Loss of alpha-tocopherol upon exposure to nitric oxide or the sydnonimine SIN-1.
SIN-1 which spontaneously decomposes to yield nitric oxide (NO.) and superoxide anion (O2.-) radicals caused a loss of microsomal alpha-tocopherol paralleled by the formation of alpha-tocopheryl quinone. The loss was partially prevented by superoxide dismutase but not by catalase. The SIN-1-induced loss of alpha-tocopherol also occurred when tocopherol was dissolved in ethanol/potassium phosphate buffer (20/80, v/v). Likewise, addition of authentic NO. to alpha-tocopherol dissolved in ethanol resulted in loss of the vitamin and quinone formation. These results suggest that NO. or its products such as peroxynitrite or nitrogen dioxide react with alpha-tocopherol, the quinone derivative being a major oxidation product. Depletion of vitamin E by NO. may contribute to tissue injury, e.g. in neuronal tissues.
de Groot
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H
Institut für Physiologische Chemie I, Heinrich-Heine-Universität Düsseldorf, Germany.
Hegi
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Sies
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D000818:Animals; D008054:Lipid Peroxides / Q000378:metabolism; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism; D008981:Molsidomine / Q000031:analogs & derivatives* / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism* / Q000494:pharmacology; D011809:Quinones / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014810:Vitamin E / Q000378:metabolism*
D008054:Lipid Peroxides; D011809:Quinones; D014810:Vitamin E; D009569:Nitric Oxide; C002385:linsidomine; D008981:Molsidomine