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It is conceivable that this general mechanism can explain Mercury-induced oxidative stress not only through a continuous depletion of the reduced glutathione pool, but also by interfering with enzymes operating through active sites based on vicinal thiol groups or which are regulated by glutathionylation of sensing cysteine residues

Consequently, inhibiting them is a crucial tactic to interfere with the continuous inflammatory process

In particular, our global metabolomic analyses revealed important therapeutic targets in LC patients

Ensuring an adequate supply of manganese in the body allows critical enzymes to effectively breakdown carbohydrates and protects the liver from oxidative stress damage induced by alcohol

Alcohol disrupts NO pathways throughout the body

During therapy, no additional environmental or pharmacological triggers were identified in our patients