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.