SciELO - Scientific Electronic Library Online

 
vol.40 número1Influencia de la radiación gamma como método de esterilización sobre el polímero poli VPAVG (Valina-Prolina-Alanina-Valina- Glicina)El Virus del Nilo Occidental: Revisión índice de autoresíndice de materiabúsqueda de artículos
Home Pagelista alfabética de revistas  

Servicios Personalizados

Revista

Articulo

Indicadores

Links relacionados

Compartir


Revista del Instituto Nacional de Higiene Rafael Rangel

versión impresa ISSN 0798-0477

Resumen

RODRIGUES DE A, Zoraida C  y  STRAUSS R, Mirian C. Cardiac stress toxic response to combined passive smoke cigarette exposition plus ethanol. INHRR [online]. 2009, vol.40, n.1, pp.36-43. ISSN 0798-0477.

Many researchers have considered oxidative stress as the main cause of tisular damage induced by alcohol and nicotine together. Oxidative stress is associated to the induction of stress proteins. However, in the case of passive smoke, it is unknown whether the stress proteins are induced and what kind of role they could have. In this regard, this work determined Hsp70 and their relationship to subcellular heart response in individual and combined ethanol and passive smoke cigarette exposition in rats. 60 female Sprague-Dawley (80-100g) rats, were randomized into four group: control; ethanol (2 g/kg c.w. 50%, oral route); passive smoke of 8 cigarettes and ethanol/smoke group. Single  dose daily treatment was given during 15 days. Once therats were killed, samples for biochemical and subcellular analysis were made from left ventricular wall. Results showed a strong relationship between bigger accumulation of Hsp70 and smaller cardiac cellular damage. Ethanol plus passive smoke treatment promoted the stress response by co-induction and an increased Hsp70 accumulation was induced. It is suggested a cardiac protective role for Hsp70.

Palabras clave : Passive smoke cigarette; Ethanol; Hsp70; Cardiac Tissue.

        · resumen en Español     · texto en Español