Effect of calcium ion on lipid peroxide formation in endotoxemic mice.

Abstract:

:The present study was conducted to determine the possible role of intracellular Ca2+ in lipid peroxide formation in endotoxin-poisoned mice. Leakages of LDH isozyme and acid phosphatase in serum of mice fed a Ca2+-deficient diet were remarkably increased after administration of 200 micrograms of endotoxin compared to that in endotoxin-nontreated Ca2+-deficient mice. Superoxide anion generation in liver of Ca2+-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 Ca2+-deficient mice as compared to that in endotoxin-nontreated Ca2+-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 Ca2+-deficient diet. In the mice treated with a Ca2+-deficient diet, free radical scavenger levels (alpha-tocopherol and nonprotein sulfhydryl) in liver tissue after endotoxin injection were markedly decreased compared to those in Ca2+-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 Ca2+ may participate in the free radical formation in the liver during endotoxemia and also that Ca2+ may play an important role in the damage of liver mitochondrial function in endotoxemic mice.

journal_name

Microbiol Immunol

authors

Sakaguchi S,Ibata H,Yokota K

doi

10.1111/j.1348-0421.1989.tb01502.x

subject

Has Abstract

pub_date

1989-01-01 00:00:00

pages

99-110

issue

2

eissn

0385-5600

issn

1348-0421

journal_volume

33

pub_type

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