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At least 469 records · Page 26Linked to original sources
PubMed1989

Manganese catalysis of dopamine oxidation.

Manganese catalysis of the oxidation of dopamine by air was studied as part of an investigation of possible manganese intoxication amongst a group of Aborigines living on manganese-rich soil on Groote Eylandt, in the Northern Territory of Australia. Manganese significantly increased the oxidation rate of dopamine, and the manganese complexes with some purines were especially efficient catalysts. An oxidation mechanism, involving a manganese(II)/(III) redox couple and a semiquinone free radical intermediate, is proposed. Stoichiometric hydrogen peroxide was produced by the oxidation, and the oxidation products of dopamine were highly toxic to the marine diatom Nitzschia closterium. Hydrogen peroxide and the superoxide radical did not oxidize dopamine at physiological pH. Some electrophilic compounds, including ascorbic acid, dehydroascorbic acid and thiamine, effectively inhibited dopamine oxidation. The Groote Eylandt Aborigines are likely to be deficient in ascorbic acid (vitamin C) and thiamine (vitamin B1), and these deficiencies, as well as their lifestyle, may predispose them to manganese intoxication.

Catalysis↗
PubMed1993

Ascorbic acid and cholesterol gallstones.

Decreased activity of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme in the catabolism of cholesterol to bile acids, is known to result in increased biliary cholesterol concentration and supersaturation of bile. Supersaturation of bile by cholesterol is a necessary condition for cholesterol gallstone formation. In guinea pigs, the hepatic concentration of ascorbic acid affects the catabolism of cholesterol: hypovitaminosis C reduces cholesterol 7 alpha-hydroxylase activity. Cholesterol gallstones are frequently found in ascorbic acid-deficient guinea pigs. Risk factors for cholesterol gallstones in humans include obesity, aging, estrogen treatment, pregnancy and diabetes. Plasma ascorbic acid levels are reduced in these groups. Vegetarian diets, which typically have high ascorbic acid contents, protect against gallstones. Since ascorbic acid effects the rate-limiting step in the catabolism of cholesterol in the guinea pig and many human risk groups for cholesterol gallstones are associated with reduced ascorbic acid levels, ascorbic acid may play a contributory role in human gallbladder disease.

Animals↗
PubMed1976

Vitamin A: not required for adrenal steroidogenesis in rats.

Previous work supporting the vitamin A dependency of adrenal function in rats neglected to take into account a secondary effect of the deficiency, a decrease in hepatic ascorbic acid biosynthesis. Vitamin A-depleted rats maintained on a diet free of ascorbate had a decrease in the activity of adrenal 3 beta-hydroxysteroid dehydrogenase, and extensive adrenocortical degeneration. The use of an ascorbate supplement prevented the symptoms. The results suggest that previous evidence for direct involvement of vitamin A in steroidogenesis may have been due to the production of a secondary deficiency, a chronic scorbutic condition.

Adrenal Glands↗
PubMed1984

Iron overload associated with congenital pyruvate kinase deficiency and high dose ascorbic acid ingestion.

Iron overload is an uncommon complication of untransfused chronic hemolytic anemias. This paper describes only the fourth reported case of erythrocyte pyruvate kinase deficiency and iron overload. Important aspects of this case are the presence of the HLA genotype commonly associated with genetic (idiopathic) hemochromatosis and a history of ingestion of large doses of ascorbic acid. Their roles in the development of iron loading and toxicity are discussed. A beneficial response to treatment with desferrioxamine was observed before significant iron removal. A mechanism for this action of desferrioxamine is proposed.

Ascorbic Acid↗
PubMed1978

Water-soluble vitamins in severe liver disease.

Biochemical deficiency of thiamine, vitamin B6, ascorbic acid or nicotinic acid occurred in 71% and 88% of patients with fulminant hepatic failure (FHF) and decompensated chronic liver disease (DCLD) respectively. Transient high plasma vitamin B6 concentrations in FHF were followed by low levels later in the illness. Although patients with DCLD of alcoholic aetiology tended to have lower circulating levels of vitamins than those with non-alcoholic DCLD, the prevalence of abnormally low concentrations did not differ. Decreased dietary nutrient intake and alcohol appeared to be less important determinants of biochemical vitamin deficiency than the presence of liver disease per se. Finally, urinary excretion of these vitamins or their major metabolites in patients with severe liver disease correlated poorly with circulating levels of vitamins.

Ascorbic Acid↗