This study demonstrates that nitric oxide modulates A-type potassium channels via methionine oxidation, a process that can be prevented by antioxidants like vitamin C.
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May implicate methionine oxidation in NO regulation of cardiac K+ channels; hypothesis-generating for human relevance.
Methionine oxidation is known to alter functional properties of a transient A-type potassium channel expressed in Xenopus oocytes. We show here that nitric oxide (NO) slows down the K+ channel inactivation time course by oxidizing a critical methionine residue in the inactivation ball domain of the channel protein. We also demonstrate that the channel protein is protected from methionine oxidation by the enzyme methionine sulfoxide reductase and the antioxidant vitamin C.
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Ciorba et al. (1999) studied this question.
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