Rubratoxin B mycotoxicosis in the hamster, gerbil and mouse

Jeffery Allen Engelhardt, Purdue University

Abstract

Studies were done to characterize the clinical, pathological, clinicopathological and biochemical features of rubratoxin B mycotoxicosis in the hamster, gerbil, and mouse. The single-dose intraperitoneal (ip) 72-hour LD$\sb{50}$ values and 95% confidence interval for the hamster, gerbil, and mouse were 0.4 (0.2-0.8), 2.0 (1.77-2.26), and 0.31 (0.22-0.43) mg/kg body weight, respectively. The principal histologic alterations were renal tubular degeneration and necrosis in the hamster, renal tubular degeneration and necrosis and focal degeneration and necrosis of hepatocytes in the gerbil, and congestion of the liver, degeneration and necrosis of hepatocytes and congestion of the spleen in the mouse. Renal tubular degeneration was an inconsistent finding in the mouse. Repeated sublethal ip doses of rubratoxin B indicated that the toxicity of rubratoxin B was cumulative with multiple doses over a wide dose range in the hamster and gerbil and a narrow dose range in the mouse. Clinicopathological alterations, characterized by increases in the serum activities of AST and ALT and increased concentration of serum urea nitrogen, correlated with the morphologic alterations observed in the liver and kidney, respectively, following single or multiple ip doses of rubratoxin B in the hamster, gerbil, and mouse. Rubratoxin B caused a 70% decrease in hepatic and a 60% decrease in renal cortical nonprotein sulfhydryl (NPSH) concentration in the hamster and gerbil. Treatment with cysteine did not greatly alter the decrease in NPSH concentration, but did decrease the severity of renal lesions. The incidence and severity of renal lesions was increased in rubratoxin B-treated hamsters and gerbils given diethyl maleate. Renal ultrastructural alterations were evident at 1 hour after hamsters were treated with 0.4 mg/kg body weight of rubratoxin B and were limited to the proximal tubule. Alterations were brush border disruption, dilation of smooth endoplasmic reticulum, mitochondrial swelling, cytoplasmic rarefication, myelin figure formation and swelling of interdigitating processes.

Degree

Ph.D.

Advisors

Carlton, Purdue University.

Subject Area

Animal diseases

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