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Effect of Calcium Ion on Lipid Peroxide Formation in Endotoxemic Mice
Author(s) -
Sakaguchi Shuhei,
Ibata Hiroshi,
Yokota Katsushi
Publication year - 1989
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1989.tb01502.x
Subject(s) - lipid peroxide , superoxide , verapamil , medicine , endocrinology , calcium , respiratory system , biology , cholesterol , biochemistry , chemistry , lipid peroxidation , enzyme , oxidative stress
The present study was conducted to determine the possible role of intracellular Ca 2+ in lipid peroxide formation in endotoxin‐poisoned mice. Leakages of LDH isozyme and acid phosphatase in serum of mice fed a Ca 2+ ‐deficient diet were remarkably increased after administration of 200 μ g of endotoxin compared to that in endotoxin‐nontreated Ca 2+ ‐deficient mice. Superoxide anion generation in liver of Ca 2+ ‐deficient mice and in mice fed a normal diet greatly increased after endotoxin administration. On the contrary, after endotoxin injection there was scarcely any difference in SOD activity of liver of Ca 2+ ‐deficient mice as compared to that in endotoxin‐nontreated Ca 2+ ‐deficient mice. In spite of an increase of superoxide anion generation there was little or no effect of endotoxin administration on lipid peroxide formation in mice given a Ca 2+ ‐deficient diet. In the mice treated with a Ca 2+ ‐deficient diet, free radical scavenger levels ( α ‐tocopherol and nonprotein sulfhydryl) in liver tissue after endotoxin injection were markedly decreased compared to those in Ca 2+ ‐deficient diet alone. Mice fed a normal diet exhibited a significant decrease of lipid peroxide level in liver by injection of endotoxin together with verapamil (10 mg/kg, s.c.). When mice fed a normal diet were injected with endotoxin, the state 3 respiratory activity showed a 49% decrease, and respiratory control ratio (RCR) of endotoxemic mice liver mitochondria was 38% lower than normal liver mitochondria. No difference could be observed in levels of state 3 and RCR between the mice given verapamil plus endotoxin and the normal mice. These findings suggest the possibility that Ca 2+ may participate in the free radical formation in the liver during endotoxemia and also that Ca 2+ may play an important role in the damage of liver mitochondrial function in endotoxemic mice.