In this review we discuss the key pathogenic and clinical aspects of gallstones, as the main clinical consequences of metabolic dysfunction-associated disease
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Elevated H 2 O 2 production by SOD activity leads to an early inhibition of EAS enzymes activity such as TrxR (Schallreuter et al., 1991a), CAT and GPx, which in turn, leads to an increase in Fenton reaction, increasing hydroxyl concentrations (Fe 2+ + H 2 O 2 Fe 3+ + OH + OH) to a toxic level, that ultimately, leads to a significant peroxidation in several cellular components (membranes, proteins, mitochondria, and DNA) (Schallreuter, 2014)
