ABSTRACT
Mowrah (M. latifolia) seeds yield 40-50% edible fat and the meal contains saponins besides protein and high level of carbohydrates. The toxicity of the meal was evaluated as it has a potential for use in animal feedstuffs. The meal was fed to young and adult rats at levels of 10 to 40% in diet. The animals showed marked inhibition of feed intake and loss of body weight resulting in mortalities. Histopathological examination revealed a gradation of damage from slight erosion of the tip of villi of intestinal mucous membrane to complete necrosis and destruction of it, with increasing amounts of mowrah seed meal in diets. The other significant change was a severe vacuolar degeneration of kidney tubular cells. Detoxification or complete removal of the toxins is necessary for utilization of the meal as animal feedingstuff.
Subject(s)
Animals , Evaluation Studies as Topic , Female , Male , Rats , Rats, Wistar , Seeds/chemistry , Toxins, Biological/toxicity , TreesABSTRACT
The effect of taurine on the serum and liver cholesterol and triglyceride levels was studied in rats fed cholesterol plus cholic acid. Four groups of 4 weeks old rats were fed control diet, hypercholesterolemic diet (HCD), HCD + 1% taurine or HCD + 2% taurine for 8 weeks. Addition of taurine in HCD diet showed a significant reduction not only in serum total cholesterol and triglyceride levels but also in liver total cholesterol, lipid and triglyceride contents compared to the animals fed HCD alone. Histological examination of organs of these animals showed severe fatty vacuolation in livers and signet ring type vacuolation in kidneys of rats fed HCD. Taurine showed ameliorating effect on these abnormalities. The animals fed taurine in HCD also showed increased bile and sterol excretion in faeces compared to rats fed HCD alone. Taurine showed significant hypocholesterolemia in rats probably by enhancing the catabolism of cholesterol and reducing the absorption of dietary cholesterol.
Subject(s)
Animals , Hypolipidemic Agents/pharmacology , Cholesterol/analysis , Cholesterol, Dietary/administration & dosage , Cholic Acid , Cholic Acids/administration & dosage , Diet, Atherogenic , Female , Hypercholesterolemia/prevention & control , Liver/chemistry , Male , Rats , Rats, Wistar/metabolism , Taurine/administration & dosage , Triglycerides/analysis , Viscera/drug effectsABSTRACT
Rat liver lipoyl transacetylase catalyzes the formation of acetyl dihydrolipoic acid from acetyl coenzyme A and dihydrolipoic acid. In an earlier paper the formation of acetyl dihydrolipoic from pyruvate and dihydrolipoic acid catalyzed by pyruvate dehydrogenase has been reported. Acetyl dihydrolipoic acid is a substrate for citrate synthase, acetyl coenzyme A carboxylase and fatty acid synthetase. The Vmax. for citrate synthase with acetyl dihydrolipoic acid was identical to acetyl coenzyme A (approximately 1 μmol citrate formed/min/mg protein) while the apparent Km was approximately 4 times higher with acetyl dihydrolipoic acid as the substrate. This may be due to the fact that synthetic acetyl dihydrolipoic acid is a mixture of 4 possible isomers and only one of them may be the substrate for the enzymatic reaction. While dihydrolipoic acid can replace coenzyme A in the activation of succinate catalyzed by succinyl coenzyme A synthetase, the transfer of coenzyme A between succinate and acetoacetyl dihydrolipoic acid catalyzed by succinyl coenzyme A: 3 oxo-acid coenzyme A transferase does not occur.
ABSTRACT
Intraperitoneal administration of lipoic acid (10 mg/100 g) does not effect changes in serum insulin levels in normal and alloxan diabetic rats, while normalising increased serum pyruvate, and impaired liver pyruvic dehydrogenase characteristic of the diabetic state. Dihydrolipoic acid has been shown to participate in activation of fatty acids with equal facility as coenzyme A. Fatty acyl dihydrolipoic acid however is sparsely thiolyzed to yield acetyl dihydrolipoic acid. Also acetyl dihydrolipoic acid does not activate pyruvate carboxylase unlike acetyl coenzyme A. The reduced thiolysis of ß-keto fatty acyl dihydrolipoic acid esters and the lack of activation of pyruvic carboxylase by acetyl dihydrolipoic acid could account for the antiketotic and antigluconeogenic effects of lipoic acid.
ABSTRACT
Relative α-lipoic acid content of diabetic livers was considerably less than that of normal livers as determined by gas chromatography. It was not possible to detect any dihydrolipoic acid in the livers. Biochemical abnormalities such as hyperglycaemia, ketonemia, reduction in liver glycogen and impaired incorporation of [2-14C] -acetate into fatty acids in alloxan diabetic rats were brought to near normal levels by the oral or intraperitoneal administration of dihydrolipoic acid. The effect of α-lipoic acid was comparable to that of dihydrolipoic acid in reducing the blood sugar levels of diabetic rabbits during a glucose tolerance test. The results suggest that the mode of action of lipoic acid was through stimulation of pyruvate dehydrogenase.