2003 年 2003 巻 Suppl3 号 p. 277-280
Xanthoascin, a hepato- and cardio-toxic metabolite of Aspergillus candidus, has been examined for in vitro toxicity to respiratory function of isolated rat liver mitochondria to elucidate the molecular mechanism of its in vivo toxicity. It was found that xanthoascin exerted dual deteriorate effects to mitochondrial respiration, exhibiting an uncoupling effect and an electron transport inhibition at NADH-UQ oxidoreductase (complex I) and cytochrome c oxidase (complex IV).