Oxidative Stress in Health and Disease

Biomedicines, Journal Year: 2023, Volume and Issue: 11(11), P. 2925 - 2925

Published: Oct. 29, 2023

Oxidative stress, resulting from the excessive intracellular accumulation of reactive oxygen species (ROS), nitrogen (RNS), and other free radical species, contributes to onset progression various diseases, including diabetes, obesity, diabetic nephropathy, neuropathy, neurological such as Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson’s (PD). stress is also implicated in cardiovascular cancer. Exacerbated oxidative leads accelerated formation advanced glycation end products (AGEs), a complex mixture crosslinked proteins protein modifications. Relatively high levels AGEs are generated AD, I diseases. Ne-carboxymethyllysine (CML) serve markers for progression. AGEs, through interaction with receptors (RAGE), initiate cascade deleterious signaling events form inflammatory cytokines, thereby further exacerbate vicious cycle. AGE inhibitors, breakers, RAGE inhibitors therefore potential therapeutic agents multiple diabetes AD. The complexity lack well-established mechanisms largely responsible effective therapeutics targeting AGE-related This review addresses role pathogenesis chronic disorders, recent progress development based on antioxidants, breakers inhibitors. Furthermore, this outlines strategies single-atom nanozymes that attenuate sequestering (ROS) (RNS).

Language: Английский

Rosmarinic acid, a natural polyphenol, has a potential pro-oxidant risk via NADH-mediated oxidative DNA damage

Genes and Environment, Journal Year: 2024, Volume and Issue: 46(1)

Published: June 3, 2024

Abstract Background Rosmarinic acid (RA) has a wide range of beneficial effects on human health. On the other hand, RA been reported to induce metal-mediated reactive oxygen species (ROS) generation and DNA damage. However, its mechanism remains unknown. In this study, clarify underlying mechanism, we analyzed damage in isolated treated with analog isorinic acid. Results plus Cu(II), but not Fe(III), significantly increased 8-oxo-7,8-dihydro-2’-deoxyguanosine (8-oxodG) formation, an indicator oxidative damage, calf thymus DNA. Furthermore, comparison 8-oxodG formation induced by suggested that catechol groups could be associated their abilities form 8-oxodG. Interestingly, Cu(II) was markedly enhanced addition NADH, endogenous reductant. To elucidate Cu(II)-induced examined 32 P-labeled presence Cu(II). caused cleavage, which piperidine treatment, suggesting causes only strand breakage also base modification. inhibited catalase (H 2 O scavenger), bathocuproine (Cu(I) chelator), methional (scavenger variety ROS than • OH) typical OH scavengers SOD, indicating involvement H , Cu(I), OH. cleavage site analysis showing RA-induced site-specific (frequently at thymine some cytosine residues) supports OH, because without specificity. Based these results, Cu(I) concomitant autoxidation lead production Cu(I)-hydroperoxide, induces o -Quinone -semiquinone radicals are likely again reduced dramatically increases particularly low concentrations RA. Conclusions physiologically relevant effectively through redox cycle reactions copper NADH.

Language: Английский