• H Maruyama, K Furukawa, and M Onda.
• First Department of Surgery, Nippon Medical School, Tokyo, Japan.
• Nippon Ika Daigaku Zasshi. 1995 Jun 1;62(3):271-82.

AbstractThe effect of coenzyme Q10 (CoQ10) on hepatocyte injury during endotoxin (ET) shock in rats was studied with special reference to the role of polymorphonuclear neutrophils (PMN). ET shock was induced by intravenous administration of 5 mg/kg ET, and CoQ10 was given at 20 mg/kg once or 3 times orally or intravenously. We examined plasma glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and glutamate dehydrogenase (GLDH) levels, superoxide production by PMN, the phagocytic activity of PMN, the cytotoxicity of PMN to liver cells, and histological changes in the liver. The CoQ10-treated rats showed lower levels of GOT, GPT, and GLDH than rats treated with ET only. When compared to the group given ET only superoxide production by PMN induced by 2-methyl-6-phenyl-3,7-dihydroimidazol [1,2-alpha]pyrazin-3-one (MCLA) was significantly inhibited in the group given CoQ10 intravenously and 3 times orally, but there was no significant difference in the group given CoQ10 once orally. However, the level of superoxide production by PMN stimulated by phorbol myristate acetate (PMA) was lower in all CoQ10-treated rats than in those given ET only. There was no difference in either peripheral PMN counts or PMN phagocytes between the CoQ10-treated group and the group given ET only. Histologically, the hepatocyte injury in all groups that received CoQ10 was milder than that in the ET-only group. No hepatocyte cytotoxicity by PMN was observed in any group that received CoQ10. These results suggest that both intravenous and oral administration of CoQ10 can modulate the endotoxin-activated PMN, and is useful for preventing hepatocyte injury during ET shock.

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