Enzyme activity and sulfhydryl status in rat renal cortex following mercuric chloride and dithiothreitol administration

Previous experiments indicated that the partial reversal of mercuric chloride-induced renal dysfunction in rats by subsequent dithiothreitol (DTT) administration was not related to increased mercury excretion, decreased renal mercury concentration, a change in renal cortical subcellular mercury distribution, or the formation of a Hg-DTT complex. The present studies investigated whether DTT, a sulfhydryl reducing agent, protected renal cortical sulfhydryl status in general, or the activity of various renal enzymes (Mg- and Na,K-ATPases, alkaline phosphatase, and glutathione peroxidase) in particular. Additionally, the occurrence of conjugated dienes was used to assess the degree of lipid peroxidation. HgCl2 produced significant decreases in renal cortical protein-bound sulfhydryl concentration, alkaline phosphatase activity, and ATPase activity within 2.5 h of administration, with no effect observed on glutathione peroxidase activity or the levels of conjugated dienes in rat renal cortex. Administration of DTT 60 min after mercury neither provided protection from inhibition nor promoted restoration of the affected enzymes or sulfhydryl status. It is concluded that the partial protection of renal function offered by DTT in the early stages of mercury toxicity does not result from maintaining the integrity of renal cortical sulfhydryl status or the activity of the enzymes investigated. Furthermore, the early stages of mercury toxicity did not appear to be related to lipid peroxidation.