Nature of dichlorvos intoxication in a freshwater prawn, Macrobrachium lamarrei (H. Milne Edwards)

Exposure of freshwater prawn (Macrobrachium lamarrei (H. Milne Edwards) to a lethal dose (96-hr LC50;0.78 mg/l) of dichlorvos for 24, 48, 72, and 96 hr induced inhibition in acetylcholinesterase and alkaline phosphatase activities and enhanced acid phosphatase activity. Hepatic glycogen values were depleted while the blood glucose level was increased up to 72 hr of exposure. After 96 hr of dichlorvos exposure hypoglycemia was recorded. The possible role of these changes in the dichlorvos intoxication is discussed.     

Dichlorvos intoxication in a freshwater prawn, Macrobrachium lamarrei (H. Milne Edwards)

Inhibition in acetylcholinesterase and alkaline phosphatase activities with an elevation in acid phosphatase activity were recorded in a freshwater prawn, Macrobrachium lamarrei (H. Milne Edwards) after sublethal dichlorvos exposure under static conditions. The possible role of these enzymes in the physiology of prawns and the probable mechanism of these changes in relation to dichlorvos intoxication are briefly discussed.     

Impact of phosphamidon on the carbohydrate metabolism of a freshwater prawn, Macrobrachium lamarrei

The effects of a lethal (96 hr LC50) and two sublethal (40 and 80% of 96 hr LC50) doses of phosphamidon on hepatic and muscle glycogen values and blood glucose level of a freshwater prawn, Macrobrachium lamarrei (H. Milne Edwards), have been studied. Pesticide exposure depleted the glycogen values in both tissues while the blood glucose level was elevated up to 72 hr, after which it was decreased. The probable explanations of phosphamidon-induced changes are discussed.     

Fluoride-induced changes in carbohydrate metabolism in the tissues of fresh water crab Barytelphusa querini

Exposure of fresh water crab Barytelphusa querini to a sublethal concentration of NaF (30 ppm) caused significant alterations in the carbohydrate metabolism. In an exposure span of 15 days the crab was observed to have marked depletion in glycogen and total free sugar levels. A significant elevation in "active" and "total" glycogen phosphorylase activity was observed. The activity changes of lactate dehydrogenase reflected changes in tissue lactate levels and succinate dehydrogenase activity had a tissue specificity.     

Influence of green tea on enzymes of carbohydrate metabolism, antioxidant defense, and plasma membrane in rat tissues

OBJECTIVE: Green tea, consumed worldwide since ancient times, is considered beneficial to human health. We hypothesized that green tea would enhance antioxidant defenses and specific metabolic activities of rat intestine, liver, and kidney to improve their functions. METHODS: The effect of green tea given to rats in the diet or drinking water for 25 d was determined on blood chemistry and on activities of enzymes of carbohydrate metabolism, brush border membrane, and antioxidant defense. RESULTS: Serum glucose, cholesterol, phosphate, and body weight decreased, whereas the activities of lactate and malate dehydrogenases and glucose-6- and fructose 1,6-bis-phosphatases increased in the intestine and kidney but slightly changed in the liver. Activity of glucose-6-phosphate dehydrogenase profoundly increased in the renal cortex but decreased in other tissues. Lipid peroxidation increased in the intestine and renal medulla and decreased in the renal cortex and liver; catalase increased in all tissues but the medulla. Superoxide dismutase activity decreased in the intestine but increased in renal tissues. Activities of brush border membrane enzymes in general increased in the intestine and kidney. CONCLUSION: Green tea consumption resulted in enhanced enzyme activities of carbohydrate metabolism and antioxidant defenses, which may lead to improved health.     

Sensitivity of the freshwater prawn, Macrobrachium lanchesteri (Crustacea: Decapoda), to heavy metals

Adult Macrobrachium lanchesteri were exposed for a 4-day period in laboratory conditions to a range of copper (Cu), cadmium (Cd), zinc (Zn) and lead (Pb) concentrations. Mortality was assessed and median lethal times (LT??) and concentrations (LC??) were calculated. At the end of the 4-day period, live prawns were used to determine bioconcentration of the metals. LT?? and LC?? increased with the decrease in mean exposure concentrations and times, respectively, for all metals. LC??s for 96 hours for Cu, Cd, Zn and Pb were 32.3, 7.0, 525.1 and 35.0 μg/L, respectively. Cu, Cd, Zn and Pb bioconcentration in M. lanchesteri increases with exposure to increasing concentrations and Cd was the most toxic to M. lanchesteri, followed by Pb, Cu and Zn. Comparison of LC?? values for metals for this species with those for other freshwater crustacean organisms reveals that M. lanchesteri is equally or more sensitive to heavy metals than most other tested crustaceans.     

Changes in oxidative metabolism in selected tissues of the crab (Scylla serrata) in response to cadmium toxicity

Changes in oxidative metabolism were studied in hepatopancreas, muscle, and hemolymph of the edible crab Scylla serrata, exposed to a sublethal concentration (2.5 ppm) of cadmium chloride. A significant decrease in glycogen, total carbohydrates, and pyruvate and an increase in lactate levels in hepatopancreas and muscle were observed. Hemolymph sugar levels were increased in experimental crabs. An increase in phosphorylase suggested increased glycogenolysis during cadmium toxicity. The decrease in lactate dehydrogenase activity and the increase in lactate content indicated reduced mobilization of pyruvate into the citric acid cycle. Krebs cycle enzymes such as succinate dehydrogenase and malate dehydrogenase were found to be decreased, suggesting impairment of mitochondrial oxidative metabolism as a consequence of cadmium toxicity. Glucose-6-phosphate dehydrogenase activity was increased, suggesting enhanced oxidation of glucose by the HMP pathway. Cytochrome-c oxidase and Mg²⁺ ATPase activity levels decreased, indicating impaired energy synthesis during cadmium stress. Acid and alkaline phosphatase activities increased, suggesting enhanced breakdown of phosphates to release energy in view of impaired ATPase system during cadmium exposure. A significant decrease in protein and free amino acid and an increase in ammonia, urea, and glutamine levels were observed in the tissues during exposure. An increase in protease, alanine aminotransaminase, and asparate aminotransaminase suggested increased proteolysis and transamination of amino acids. The increase in glutamate dehydrogenase, AMP deaminase, and adenosine deaminase indicated increased ammonia production. The increased arginase and glutamine synthetase suggested the detoxification or mobilization of ammonia toward the production of urea and glutamine. These results suggest that cadmium affects oxidative metabolism and induces hyperammonemia, and crabs switch over their metabolic profiles toward compensatory mechanisms for the survivability in cadmium-polluted habitats.