Modification of Liver and Serum Enzymes by Paraquat Treatment in Rabbits

Abstract

Paraquat (PQ) is known to cause progressive interstitial fibrosis in the lungs. Previous investigations have indicated that PQ acts by lipid peroxidation of the membrane. However, there are few reports on the action of PQ on hepatic enzymes. This work was carried out to investigate the modulation of various hepatic enzymes by PQ in rabbits. Paraquat was administered at a dose of 3, 6 or 12 mg/kg b. wt/day intraperitoneally to male rabbits for different periods of time. Administration of paraquat resulted in a significant decrease in plasma activities of transaminase enzymes, alkaline phosphatase and liver transketolase. No significant change was found in the activities of plasma and hepatic lactate dehydrogenase and alkaline phosphatase. A marked increase in blood glucose was noticed 48 hours after paraquat administration.

Hepatotoxicity Related to Paraquat and Diquat Absorption Through Intact Skin

“…observed in animal models of paraquat-induced hepatotoxicity [5,6], and previously reported cases of paraquat-induced liver toxicity after accidental dermal exposition showed a cholangiodestructive cholestasis probably produced by a direct corrosive effect of paraquat [7][8][9].…”

Effect of <i>Manasamitra vatakam</i>, an Ayurvedic Formulation, on Aluminium-Induced Neurotoxicity in Rats

“…Increase in blood glucose level may have disrupted carbohydrate metabolism due to enhanced breakdown of liver glycogen, possibly mediated by increase in adrenocorticotrophic and glucagon hormones and/or reduced insulin activity [17]. Sallam et al [18] reported that Al accumulation in the liver leads to liver damage as a result of increased enzymes levels of ALP, SGOT, SGPT and glucose in the serum.…”

Deltamethrin-induced oxidative damage and biochemical alterations in rat and its attenuation by Vitamin E

“…Reduction of hepatic glycogen indicates expenditure of energy because of stress caused by deltamethrin. The rise in blood glucose by pesticide treatment may indicate disrupted carbohydrate metabolism due to enhanced breakdown of liver glycogen, possibly mediated by increase in adrenocorticotrophic and glucagon hormones and/or reduced insulin activity (Raja et al, 1992). Elevated blood urea is correlated with an increased protein catabolism in mammalian body or from more efficient conversion of ammonia to urea as a result of increased synthesis of enzyme involved in urea production (Rodwell, 1979).…”