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First, hyperhomocysteinemia detected only in the fasting state (approximately 23% of patients), which might mainly result from an inhibition of the homocysteine remethylation pathway (folate, cobalamin, or functional methionine synthase deficiencies or thermolabile MTHFR mutation), and which increases the cardiovascular risk 1.6-fold

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The definite toxicity, safety margin and potential adverse reactions have not been reported

reported that ASX mitigated oxidative stress, apoptotic cell death, behavioral impairment, and dopaminergic neuron loss in a paraquat-induced PD mouse model [10]

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