Utilize este identificador para referenciar este registo: https://hdl.handle.net/1822/9186

TítuloDrinking of Salvia officinalis tea increases CCl4-induced hepatotoxicity in mice
Autor(es)Lima, Cristóvão F.
Ferreira, Manuel Fernandes
Wilson, Cristina Pereira
Palavras-chaveSalvia officinalis L. infusion
Mice
CCl4-induced hepatotoxicity
Herb–drug interaction
Gender differences
CCl -induced hepatotoxicity 4
DataMar-2007
EditoraElsevier Ltd.
RevistaFood and Chemical Toxicology
Citação"Food and Chemical Toxicology." ISSN 0278-6915. 45:3 (Mar. 2007) 456–464.
Resumo(s)In a previous study, the drinking of a Salvia officinalis tea (prepared as an infusion) for 14 days improved liver antioxidant status in mice and rats where, among other factors, an enhancement of glutathione-S-transferase (GST) activity was observed. Taking in consideration these effects, in the present study the potential protective effects of sage tea drinking against a situation of hepatotoxicity due to free radical formation, such as that caused by carbon tetrachloride (CCl4), were evaluated in mice of both genders. Contrary to what was expected, sage tea drinking significantly increased the CCl4-induced liver injury, as seen by increased plasma transaminase levels and histology liver damage. In accordance with the previous study, sage tea drinking enhanced significantly GST activity. Additionally, glutathione peroxidase was also significantly increased by sage tea drinking. Since CCl4 toxicity results from its bioactivation mainly by cytochrome P450 (CYP) 2E1, the expression level of this protein was measured by Western Blot. An increase in CYP 2E1 protein was observed which may explain, at least in part, the potentiation of CCl4-induced hepatotoxicity conferred by sage tea drinking. The CCl4-induced hepatotoxicity was higher in females than males. In conclusion, our results indicate that, although sage tea did not have toxic effects of its own, herb–drug interactions are possible and may affect the efficacy and safety of concurrent medical therapy with drugs that are metabolized by phase I enzymes.
TipoArtigo
URIhttps://hdl.handle.net/1822/9186
DOI10.1016/j.fct.2006.09.009
ISSN0278-6915
Versão da editorahttp://www.elsevier.com/
Arbitragem científicayes
AcessoAcesso aberto
Aparece nas coleções:DBio - Artigos/Papers

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