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S NOS of its substrate L-arginine; antagonizes the increased ET-1 expression that promotes vasoconstriction and inflammation; upregulates SOD-1 expression to combat oxidative/nitrosative stress; and finally, causes partial reversal of dephosphorylation of eNOS, which impairs NO generation. Others have confirmed the SOD-1 finding and also reported elevated SOD-2 expression (Collino et al., 2013). T

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