Homocysteine alters glutamate uptake and Na(+),K (+)-ATPase activity and oxidative status in rats hippocampus: protection by vitamin C.

06:29 EDT 5th August 2015 | BioPortfolio

Summary of "Homocysteine alters glutamate uptake and Na(+),K (+)-ATPase activity and oxidative status in rats hippocampus: protection by vitamin C."

In the present study we investigate the effect of homocysteine on glutamate uptake, Na(+),K(+)-ATPase, enzymatic antioxidant defenses, as well as reactive species levels in hippocampus of rats. The influence of vitamin C, a classic antioxidant, on the effects elicited by homocysteine was also tested. Results showed that chronic hyperhomocysteinemia decreased glutamate uptake and the activities of Na(+),K(+)-ATPase, catalase and superoxide dismutase in hippocampus of rats. Reactive species levels were increased by chronic homocysteine administration. Concomitant administration of vitamin C significantly prevented these alterations caused by homocysteine. According to our results, it seems possible to suggest that the reduction in glutamate uptake and Na(+),K(+)-ATPase activity may be mediated by oxidative stress, since vitamin C prevented these effects. We suggest that the administration of antioxidants should be considered as an adjuvant therapy to specific diet in homocystinuria.

Affiliation

Laboratório de Neuroproteção e Doença Metabólica, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, CEP 90035-003, Porto Alegre, RS, Brazil.

Journal Details

This article was published in the following journal.

Name: Metabolic brain disease
ISSN: 1573-7365
Pages:

Links

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Medical and Biotech [MESH] Definitions

Drugs that inhibit the transport of neurotransmitters into axon terminals or into storage vesicles within terminals. For many transmitters, uptake determines the time course of transmitter action so inhibiting uptake prolongs the activity of the transmitter. Blocking uptake may also deplete available transmitter stores. Many clinically important drugs are uptake inhibitors although the indirect reactions of the brain rather than the acute block of uptake itself is often responsible for the therapeutic effects.

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