Effect of carnitine supplementation on mitochondrial enzymes in liver and skeletal muscle of rat after dietary lipid manipulation and physical activity.

Effect of carnitine supplementation in enhancing fat utilization was investigated by looking into its effects on mitochondrial respiratory enzymes activity in liver and muscle as well as on membrane fatty acid profile in rats fed with hydrogenated fat (HF) and MUFA-rich peanut oil (PO) with or without exercise. Male Wistar rats were fed HF-diet (4 groups, 8 rats in each group) or PO-diet (4 groups, 8 rats in each group), with or without carnitine for 24 weeks. One group for each diet acted as sedentary control while the other groups were allowed swimming for 1 hr a day, 6 days/week, for 24 weeks. The PO diet as well as exercise increased the activities of mitochondrial enzymes, NADH dehydrogenase, NADH oxidase, cytochrome C reductase, cytochrome oxidase, while carnitine supplementation further augmented the oxidative capacity of both liver and muscle significantly by enhancing the activity of carnitine palmitoyl transferase and the respiratory chain enzymes. These effects can be attributed to the enhanced unsaturated fatty acids in phospholipids of mitochondria and may be due to increased fluidity of the membrane in these rats. Results of this study show a significant health promoting effects of carnitine supplementation which could be further augmented by regular exercise.

Response of antioxidant system in rats to dietary fat and physical activity.

The influence of feeding hydrogenated fat (HF) or refined peanut oil (PO) diet and regular swimming exercise on hepatic and skeletal muscle antioxidant enzymes i.e., catalase ,and glutathione peroxidase (GPX) as well as tissue lipid peroxidation was investigated in male Wistar rats. Two groups of rats were fed diet with HF or PO as the only fat source. Both the groups were further divided into 4 subgroups each according to physical activity: Two each for sedentary (HFS3, POS3) and two for swimming, HFE3 and POE3 [30 minutes a day, 6 days a week, for 3 months or HFS6, POS6, HFE6 and POE6 for 6 months. A mild increase in lipid peroxidation was observed in both liver and muscle tissues of PO-diet fed rats of E1. Swimming augmented further the lipid peroxidation in liver. GSH level was decreased in the liver of exercising rats, in contrast, it was increased in skeletal muscle by 70% in POE6 and 26% in HFE6. Compared to POS3 swimming elevated GPX activity of about 70% in liver from POE3 as well as about 60% in skeletal muscle from POE3 and POE6. The catalase activity was enhanced in muscle of HFE3 and POE3 by 250% while it remained unaltered in rats of 6 months. These data indicate an adaptive-response of antioxidant enzymes in liver and skeletal muscle to reduce oxidative stress induced by unsaturated fat (PO) and exercise.

Molluscicidal effect of nicotinanilide and its intermediate compounds against a freshwater snail Lymnaea luteola, the vector of animal schistosomiasis

The molluscicidal effect of nicotinanilide was evaluated and compared with niclosamide (2',5-dichloro-4'-nitrosalicylanilide, ethanolamide salt) against different stages of the freshwater snail Lymnaea luteola i.e., eggs, immature, young mature, and adults. Calculated values of lethal concentrations (LC50 and LC90 ) showed that both nicotinanilide and niclosamide as toxic against eggs, immature, and adults. The young mature stage of the snails was comparatively more tolerant to both molluscicides than the other stages. The toxicity of the intermediate compounds of nicotinanilide against the young mature stage of the snails showed them as ineffective. The mortality pattern of the snails exposed to LC90 concentration of these molluscicides showed niclosamide to kill faster (within 8 to 9 h) than nicotinanilide (26 to 28 h). In view of the above studies it may be concluded that both molluscicides are toxic against all the stages of the L. luteola snails.

Physiological, biochemical and histological changes due to physostigmine in monkeys.

Physostigmine (Phy), a short-acting reversible anticholinesterase agent is considered to be a potent prophylactic antidote for the highly toxic organophosphorous (OP) compounds. The toxic effects, if any, of the probable prophylactic doses of Phy have been evaluated by studying its physiological, biochemical and histological effects in monkeys. Phy only at 100 micrograms/kg resulted in certain cholinergic signs such as salivation, lacrymation and muscular faciculations; physiological changes such as mild tachycardia, tachypnea, higher amplitude in electrical activity of the brain, clinico-chemical effects like fall in PO2, PCO2 and alkalosis and histologically an inflammatory reaction in the lungs. On the other hand, the lower dose, i.e. 50 micrograms/kg appeared to be devoid of cholinergic signs and symptoms. However, we observed a significant inhibition of both plasma and erythrocyte ChE and increase in the rectal temperature in both the Phy treated groups. From this study, Phy at a dose of 50 micrograms/kg could be inferred as a safe, sign free intramuscular dose and may probably be used in pretreatment regimen against nerve agents.

Acute histopathological changes induced by methyl isocyanate in lungs, liver, kidneys & spleen of rats.

Methyl isocyanate (MIC), inhaled or administered subcutaneously (sc) at lethal concentration/dose caused essentially similar histopathological changes in all the viscera except for the lungs. The observed congestion of the viscera, foci of hepatocellular necrosis with widening of Disse's spaces in the liver and tubulo-rhexis with degeneration in the kidneys are attributable mostly to the initial shock. In addition, the lungs revealed more distinct route specific patterns of histopathological lesions. Inhaled MIC caused acute eosinophilic necrosis of the bronchial epithelium and frank alveolar edema, while MIC administered sc led to prominent vascular endothelial damage and severe interstitial pneumonitis with normal bronchial epithelium. The differential loci of damage in the lungs may be attributed to the immediate contact surface available for interaction with MIC.

Effects of topically applied sulphur mustard on tissue glycogen, blood glucose, lactate and pyruvate in mice.

Bis-2-Chloroethyl sulphide, commonly known as sulphur mustard (SM) or mustard gas, an alkylating agent, is frequently used as a chemical warfare agent. Inhibition of glycolysis has been related to skin injury and cell death. The effects of SM on tissue glycogen, blood glucose, lactate/pyruvate ratio were investigated in the present study. After a single dermal application of 1.0 LD50 SM in mice, a significant hyperglycemia was observed at 24 hr post exposure. There was a corresponding decrease in liver glycogen content, with no alteration in glycogen content of brain, muscles and kidney. Blood pyruvate and lactate levels were not appreciably altered.