The effect of depletion of nonprotein sulfhydryls by diethyl maleate plus buthionine sulfoximine on renal uptake of mercury in the rat

Disposition of Inorganic Mercury Following Biliary Obstruction and Chemically Induced Glutathione Depletion: Dispositional Changes One Hour after the Intravenous Administration of Mercuric Chloride

“…In the present study, animals pretreated with either BSO or DEM did not receive an initial priming dose of DEM 24 h prior to pretreatment, which was used in our previous study and likely had an added effect on the magnitude of reduction in the renal burden of inorganic mercury. In support of this contention, are the findings of Baggett and Berndt (1986), who demonstrated that nonprotein thiol content in the kidneys decreased by approximately 60% in rats pretreated with two doses of DEM (as in our previous study) while it decreased by only about 40% in rats pretreated with a single dose (as in the present study). Further support for this contention comes from the present study.…”

“…Rats that were pretreated with DEM received a 3.37-mmol/kg dose ip in 2.0 ml/kg corn oil. Baggett and Berndt (1986) have shown that this type of pretreatment with DEM causes the nonprotein thiol content in the kidneys and liver to decrease by approximately 40 and 68%, respectively. Two hours after pretreatment with either BSO or DEM, the animals received the nonnephrotoxic 0.5-mol/kg iv dose of mercuric chloride.…”

How can a chemical element elicit complex immunopathology? Lessons from mercury-induced autoimmunity

“…GSH, the most abundant source of intracellular thiols, imparts changes in patterns of cytokine expression. Cellular levels of GSH impact mercury uptake, accumulation and toxicity [85]. GSH is required for induction of IFN-g by the T cell mitogen concanavalin A in vivo [86] and therefore suppression of IFN-g production by mercury in susceptible rats might be due to interactions with GSH [87].…”

Interactive toxicity of inorganic mercury and trichloroethylene in rat and human proximal tubules: Effects on apoptosis, necrosis, and glutathione status

“…Both protein and non-protein sulfhydryl-containing compounds bind Hg 2+ with high affinity and are the major ligands for Hg 2+ in both the extracellular and intracellular space (Zalups and Lash, 1994). The cellular content of thiols, particularly that of glutathione (GSH), can modulate the intracellular uptake, cellular accumulation, and toxicity of Hg 2+ in the renal proximal tubule (Baggett and Berndt, 1986;Berndt et al, 1985;Burton et al, 1995;de Ceaurriz et al, 1994;Girardi and Elias, 1993;Lash et al, 1998aLash et al, ,1999aZalups and Lash, 1997). Conversely, prior exposure of rats to Hg 2+ alters cellular GSH status, with subtoxic concentrations increasing and toxic concentrations depleting GSH concentrations in the cortex and outer stripe of the outer medulla (Lash and Zalups, 1996;Zalups and Lash, 1990).…”