM NAC; however, 2 mM NAC alone resulted in 100% mortality, indicating antioxidant toxicity at high doses. NAC (1 mM) did not prevent sodium arsenite-induced increase in motor neurons, suggesting that arsenic-induced apoptosis and supernumerary motor neuron development are mediated via distinct pathways. To determine whether NAC prevented arsenic-induced apoptosis via reactive oxygen species (ROS) signaling, we assessed ROS levels and oxidative modification of proteins (carbonylation) using an OxyBlot assay. Neither sodium arsenite nor NAC altered protein oxidation, ROS levels, or p53, a pro-apoptotic protein, transcript levels. Additionally, dicoumarol, an inducer of p53 protein degradation, did not inhibit sodium arsenite-induced apoptosis. These results indicate that protein oxidation and p53 signaling are not involved in arsenic-induced apoptosis and that NAC prevents arsenic toxicity in zebrafish embryos through a hitherto unknown mechanism. Full article