Impaired enzymatic reactive aldehyde-detoxifying capacity and glutathione peroxidase activity in the aged human arterial tissue

脂质过氧化 醛脱氢酶 谷胱甘肽过氧化物酶 氧化应激 化学 谷胱甘肽 生物化学 ALDH2 内分泌学 抗氧化剂 内科学 谷胱甘肽还原酶 4-羟基壬醛 医学
作者
Domenico Lapenna,Giuliano Ciofani,G. Obletter,Sante D. Pierdomenico,Francesco Cipollone,Roberto Cotellese,Massimo Cieri,Ettore Porreca
出处
期刊:Experimental Gerontology [Elsevier]
卷期号:116: 7-13 被引量:6
标识
DOI:10.1016/j.exger.2018.11.013
摘要

It is not known whether aging alters the enzymatic reactive aldehyde- and lipid hydroperoxide-detoxifying capacity of the human arterial tissue favoring vascular oxidative stress. To address this issue, we studied the specific enzymatic activities of class 1, 2 and 3 aldehyde dehydrogenase (ALDH1, ALDH2 and ALDH3), glutathione S‑transferase (isozyme A4-4, GSTA4-4) and aldose reductase (AR), namely the major reactive aldehyde-scavenging enzymes, together with the activity of the lipid hydroperoxide-removing enzyme glutathione peroxidase (GSH-Px), in superior thyroid arteries (STA) specimens obtained in the thyroid surgery setting in aged subjects (age 72.3 ± 3.6 years) and young adult controls (age 31.9 ± 3.5 years). Vascular lipid peroxidation was also studied by assessing in STA fluorescent damage products of lipid peroxidation (FDPL), which reflect oxidant-induced 4‑hydroxynonenal and lipid hydroperoxide formation. Remarkably, the activities of ALDH1, ALDH2, ALDH3, GSTA4-4, AR and GSH-Px were significantly lower, and FDPL levels higher, in the arterial tissue of the aged subjects than in that of the young adult controls. Moreover, the enzymatic activities were inversely and significantly correlated with the levels of FDPL in the arterial tissue of both the aged and young subjects, highlighting their vascular antioxidant/antilipoperoxidative role in vivo. Thus, aging impairs the enzymatic reactive aldehyde-detoxifying capacity and GSH-Px activity of the human arterial tissue eventually favoring vascular oxidative stress.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
beautyy发布了新的文献求助10
1秒前
科研小易发布了新的文献求助10
1秒前
leo发布了新的文献求助10
2秒前
魏万天发布了新的文献求助10
2秒前
3秒前
yichun完成签到,获得积分10
3秒前
浅尝离白给紧张的如南的求助进行了留言
4秒前
华仔应助郝宝真采纳,获得10
5秒前
安静成威完成签到 ,获得积分10
5秒前
难过的微生物完成签到,获得积分10
7秒前
wil发布了新的文献求助10
8秒前
weslywang完成签到 ,获得积分10
8秒前
愉快的老三完成签到,获得积分10
9秒前
Zxx完成签到,获得积分10
9秒前
科研小易完成签到,获得积分20
9秒前
何博洋完成签到,获得积分10
10秒前
joshar完成签到,获得积分10
10秒前
涂惠芳完成签到,获得积分10
11秒前
完美世界应助Cherry采纳,获得10
11秒前
搜集达人应助leo采纳,获得30
11秒前
有魅力的书本完成签到 ,获得积分10
11秒前
12秒前
SchurrleHao完成签到,获得积分10
12秒前
JJH完成签到,获得积分10
12秒前
zmy完成签到,获得积分10
13秒前
善学以致用应助寒冷乐驹采纳,获得10
15秒前
科目三应助strings采纳,获得10
16秒前
斯文败类应助涂惠芳采纳,获得30
16秒前
VPN不好用完成签到,获得积分10
18秒前
19秒前
20秒前
科研通AI2S应助六日采纳,获得30
20秒前
zmy发布了新的文献求助20
21秒前
无私萧发布了新的文献求助10
21秒前
23秒前
zzd12318发布了新的文献求助10
23秒前
23秒前
一味地丶逞强完成签到,获得积分10
25秒前
26秒前
冷傲的灵安完成签到,获得积分10
26秒前
高分求助中
Evolution 10000
The Young builders of New china : the visit of the delegation of the WFDY to the Chinese People's Republic 1000
юрские динозавры восточного забайкалья 800
English Wealden Fossils 700
Foreign Policy of the French Second Empire: A Bibliography 500
Chen Hansheng: China’s Last Romantic Revolutionary 500
China's Relations With Japan 1945-83: The Role of Liao Chengzhi 400
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3147946
求助须知:如何正确求助?哪些是违规求助? 2798939
关于积分的说明 7832669
捐赠科研通 2456017
什么是DOI,文献DOI怎么找? 1307045
科研通“疑难数据库(出版商)”最低求助积分说明 628043
版权声明 601620