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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Vitamin C prevents DNA damage induced by renovascular hypertension in multiple organs of Wistar rats

Texto completo
Autor(es):
Nishi, Erika Emy [1] ; Campos, Ruy Ribeiro [1] ; Bergamaschi, Cassia Toledo [2, 1] ; de Almeida, Vitor Rossi [2] ; Ribeiro, Daniel Araki [2]
Número total de Autores: 5
Afiliação do(s) autor(es):
[1] Univ Fed Sao Paulo, UNIFESP, Dept Physiol, Paulista Med Sch, Cardiovasc Div, Santos, SP - Brazil
[2] Univ Fed Sao Paulo, UNIFESP, Dept Biosci, Santos, SP - Brazil
Número total de Afiliações: 2
Tipo de documento: Artigo Científico
Fonte: HUMAN & EXPERIMENTAL TOXICOLOGY; v. 29, n. 7, p. 593-599, JUL 2010.
Citações Web of Science: 17
Resumo

The aim of this study was to investigate, through the single-cell gel (comet) assay, whether vitamin C is able to protect against renovascular hypertension-induced genotoxicity in multiple organs. A total of 32 male Wistar rats were divided into four groups: negative control (n = 6); animals treated with vitamin C (n = 6); hypertensive rats (n = 10) and hypertensive rats and treated with vitamin C (n = 10). Hypertension was induced as a result of partial obstruction of the left renal artery by means of a silver clip during 6 weeks. Vitamin C was administered at 150 mg/kg during 7 consecutive days before the end of the experimental period. The results showed that vitamin C was able to protect blood cells against hypertension-induced genotoxicity. Brain, liver and heart cells were also protected by vitamin C following hypertension-induced genotoxic damage. Regarding blood pressure, vitamin C reduced the hypertensive state. In conclusion, our results suggest that vitamin C can prevent hypertension-induced DNA damage in blood, liver, brain and heart cells as well as to normalize the blood pressure of rats. (AU)

Processo FAPESP: 07/01228-4 - Carcinogênese bucal quimicamente induzida pela 4-nitroquinolina 1-óxido em ratos: possíveis biomarcadores envolvidos em sua patogênese
Beneficiário:Daniel Araki Ribeiro
Linha de fomento: Auxílio à Pesquisa - Apoio a Jovens Pesquisadores