An in vivo study of common carp (Cyprinus carpio L.) liver during prolonged hypoxia

被引:32
作者
Poon, W. L. [1 ]
Hung, C. Y. [1 ]
Nakano, K. [1 ]
Randall, D. J. [1 ]
机构
[1] City Univ Hong Kong, Dept Biol & Chem, Kowloon, Hong Kong, Peoples R China
来源
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY D-GENOMICS & PROTEOMICS | 2007年 / 2卷 / 04期
关键词
apoptosis; arrest; carp; hypoxia; liver; CANCER-CELL-LINES; INDUCED APOPTOSIS; INDEPENDENT PATHWAYS; MEDIATED APOPTOSIS; ENDOTHELIAL-CELLS; CYCLE ARREST; ACTIVATION; EXPRESSION; METABOLISM; GLUCOSE;
D O I
10.1016/j.cbd.2007.05.002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Hypoxia induced apoptosis has been studied extensively in many mammalian cell lines but there are only a few studies using whole animal models. We investigated the response of the intact liver to hypoxia in a hypoxia tolerant fish, the carp (Cyprinus carpio, L). We exposed carp to hypoxia for up to 42 days, using oxygen level (0.5 mgO(2)/L) that were slightly higher than the critical oxygen level of carp. There was extensive DNA damage in liver cells, especially during the first week of exposure, indicated by a massive TUNEL signal. However there was no change in cell proliferation, cell number or size, no increase in caspase-3 activity, no increase in single stranded DNA and this, combined with a number of other observations, led us to conclude there was no increase in apoptosis in the liver during hypoxia. There was up-regulation of some antiapoptotic genes and proteins (Bcl-2, HSP70, p27) and down-regulation of some pro-apoptotic genes (Tetraspanin 5 and Cell death activator). The cells appeared to enter cell cycle arrest, presumably to allow repair of damaged DNA. As there was no change in cell proliferation and cell number, the damaged cells were not entering apoptosis and must have recovered during prolonged hypoxia. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:295 / 302
页数:8
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