Beneficial role of L-thyroxine on hepato-renal toxicity induced by amikacin and potassium dichromate

Amikacin aminoglycoside antibiotic, potassium dichromate and L- thyroxine were employed to study the induction of hepatonephrotoxicity changes using potassium dichromate; the effect of amikacin sulfate aminoglycoside antibiotic on liver and kidney functions in normal rats and in rats subjected to potassium dichromate induced hepatonephrotoxicity and to minimize the undue effect of both potassium dichromate and amikacin by either concomitant or pre-administration of L- thyroxine. The following test parameters were carried out in serum: ALT, AST, isocitrate dehydrogenase, glucose-6- phospatase, total protein, albumin, urea, creatinine and N- acetyl-B- glucosaminidase. The results indicated that the efficient potassium dichromate induced renal impairment required the use of adult rats weighing 250-350 g. The well-marked changes of all the previous test parameters were investigated throughout the experimental period. Among these parameters, serum albumin level seemed to be of a special concern as a risk factor for aminoglycoside nephrotoxicity. The administration of L- thyroxine [10 mug/100 g body wt.] caused an improvement of kidney and liver functions of rats receiving amikacin or potassium dichromate, respectively

Prophylactic and protective effect of L-thyroxine on hepato-renal dysfunction induced by amika.cin and potassium dichromate

The present study was concerned with amikacin's hepatorenal hazards on certain kidney and liver tissue enzymes in normal rats as well as rats subjected to potassium dichromate induced hepatorenal toxicity. Minimizing the undue effects of both amikacin and potassium dichromate by either concomitant or pre-administration of L-thyroxine was also undertaken. Specific enzyme activity of N-acetyl-beta-D- glucosaminidase, NAG [as a marker of lysosomal enzyme], Na-K- ATPase [as a marker of basolateral membrane enzyme] and glucosed-6-phosphatase, G-6-Pase [as a marker of endoplasmic reticulum] as well as liver 5-nucleotidase specific enzyme activity were measured. The association of potassium dichromate, amikacin or both with the membrane binding caused increased lysosomal hydrolase specific enzyme activity extracted from the liver and kidney tissues, reduction of Na- K-ATPase, G-6-Pase and liver 5-nucleotidase activities, membrane damage in renal tubule of the rats as well as the induction of ultrastructural alterations of the liver. Thyroid hormone had an important stimulatory action on the plasma membrane pump that maintained cellular constancy of sodium and potassium. The recorded data may suggest that L- thyroxine administration may enable the cell to resist liver and kidney injury