RESUMO
Dietary supplementation of ascorbic acid was found to be effective in modifying the composition of essential biomolecules. A relative investigation on effects of exogenous dietary supplementation of 0.2% ascorbic acid on the fifth instar larvae of silkworm, Bombyx mori exposed to a high thermal stress of range 40 ± 2 °C was carried out in the lab-set conditions. The observed elevation in various biomolecules, viz., DNA, RNA, protein, lipids, and carbohydrates were quantified in both the thermal stress-induced test groups and in the control, set aside. The test results so obtained were proven to be statistically significant. The present study reveals that foliar supplementation of ascorbic acid has been effective in positively-modulating the biochemical performance in larvae exposed to thermal stress. Moreover, the study also uncovers the possibilities of ascorbic acid as a potential candidate, capable of facilitating the production of good quality cocoons, from larvae exposed to thermal stress.
Assuntos
Ácido Ascórbico/farmacologia , Bombyx/fisiologia , Larva/fisiologia , Animais , Fenômenos Bioquímicos/efeitos dos fármacos , Bombyx/genética , Bombyx/metabolismo , Suplementos Nutricionais , Estresse Fisiológico , TemperaturaRESUMO
The effects of a mega dose of ascorbic acid (AA) on alcohol induced peroxidative damages were investigated in guinea pigs. In the present study, four groups of male guinea pigs were maintained for 30 days as follows. (1) Control group (1 mg AA/100 g body wt); (2) Ethanol group (1 mg AA/100 g body wt. + 9 g ethanol/kg body wt); (3) AA group (25 mg AA/100 g body wt); (4) AA + ethanol group (25 mg AA/100 g body wt. + 9 g ethanol/kg). Results revealed that alcohol induced significant lipid peroxidation, since the lipid peroxidation products malondialdehyde (MDA), hydroperoxides and conjugated dienes were elevated. The activities of scavenging enzymes superoxide dismutase (SOD), catalase were reduced. However, supplementation of AA along with alcohol reduced the lipid peroxidation products in the liver and enhanced the activities of scavenging enzymes. Activities of glutathione peroxidase and reductase were also greater in guinea pigs given alcohol + AA in comparison with those given alcohol alone. Administration of ascorbic acid also reduced the activity of gamma-glutamyl transpeptidase (GGT), the marker enzyme of alcohol induced toxicity. The vitamin E level, which was reduced by alcohol intake, was raised by the co-administration of AA and alcohol. These studies suggest that a mega dose of AA helps in the prevention of alcohol induced oxidative stress by enhancing the antioxidant capacity and also by reducing the lipid peroxidation products.
Assuntos
Antioxidantes/administração & dosagem , Ácido Ascórbico/administração & dosagem , Dieta , Etanol/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Animais , Encéfalo/metabolismo , Catalase/metabolismo , Relação Dose-Resposta a Droga , Ácidos Graxos não Esterificados/metabolismo , Glutationa Redutase/metabolismo , Cobaias , Intubação Gastrointestinal , Rim/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/metabolismo , Masculino , Malondialdeído/metabolismo , Miocárdio/metabolismo , Superóxido Dismutase/metabolismo , Vitamina E/metabolismo , gama-Glutamiltransferase/metabolismoRESUMO
Ascorbic acid metabolism was studied in guinea pigs and rats after the administration of ethanol and a high dose of ascorbic acid (AA). Male guinea pigs were maintained for 30 days as follows: (1) controls (1 mg AA/100 g body wt.); (2) ethanol (1 mg AA/100 g body wt. + 900 mg ethanol/100 g body wt); (3) ascorbic acid (25 mg AA/100 g body wt.); (4) ascorbic acid + ethanol (25 mg AA/100 g body wt. + 900 mg ethanol/100 g body wt.). Rats were also grouped into four groups as in the case of guinea pigs, but the dose of AA was 200 mg/100 g body weight. Rats adjusted to ethanol intoxication by enhancing the biosynthesis of ascorbate as evidenced by elevated activity of L-gulono lactone oxidase (GLO). Hence ascorbate levels were not lowered in rats after administration of alcohol. However, alcohol administration lowered tissue levels of ascorbate in guinea pigs. But the supplementation of ascorbate along with alcohol raised the tissue level of this vitamin. Guinea pigs responded to the ascorbate deficiency during alcohol administration by lowering the degradation of ascorbate, as seen by the lower activity of the degrading enzyme gulono lactone hydrolase. It is concluded that on the administration of alcohol, guinea pigs are dependent upon additional exogenous supplies of ascorbic acid, whereas rats are not.
Assuntos
Ácido Ascórbico/metabolismo , Etanol/administração & dosagem , Animais , Ácido Ascórbico/farmacocinética , Cobaias , Masculino , Ratos , Ratos Sprague-Dawley , Distribuição TecidualRESUMO
The objective of this study was to determine the effects of a country liquor Toddy (Coconut palm wine) and an equivalent quantity of ethanol on liver function and lipid metabolism in utero. Female albino rats with an average weight of 125 +/- 5 g were exposed to Toddy from coconut palm (24.5 ml/kg body weight/day) and ethanol (0.52 ml/kg body weight/day) for 15 days before conception and during pregnancy. On day 13 and day 19 of gestation, altered liver function and hyperlipidemia were seen in the fetuses of both the treated groups. Altered liver function was evidenced by the increased activity of alcohol dehydrogenase, aldehyde dehydrogenase, glutamic oxaloacetic transaminase (aspartate amino transferase (GOT)), glutamic pyruvic transaminase (alanine amino transferase (GPT)). Hyperlipidemia was caused by increased biosynthesis since the incorporation of 14C acetate into lipids and activities of HMG CoA reductase and lipogenic enzymes were elevated. Toddy treated fetuses were more severely affected than those exposed to an equivalent quantity of ethanol. Toddy seemed to potentiate the toxicity induced by alcohol suggesting the role of non alcoholic components. Hepatic functions of the day 13 fetuses were effected to a lesser degree than those in the day 19 hepatic liver.