Developed resistance to mercuric chloride nephrotoxicity: Failure to protect against other nephrotoxicants

Abstract

Daily, oral treatment of rats for 14 days with 5 mg kg of mercuric chloride (HgCl 2) caused hypertrophy of the kidney, but no change in percent tissue water, or serum urea nitrogen (BUN) or creatinine concentrations. Upon histological examination, hypercellularity and increased basophilia of the outer medulla were observed. A single, subcutaneous injection of 20 mg kg of potassium chromate (K 2CrO 4) increased kidney size and water content, as well as BUN and serum creatinine concentrations, and produced coagulative necrosis of the proximal convoluted tubules. Intraperitoneal injection of 125 mg kg of hexachloro-1,3-butadiene (HCBD) increased kidney weight, percent water, BUN and serum creatinine, and produced necrosis of the proximal straight tubules in approximately half of the animals. 1 g kg biphenyl, orally, produced only diffuse tubular swelling. Rats treated with 20 mg kg K 2CrO 4, 125 mg kg HCBD or 1 g kg biphenyl following 14 days of treatment with 5 mg kg HgCl 2 generally displayed the symptoms of both types of treatment, and the severity of the K 2CrO 4, HCBD and biphenyl effects were substantially the same as in those without HgCl 2 pretreatment. Developed resistance to HgCl 2 nephrotoxicity, therefore, appears to have little effect on response of the kidney to other nephrotoxicants.