Manganese toxicity: lipid peroxidation in rat brain.
Albino rats were given intraperitoneally manganese chloride (Mn2+, 4mg/kg) daily for a period of 30 days. Manganese significantly inhibited the lipid peroxidation potential of treated rat brain without altering the contents of iron and ascorbic acid, the two prooxidant factors. In vitro lipid peroxidation studies in the fresh and heated brain homogenates showed almost a non-enzymatic mechanism of inhibition by this metal ion. 30 micrometers Mn2+ concentrations completely inhibited the formation of malonaldehyde (MDA) at 3 hours of incubation. Iron was found to reverse, to some extent, the effect of manganese on in vitro lipid peroxide formation in the mitochondrial fraction of brain and at concentrations of 5 micrometers Fe2+ the amount of MDA formed is comparable to that observed with 1 micro meter Fe2+ in the mitochondrial fraction without manganese. These observations suggest that the central nervous system toxicity of manganese may not be associated with accelerated in vivo lipid peroxidation. However, the mechanism of iron induced reversal on in vitro inhibition of lipid peroxidation by manganese is not understood, at present.
D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D007501:Iron / Q000378:metabolism; D008054:Lipid Peroxides / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000037:antagonists & inhibitors; D008345:Manganese / Q000494:pharmacology*; D020149:Manganese Poisoning; D008928:Mitochondria / Q000187:drug effects; D051381:Rats
D008054:Lipid Peroxides; D008345:Manganese; D008315:Malondialdehyde; D007501:Iron; D001205:Ascorbic Acid