Oxidative and Nitrous Stress Underlies Vascular Malfunction Induced by Ionizing Radiation and Diabetes.

IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
Cardiovascular Toxicology Pub Date : 2024-08-01 Epub Date: 2024-06-25 DOI:10.1007/s12012-024-09878-x
Anatoly Soloviev, Vadym Sydorenko
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引用次数: 0

Abstract

Oxidative stress results from the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in quantities exceeding the potential activity of the body's antioxidant system and is one of the risk factors for the development of vascular dysfunction in diabetes and exposure to ionizing radiation. Being the secondary products of normal aerobic metabolism in living organisms, ROS and RNS act as signaling molecules that play an important role in the regulation of vital organism functions. Meanwhile, in high concentrations, these compounds are toxic and disrupt various metabolic pathways. The various stress factors (hyperglycemia, gamma-irradiation, etc.) trigger free oxygen and nitrogen radicals accumulation in cells that are capable to damage almost all cellular components including ion channels and transporters such as Na+/K+-ATPase, BKCa, and TRP channels. Vascular dysfunctions are governed by interaction of ROS and RNS. For example, the reaction of ROS with NO produces peroxynitrite (ONOO-), which not only oxidizes DNA, cellular proteins, and lipids, but also disrupts important signaling pathways that regulate the cation channel functions in the vascular endothelium. Further increasing in ROS levels and formation of ONOO- leads to reduced NO bioavailability and causes endothelial dysfunction. Thus, imbalance of ROS and RNS and their affect on membrane ion channels plays an important role in the pathogenesis of vascular dysfunction associated with various disorders.

Abstract Image

氧化应激和亚硝应激是电离辐射和糖尿病诱发血管功能失调的基础
氧化应激源于活性氧(ROS)和活性氮(RNS)的产生,其数量超过了机体抗氧化系统的潜在活性,是导致糖尿病血管功能障碍和暴露于电离辐射的风险因素之一。作为生物体内正常有氧代谢的次级产物,ROS 和 RNS 是信号分子,在调节生物体的重要功能方面发挥着重要作用。同时,在高浓度下,这些化合物具有毒性,会破坏各种代谢途径。各种应激因素(高血糖、伽马射线照射等)都会引发细胞内自由氧和氮自由基的积累,这些自由氧和氮自由基能够破坏几乎所有的细胞成分,包括离子通道和转运体,如 Na+/K+-ATPase、BKCa 和 TRP 通道。血管功能障碍受 ROS 和 RNS 相互作用的影响。例如,ROS 与 NO 反应会产生过亚硝酸盐(ONOO-),它不仅会氧化 DNA、细胞蛋白和脂质,还会破坏调节血管内皮阳离子通道功能的重要信号通路。ROS 水平的进一步升高和 ONOO- 的形成会导致 NO 的生物利用率降低,从而引起血管内皮功能障碍。因此,ROS 和 RNS 的失衡及其对膜离子通道的影响在与各种疾病相关的血管功能障碍的发病机制中起着重要作用。
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来源期刊
Cardiovascular Toxicology
Cardiovascular Toxicology 医学-毒理学
CiteScore
6.60
自引率
3.10%
发文量
61
审稿时长
>12 weeks
期刊介绍: Cardiovascular Toxicology is the only journal dedicated to publishing contemporary issues, timely reviews, and experimental and clinical data on toxicological aspects of cardiovascular disease. CT publishes papers that will elucidate the effects, molecular mechanisms, and signaling pathways of environmental toxicants on the cardiovascular system. Also covered are the detrimental effects of new cardiovascular drugs, and cardiovascular effects of non-cardiovascular drugs, anti-cancer chemotherapy, and gene therapy. In addition, Cardiovascular Toxicology reports safety and toxicological data on new cardiovascular and non-cardiovascular drugs.
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