title: 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.
authors.affiliation: First Department of Hygienic Chemistry, Tohoku College of Pharmacy, Miyagi.
authors.forename: S
authors.initials: S
authors.lastname: Sakaguchi
authors.forename: H
authors.initials: H
authors.lastname: Ibata
authors.forename: K
authors.initials: K
authors.lastname: Yokota
mesh_terms: D000818:Animals; D002118:Calcium / Q000172:deficiency / Q000378:metabolism*; D004731:Endotoxins / Q000633:toxicity; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008054:Lipid Peroxides / Q000096:biosynthesis*; D008099:Liver / Q000378:metabolism; D008297:Male; D051379:Mice; D010101:Oxygen Consumption; D013481:Superoxides / Q000378:metabolism; D014115:Toxemia / Q000378:metabolism*
chemical_list: D004731:Endotoxins; D007527:Isoenzymes; D008054:Lipid Peroxides; D013481:Superoxides; D007770:L-Lactate Dehydrogenase; D002118:Calcium