Effect of 2,4-dinitrophenol and other metabolic inhibitors on the renal deposition and excretion of mercury

Abstract

Observations are reported on the effects of administration of 2,4-dinitrophenol (DNP), probenecid, sodium fluoroacetate, sodium fluoride and sodium malonate on the ability of the rat kidney to accumulate inorganic mercury. Mercury was injected into female rats, body wt. 240 g, as mercuric chloride or mercuric cysteine (100 μg Hg per animal, i.m.) and the metabolic inhibitors were given subcutaneously in doses approaching the ld 50 dose. Mercury levels were measured in urine, blood and kidney. DNP inhibited the renal accumulation of mercury. The other inhibitors were ineffective. DNP was effective only when given just prior to the injection of mercury. The dose of DNP capable of inhibiting renal uptake or mercury was without effect on renal hemodynamics and either did not influence, or only slightly influenced, the excretion of various urinary solutes and water. DNP did not increase the urinary excretion of mercury. It was concluded that the selective accumulation of mercury by kidney is because of energy-dependent processes and that most of this accumulation took place directly into renal tissue from the peritubular capillaries and not by way of glomerular filtration.