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Hydrogen sulfide inhibits myocardial injury induced by homocysteine in rats
Chang, Lin1; Geng, Bin1,2; Yu, Fang2; Zhao, Jing2; Jiang, Hongfeng2; Du, Junbao3; Tang, Chaoshu1,2
关键词Homocysteine Hydrogen Sulfide Sulfur Containing Amino Acids Oxidative Stress Endoplasmic Reticulum Stress
刊名AMINO ACIDS
2008-05-01
DOI10.1007/s00726-007-0011-8
34期:4页:573-585
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology
研究领域[WOS]Biochemistry & Molecular Biology
关键词[WOS]INDUCED OXIDATIVE STRESS ; PROGRAMMED CELL-DEATH ; CARDIOVASCULAR-DISEASE ; ENDOTHELIAL DYSFUNCTION ; MITOCHONDRIAL-FUNCTION ; SUPEROXIDE-DISMUTASE ; RESPIRATORY-FUNCTION ; OXIDASE INHIBITION ; CARDIAC-MUSCLE ; FOLIC-ACID
英文摘要

Hyperhomocysteinemia (HHcy) is a critical independent risk factor for cardiovascular diseases. However, to date, no satisfactory strategies to prevent HHcy exist. Since homocysteine (Hcy) and endogenous H2S are both metabolites of sulfur-containing amino acids, we aimed to investigate whether a metabolic product of Hcy and H2S, may antagonize in part the cardiovascular effects of Hcy. In the HHcy rat model injected subcutaneously with Hcy for 3 weeks, H2S levels and the H2S-generating enzyme cystathionine gamma lyase (CSE) activity in the myocardium were decreased. The intraperitoneal injection of H2S gas saturation solution significantly reduced plasma total Hcy (tHcy) concentration and decreased lipid peroxidation formation (i.e., lowered manodialdehyde and conjugated diene levels in myocardia and plasma). The activities of myocardial mitochondrial respiratory enzymes succinate dehydrogenase, cytochrome oxidase, and manganese superoxide dismutase, related to reactive oxygen species metabolism, were significantly dysfunctional in HHcy rats. The H2S administration restored the level of enzyme activities and accelerated the scavenging of H2O2 and superoxide anion generated by Hcy in isolated mitochondria. The H2S treatment also inhibited the expression of glucose-regulated protein 78, a marker of endoplasmic reticulum (ER) stress, induced by Hcy in vivo and in vitro. Thus, HHcy impaired the myocardial CSE/H2S pathway, and the administration of H2S protected the myocardium from oxidative and ER stress induced by HHcy, which suggests that an endogenous metabolic balance of sulfur-containing amino acids may be a novel strategy for treatment of HHcy.

语种英语
WOS记录号WOS:000255613300009
引用统计
被引频次:107[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/53365
专题北京大学第一临床医学院_心血管内科
北京大学医学部管理机构_医学部
北京大学基础医学院
北京大学第一临床医学院_儿科
北京大学第二临床医学院_风湿免疫科
作者单位1.Peking Univ, Inst Cardiovasc Res, Beijing 100034, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Dept Physiol, Beijing 100871, Peoples R China
3.Peking Univ, Hosp 1, Dept Pediat, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Chang, Lin,Geng, Bin,Yu, Fang,et al. Hydrogen sulfide inhibits myocardial injury induced by homocysteine in rats[J]. AMINO ACIDS,2008,34(4):573-585.
APA Chang, Lin.,Geng, Bin.,Yu, Fang.,Zhao, Jing.,Jiang, Hongfeng.,...&Tang, Chaoshu.(2008).Hydrogen sulfide inhibits myocardial injury induced by homocysteine in rats.AMINO ACIDS,34(4),573-585.
MLA Chang, Lin,et al."Hydrogen sulfide inhibits myocardial injury induced by homocysteine in rats".AMINO ACIDS 34.4(2008):573-585.
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