Lipid profiles in cerebral and hepatic tissues of wistar rats during chronic phosphamidon toxicity.

The possibility of alterations in function of lipids in structural components of membranes such as storage, protective coating on the surface, cell recognition, and tissue immunity during phosphamidon stress, prompted the present investigation. Specifically chosen doses of phosphamidon, viz, acute dose (AD) (1/2 LD50, 6.63 mg/kg body wt/day), and subacute dose (ASD) (1/3 LD50; 0.10 mg/kg body wt/day) were administered to male Wistar rats orally by gavage. After the stipulated treatment period, brain and liver from these rats were examined for lipid profiles such as cholesterol triglycerides and phospholipids, using standard biochemical procedures. An increase in lipid peroxidation in conjunction with reduced levels of lipid profiles indicated that the lipid profiles were variously affected depending on different altered chemical reactons in the tissues of animal under stress. The study shows that induced lipid peroxidation was on par with the reduced levels of lipid profiles, indicating that the lipid profiles under continued daily dosing of phosphamidon could generate free radicals, in spite of elevation in the levels of antioxidants, or antioxidant enzyme activity, or both.

Arginine protection against ammonia toxicity in exhausted rat.

Arginine administration (5 m moles/kg/day) to albino rats for 7 days, revealed that this vital basic amino acid possesses latent potentiality for the accentuation of urea cycle or at least for arginase activity. The mitigation of ammonia toxicity was observed to be more effective in the case of gastrocnemius and red vastus as compared to white vastus. Further, ammonia and lactate levels were also decreased by arginine in blood and thereby delaying the onset of fatigue by preventing ammonotoxemia and lactic acidemia.

Alterations in some dehydrogenase profiles of sciatectomized toad gastrocnemius muscle-metabolic modifications by malate.

Sciatectomized toad gastrocnemius has shown a progressive loss in lactate (LDH), succinate (SDH) and malate (MDH) dehydrogenase activities and elevation of glutamate dehydrogenase (GDH) activity during post-neurectemic days. The possible role of malate in the restoration of metabolic homeostasis in denervated muscle is discussed.