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Dietary pantothenic acid requirement of juvenile grass shrimp, Penaeus monodon.

A feeding trial was conducted to estimate the minimal dietary pantothenic acid (PA) requirement for juvenile grass shrimp, Penaeus monodon. Purified diets with seven levels (0, 20, 40, 60, 120, 240, and 480 mg/kg) of supplemental PA were fed to P. monodon (mean weight 0.88 +/- 0.01 g) for 8 wk. The level of PA detected in the unsupplemented diet was 0.02 mg/kg. Each diet was fed to three replicate groups of shrimp. Feed efficiencies (FE) and protein efficiency ratios were highest in shrimp fed the diets supplemented with 120, 240, and 480 mg PA/kg diet, followed by the groups fed 60 mg/kg, then 40 mg/kg, and finally the unsupplemented control group (P < 0.05). Shrimp fed diets supplemented with PA had significantly higher survival percentages and lower hepatopancreatic lipid concentration than those fed the unsupplemented, control diets. Broken-line regression analyses of weight gain percentage and hepatopancreatic CoA and PA concentrations of the shrimp indicated that the adequate dietary PA concentration in growing P. monodon is 101-139 mg/kg.

Animals↗

Protection by pantethine, pantothenic acid and cystamine against carbon tetrachloride-induced hepatotoxicity in the rat.

The daily ip administration of pantethine (500 mg/kg), pantothenic acid (100 mg/kg) or cystamine (50 mg/kg) for 5 days conferred significant protection against the hepatotoxic and peroxidative actions of a 0.5 mL/kg ip dose of CCl4 in rats. All three treatments lessened the increases in serum ALT and liver TBARS values, and the reductions in serum triglyceride levels, and prevented the development of hepatic steatosis caused by the halocarbon. Pantethine was found to offer the greatest protection.

Alanine Transaminase↗

Gross and histological signs of dietary deficiencies of biotin and pantothenic acid in lake trout, Salvelinus namaycush.

We describe the pathologic changes of single or simultaneous dietary deprivations of biotin (B) and pantothenic acid (PA) in lake trout, Salvelinus namaycush. A deficiency of PA produced gross signs of anorexia, inanition, emaciation, gill abnormalities and high mortality. In B-deficient fish, growth retardation reached statistically significant levels (P less than 0.05) after week 10, but gill and liver lesions were observed earlier. Anorexia and reduced weight gain were observed earlier in fish deprived of both nutrients than in those deficient in B alone. All B-deficient trout fed PA survived the study, and were less anorexic, anemic and emaciated than were those fed B without PA. Deposition of glycogen was greater in kidney tubules of B-deficient fish than in those lacking both vitamins. However, lesions interpreted to be mitochondrial conglutination and cellular necrosis of renal tubules and pancreatic acini were more exaggerated in fish fed neither nutrient than in those deprived of only one. Both vitamins are needed for energy transfer metabolism and their absence in metabolically active tissues causes lesions that resemble those reported for cellular anoxia.

Animal Nutritional Physiological Phenomena↗

Enhancement of muscular performance by a coformulation of propionyl-L-carnitine, coenzyme Q10, nicotinamide, riboflavin and pantothenic acid in the rat.

A coformulation of essential factors, i.e. propionyl-L-carnitine (PLC), coenzyme Q10 (CoQ10), nicotinamide (NAM), riboflavin and pantothenic acid, was administered orally to Wistar rats for 7 weeks and its efficacy was tested through in vivo and in vitro techniques in improving motor functions of striated, cardiac and smooth musculature of the rat. In vivo experiments showed that long-term supplementation significantly improved horizontal locomotor activity by about 19% in male and 26% in female rats. Maximum values of shortening velocity, work and power were significantly increased (P<.05) in papillary muscle isolated from treated rats. A positive inotropic effect was also observed on colonic smooth muscle strips upon treatment. Work was the most affected parameter and it increased by 160% in smooth muscle from treated animals. The present results indicate that supplementation with the combination of the above mentioned substances elicits positive functional changes on motor performance of skeletal, cardiac and smooth muscle of the rat.

Animals↗

[Proteinization and biotransformation of pantothenic acid in the liver during the activation of lipogenesis].

White female rats received a balanced synthetic ration (control) or a ration devoid of pantothenic acid (PAA) during 3 weeks. After 36-hour fasting adaptive hyperlipogenesis was induced by feeding the animals with a high-carbohydrate ration, then [114-C]-PAA (sodium salt, 182 nmol/kg) was administered with intervals of 3, 6, 24 hours up to 1 hour before decapitation. Radioactivity of the rats' boiled liver extracts depended on the hyperlipogenesis stage, its level rose progressively, in the control and reached the maximum in PAA-deficient animals by hour 6 after the feeding resumption. The PAA-deficient animals possessed a high PAA-accumulating capacity of the liver and cytosole of the liver including non-covalent radionuclide binding by protein complexes. CoA-synthesizing capacity of the liver in the control animals, evaluated by the biotransformation of the labeled vitamin with CoA precursors of CoA, was intensified with the lipogenesis activation; in vitamin-deficiency CoA biosynthesis was accelerated more than two-fold as compared to the control at the initial and extended periods of hyperlipogenesis (3.6 h). The differences in proteinization and biotransformation of PAA in the liver of control and PAA-deficient animals disappeared by 25 h of adaptive hyperlipogenesis.

Animals↗

The effects of high dietary supplements of copper sulphate on pantothenic acid metabolism in the chick.

1. The effects of incorporation of copper sulphate supplying 250 mg copper/kg semi-purified diet with graded amounts of calcium pantothenate (CaPa) were studied in chicks. 2. When the doses of CaPa were marginally adequate or less the Cu supplementation induced severe signs of pantothenic acid (PaA) deficiency. 3. Livers of the Cu-treated birds given low doses of PaA had lower concentrations of total and bound PaA than those of the corresponding control birds. The bound:total PaA value was also reduced. 4. The amount and concentration of coenzyme A (CoA) were significantly less in the livers of Cu-treated chicks. Fatty acid synthetase activity was not reduced. 5. It is suggested that high dietary supplements of CuSO4 induce PaA deficiency through interference in the biosynthesis of CoA.

Animals↗