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When tissue folate and cobalamin stores are intact, an abnormal increment of postmethionine-load homocysteinemia may also reveal a saturation of the transsulfuration pathway caused by dietary methionine excess that might be combined with transsulfuration defects (in cases with basal hyperhomocysteinemia) or with the homozygous thermolabile MTHFR defect (in cases with normal fasting homocysteine) (Cattaneo, 1999)
Well-designed randomized clinical studies are needed to systematically evaluate the evidence for the use of these hepatoprotective agents as treatment options for APAP-induced liver injury, to determine the timing of initiation of the therapy, and to further define the optimal treatment regimen
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When liver metabolism is overburdened, oxidative stress may rise while glutathione, methylation capacity and cellular energy are consumed more rapidly
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