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The effect of thyroxine or carbimazole treatment on gentamicin nephrotoxicity in rats

Desert and Marine Environment Research Centre, UAE University, PO Box: 17777, Al Ain, UAE

A.A. Bashir

Department of Pharmacology, Faculty of Medicine, Al Arab Medical University, Benghazi, Libya

M.O.M. Tanira

Department of Pharmacology and Therapeutics, Faculty of Medicine and Health Sciences, UAE University, Al Ain, UAE

1 This study examines the effect of treating rats with gen tamicin (80 mg kg^-1 day^-1 intramuscularly (i.m.), for 6 days) alone or with either L-thyroxine or the anti-thyroid drug carbimazole.

2 Gentamicin produced significant increases in serum creatinine and urea concentrations, and significantly reduced the activity of Na⁺,K⁺ATPase in renal cortex. The concentration of serum triiodothyronine (T₃) was unaffect ed by graded doses (20, 40 and 80 mg kg-1) of the antibiot ic. Histopathologically, gentamicin produced necrosis of proximal tubules in the renal cortical tissues of treated rats.

3 Treatment of rats with either L-thyroxine or carbima zole alone did not significantly affect any of the biochemi cal variables investigated. Carbimazole alone produced only mild tubular necrosis.

4 Treatment of rats with either L-thyroxine (100 µg kg^-1 day^-1, subcutaneously) for 10 days, and gentamicin (80 mg kg^-1, i.m. daily during the last 6 days of treatment signifi cantly reduced the gentamicin-induced increases in serum creatinine and urea concentrations, and increased the activity of cortical N⁺,K⁺ATPase to control levels. Histopathologically, the severity of gentamicin-induced tubular necrosis was reduced by L-thyroxine treatment.

5 Carbimazole (12 mg ml-1 in drinking water for 21 days) and gentamicin (80 mg kg^-1 i.m.) daily during the last 6 days of treatment, stimulated the increase in serum urea concentration produced by gentamicin, but did not signifi cantly affect the gentamicin-induced changes in serum creatinine or cortical N⁺,K⁺ATPase.

Key Words: thyroxine • carbimazole • gentamicin • nephrotoxi city • nephroprotection.

Human & Experimental Toxicology, Vol. 14, No. 1, 13-17 (1995)
DOI: 10.1177/096032719501400103


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