Disorders of immune state parameters and lipid peroxidation under experimental exposure to radiation

O. Ilderbayev, S. Kashanskiy, L. Chulenbayeva, Masygut R. Mynzhanov, G. Ilderbayeva
{"title":"Disorders of immune state parameters and lipid peroxidation under experimental exposure to radiation","authors":"O. Ilderbayev, S. Kashanskiy, L. Chulenbayeva, Masygut R. Mynzhanov, G. Ilderbayeva","doi":"10.31089/1026-9428-2018-11-16-21","DOIUrl":null,"url":null,"abstract":"The article presents experimental data on the impact of high dose gamma-radiation exposure (6 Gy) on immune system, lipid oxidation products (LOPs) and antioxidant defense system (AODS) enzymes activity. The study revealed that high dose radiation exposure suppressed the cell-mediated immunity especially with respect to T-lymphocytes and their subpopulations as well as immune defense and adaptation mechanisms. Ionizing radiation exposure led to increase of conjugated lipid dienes and malondialdehyde (MDA), and to inhibition of catalase and glutathione peroxidise activity, thus promoting oxidative stress in most of the examined samples. The results indicate dramatic changes in lipid peroxidation and antioxidant defense system under the radiation stress. Both cell-mediated and humoral immunity inhibition, mononuclear phagocyte system suppression and lipid peroxidation / antioxidant defense imbalance provide a background for immunopathological disorders, provoking radiation-related carcinogenesis. Impairment of functional network related to glutathione-dependent redox catalytic system decreases human antioxidant status, that necessitates specification of new promising methods correcting adaptation.","PeriodicalId":229714,"journal":{"name":"Occupational Health and Industrial Ecology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2019-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Occupational Health and Industrial Ecology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.31089/1026-9428-2018-11-16-21","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

The article presents experimental data on the impact of high dose gamma-radiation exposure (6 Gy) on immune system, lipid oxidation products (LOPs) and antioxidant defense system (AODS) enzymes activity. The study revealed that high dose radiation exposure suppressed the cell-mediated immunity especially with respect to T-lymphocytes and their subpopulations as well as immune defense and adaptation mechanisms. Ionizing radiation exposure led to increase of conjugated lipid dienes and malondialdehyde (MDA), and to inhibition of catalase and glutathione peroxidise activity, thus promoting oxidative stress in most of the examined samples. The results indicate dramatic changes in lipid peroxidation and antioxidant defense system under the radiation stress. Both cell-mediated and humoral immunity inhibition, mononuclear phagocyte system suppression and lipid peroxidation / antioxidant defense imbalance provide a background for immunopathological disorders, provoking radiation-related carcinogenesis. Impairment of functional network related to glutathione-dependent redox catalytic system decreases human antioxidant status, that necessitates specification of new promising methods correcting adaptation.
实验照射下免疫状态参数和脂质过氧化的紊乱
本文介绍了高剂量γ辐射照射(6 Gy)对免疫系统、脂质氧化产物(LOPs)和抗氧化防御系统(AODS)酶活性影响的实验数据。研究表明,高剂量辐射暴露抑制了细胞免疫,特别是t淋巴细胞及其亚群,以及免疫防御和适应机制。电离辐射暴露导致共轭脂质二烯和丙二醛(MDA)的增加,并抑制过氧化氢酶和谷胱甘肽过氧化物活性,从而促进大多数检测样品的氧化应激。结果表明,在辐射胁迫下,脂质过氧化和抗氧化防御系统发生了显著变化。细胞介导和体液免疫抑制、单核吞噬细胞系统抑制和脂质过氧化/抗氧化防御失衡为免疫病理障碍提供了背景,引发了辐射相关的致癌作用。与谷胱甘肽依赖的氧化还原催化系统相关的功能网络的损伤降低了人体的抗氧化状态,这就需要规范新的有前途的方法来纠正适应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信