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

ABSTRACT

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