Abstract
The influence of hyperthyroidism on the capacity of the liver to synthesize glutathione (GSH) was evaluated as a possible mechanism of depletion of the tripeptide. For this purpose, the effect of daily doses of 0.1 mg 3,3′,5-triiodothyronine (T 3)/kg for 3 consecutive days on hepatic GSH biosynthetic capacity was assessed by a combined assay measuring gamma-glutamylcysteinyl synthase and GSH synthase simultaneously. T 3 treatment induced a significant 56% depletion of liver GSH in parallel with an increase in the rate of GSH synthesis, the latter effect being completely abolished by l-buthionine sulfoximine. According to these data, the fractional rate of hepatic GSH turnover exhibited a 3.2-fold enhancement in hyperthyroid rats compared to control animals. It is concluded that the enhanced GSH utilization in the liver of hyperthyroid rats previously observed [Fernández et al., Endocrinology 129, 85–91, 1991], is accompanied by an increment in GSH synthesis that is insufficient to sustain the basal levels of the tripeptide observed in euthyroid animals, thus establishing a low steady-state content of GSH in the tissue.
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