“…In addition to the oxidative modification of lipids, oxygen radicals can alter the structure and function of proteins using any of the following: protein-peptide chain breakage, cross-linking and polymerization, the oxidative deamination of amino acids, attacking protein reducing groups, or causing secondary reactions with lipid peroxidation products. 51 Formed as chemically stable protein oxidation products, protein carbonyls and the protein nitrotyrosine are extensively employed as biomarkers in SLE, with the former being more addressed these years owing to its longer circulation durations in the blood. Protein nitrotyrosine is delivered on tyrosine residues by RNS.…”
Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease with complex pathogenesis, the treatment of which relies exclusively on the use of immunosuppressants. Increased oxidative stress is involved in causing inflammatory and cellular defects in the pathogenesis of SLE. Various inflammatory and cellular markers including oxidative modifications of proteins, lipids, and DNA contribute to immune system dysregulation and trigger an aggressive autoimmune attack through molecular mechanisms like enhanced NETosis, mTOR pathway activation, and imbalanced T-cell differentiation. Accordingly, the detection of inflammatory and cellular markers is important for providing an accurate assessment of the extent of oxidative stress. Oxidative stress also reduces DNA methylation, thus allowing the increased expression of affected genes. As a result, pharmacological approaches targeting oxidative stress yield promising results in treating patients with SLE. The purpose of this review is to examine the involvement of oxidative stress in the pathogenesis and management of SLE.
“…In addition to the oxidative modification of lipids, oxygen radicals can alter the structure and function of proteins using any of the following: protein-peptide chain breakage, cross-linking and polymerization, the oxidative deamination of amino acids, attacking protein reducing groups, or causing secondary reactions with lipid peroxidation products. 51 Formed as chemically stable protein oxidation products, protein carbonyls and the protein nitrotyrosine are extensively employed as biomarkers in SLE, with the former being more addressed these years owing to its longer circulation durations in the blood. Protein nitrotyrosine is delivered on tyrosine residues by RNS.…”
Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease with complex pathogenesis, the treatment of which relies exclusively on the use of immunosuppressants. Increased oxidative stress is involved in causing inflammatory and cellular defects in the pathogenesis of SLE. Various inflammatory and cellular markers including oxidative modifications of proteins, lipids, and DNA contribute to immune system dysregulation and trigger an aggressive autoimmune attack through molecular mechanisms like enhanced NETosis, mTOR pathway activation, and imbalanced T-cell differentiation. Accordingly, the detection of inflammatory and cellular markers is important for providing an accurate assessment of the extent of oxidative stress. Oxidative stress also reduces DNA methylation, thus allowing the increased expression of affected genes. As a result, pharmacological approaches targeting oxidative stress yield promising results in treating patients with SLE. The purpose of this review is to examine the involvement of oxidative stress in the pathogenesis and management of SLE.
“…Additionally, protein oxidation adducts inhibit 26S proteasomal activity, resulting in intracellular accumulation of damaged proteins. Protein carbamylation contributes to a decrease in cardiac and kidney functions and increased myocardial apoptosis after ischemia/reperfusion shown in humans [ 51 ]. Older participants have been reported to demonstrate increased levels of carbamylated proteins compared to younger subjects in a research study [ 52 ].…”
Evidence from research studies reports that wine consumption is associated with lower cardiovascular disease risk, partly through the amelioration of oxidative stress. The aim of the present study was to examine the effect of regular light to moderate wine consumption from coronary heart disease (CHD) patients compared to the effect induced by alcohol intake without the presence of wine microconstituents, on oxidation-induced macromolecular damage as well as on endogenous antioxidant enzyme activity. A randomized, single-blind, controlled, three-arm parallel intervention was carried out, in which 64 CHD patients were allocated to three intervention groups. Group A consumed no alcohol, and Group B (wine) and Group C (ethanol) consumed 27 g of alcohol/day for 8 weeks. Blood and urine samples were collected at baseline and at 4 and 8 weeks. Urine oxidized guanine species levels, protein carbonyls, thiobarbituric acid substances (TBARS) levels, as well as superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, were measured. Oxidized guanine species and protein carbonyl levels were significantly increased in the ethanol group during the intervention and were significantly decreased in the wine group. These results support the idea that wine’s bioactive compounds may exert antioxidant actions that counteract the macromolecular oxidative damage induced by alcohol in CHD patients.
“…Polybrominated diphenyl ethers BDE-153 and BDE-100 induced autophagy in human liver HepG2 cells through oxidative stress and mitochondrial dysfunction (mitophagy) [ 53 ]. Recent research suggests that direct oxidation of catalytic thiol-groups on autophagy-related 3 (ATG3) and 7 (ATG7) might block LC3’s conjugation with phosphatidylethanolamine, which is essential for effective autophagy [ 54 ]. ER stress promotes ROS production and can affect redox equilibrium in the cell.…”
Section: Effects Of Pesticides and Other Small Molecular Weight Envir...mentioning
Autophagy is an evolutionarily conserved cellular system crucial for cellular homeostasis that protects cells from a broad range of internal and extracellular stresses. Autophagy decreases metabolic load and toxicity by removing damaged cellular components. Environmental contaminants, particularly industrial substances, can influence autophagic flux by enhancing it as a protective response, preventing it, or converting its protective function into a pro-cell death mechanism. Environmental toxic materials are also notorious for their tendency to bioaccumulate and induce pathophysiological vulnerability. Many environmental pollutants have been found to influence stress which increases autophagy. Increasing autophagy was recently shown to improve stress resistance and reduce genetic damage. Moreover, suppressing autophagy or depleting its resources either increases or decreases toxicity, depending on the circumstances. The essential process of selective autophagy is utilized by mammalian cells in order to eliminate particulate matter, nanoparticles, toxic metals, and smoke exposure without inflicting damage on cytosolic components. Moreover, cigarette smoke and aging are the chief causes of chronic obstructive pulmonary disease (COPD)-emphysema; however, the disease’s molecular mechanism is poorly known. Therefore, understanding the impacts of environmental exposure via autophagy offers new approaches for risk assessment, protection, and preventative actions which will counter the harmful effects of environmental contaminants on human and animal health.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.