Hydrogen Sulfide as an Endogenous Modulator in Mitochondria and Mitochondria Dysfunction

被引:80
作者
Guo, Wei [1 ]
Kan, Jun-tao [1 ]
Cheng, Ze-yu [1 ]
Chen, Jie-fang [1 ]
Shen, Ya-qi [1 ]
Xu, Jie [1 ]
Wu, Dan [1 ]
Zhu, Yi-zhun [1 ,2 ,3 ]
机构
[1] Fudan Univ, Sch Pharm, Dept Pharmacol, Shanghai 201203, Peoples R China
[2] Fudan Univ, Inst Biomed Sci, Shanghai 201203, Peoples R China
[3] Natl Univ Singapore, Dept Pharmacol, Singapore 117597, Singapore
关键词
OXIDATIVE STRESS; INHIBITION; ISCHEMIA; LUNG; H2S; ANTIOXIDANT; METABOLISM; DISORDERS; MECHANISM; CHANNELS;
D O I
10.1155/2012/878052
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Hydrogen sulfide (H2S) has historically been considered to be a toxic gas, an environmental and occupational hazard. However, with the discovery of its presence and enzymatic production through precursors of L-cysteine and homocysteine in mammalian tissues, H2S has recently received much interest as a physiological signaling molecule. H2S is a gaseous messenger molecule that has been implicated in various physiological and pathological processes in mammals, including vascular relaxation, angiogenesis, and the function of ion channels, ischemia/reperfusion (I/R), and heart injury. H2S is an endogenous neuromodulator and present studies show that physiological concentrations of H2S enhance NMDA receptor-mediated responses and aid in the induction of hippocampal long-term potentiation. Moreover, in the field of neuronal protection, physiological concentrations of H2S in mitochondria have many favorable effects on cytoprotection.
引用
收藏
页数:9
相关论文
共 63 条
[1]
Abe K, 1996, J NEUROSCI, V16, P1066
[2]
Oxidative stress and anxiety Relationship and cellular pathways [J].
Bouayed, Jaouad ;
Rammal, Hassan ;
Soulimani, Rachid .
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2009, 2 (02) :63-67
[3]
Transmission of mitochondrial DNA disorders: possibilities for the future [J].
Brown, D. T. ;
Herbert, M. ;
Lamb, V. K. ;
Chinnery, P. F. ;
Taylor, R. W. ;
Lightowlers, R. N. ;
Craven, L. ;
Cree, L. ;
Gardner, J. L. ;
Turnbull, D. M. .
LANCET, 2006, 368 (9529) :87-89
[4]
Mitochondria in the diabetic heart [J].
Bugger, Heiko ;
Abel, E. Dale .
CARDIOVASCULAR RESEARCH, 2010, 88 (02) :229-240
[5]
Hydrogen sulfide-releasing NSAIDs inhibit the growth of human cancer cells: A general property and evidence of a tissue type-independent effect [J].
Chattopadhyay, Mitali ;
Kodela, Ravinder ;
Nath, Niharika ;
Dastagirzada, Yosef M. ;
Velazquez-Martinez, Carlos A. ;
Boring, Daniel ;
Kashfi, Khosrow .
BIOCHEMICAL PHARMACOLOGY, 2012, 83 (06) :715-722
[6]
Hydrogen sulfide: third gaseous transmitter, but with great pharmacological potential [J].
Chen, Chang-qing ;
Xin, Hong ;
Zhu, Yi-zhun .
ACTA PHARMACOLOGICA SINICA, 2007, 28 (11) :1709-1716
[7]
Is mitochondrial generation of reactive oxygen species a trigger for autophagy? [J].
Chen, Yongqiang ;
Gibson, Spencer B. .
AUTOPHAGY, 2008, 4 (02) :246-248
[8]
Mitochondria [J].
Chinnery, PF ;
Schon, EA .
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 2003, 74 (09) :1188-1199
[9]
Cytochrome oxidase inhibition induced by acute hydrogen sulfide inhalation: Correlation with tissue sulfide concentrations in the rat brain, liver, lung, and nasal epithelium [J].
Dorman, DC ;
Moulin, FJM ;
McManus, BE ;
Mahle, KC ;
James, RA ;
Struve, MF .
TOXICOLOGICAL SCIENCES, 2002, 65 (01) :18-25
[10]
Regulation of cardiovascular cell function by hydrogen sulfide (H2S) [J].
Elsey, David J. ;
Fowkes, Robert C. ;
Baxter, Gary F. .
CELL BIOCHEMISTRY AND FUNCTION, 2010, 28 (02) :95-106