The role of iron in the NADPH-dependent lipid peroxidation due to glutathione depletion by phorone.
Enhanced NADPH-dependent LPO in rat liver postmitochondrial supernatants in vitro due to depletion of GSH by treatment with phorone (diisopropylidene acetone) in vivo was inhibited by Fe2+-chelating agents (desferrioxamine, DETAPAC), but not by scavengers of .O2-, H2O2, singlet oxygen or .OH-radicals, indicating that a perferryl ion (Fe2+ . O2) is needed as an initiating factor. In vivo, rats treated with phorone (250 mg/kg i.p.) exhaled 1.4 times as much ethane within 4 h as compared to controls. Pretreatment with FeSO4 resulted in a 6.9-fold enhancement of LPO as compared to Fe2+-pretreated controls. Our results indicate that GSH-depletion results in a strong enhancement of NADPH-dependent LPO also in vivo, provided that an initiating factor is present.
D000818:Animals; D004980:Ethane / Q000378:metabolism; D005978:Glutathione / Q000172:deficiency* / Q000502:physiology; D066298:In Vitro Techniques; D007501:Iron / Q000502:physiology*; D007659:Ketones / Q000494:pharmacology*; D008054:Lipid Peroxides / Q000096:biosynthesis*; D008099:Liver / Q000378:metabolism*; D008297:Male; D009249:NADP / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains
D007659:Ketones; D008054:Lipid Peroxides; D009249:NADP; C018637:phorone; D007501:Iron; D005978:Glutathione; D004980:Ethane