Acetaldehyde acumulation and oxidative stress in rat breast. Their role in ethanol induced cancer

CASTRO GD; DELGADO DE LAYÑO AMA; FANELLI SL; MACIEL ME; DÍAZ GÓMEZ MI,; CASTRO JA.

Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB)

Congreso; XLII Reunión Anual Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB); 2006

Rosario, Santa Fe

In previous studies we reported the presence of several pathways of activation of ethanol to acetaldehyde (AC) and hydroxyl free radicals as well as the promotion of  oxidative stress. In the present studies we tested the possibility that after alcohol drinking, AC accumulated in mammary tissue to reach concentrations higher than in blood. Three different doses of alcohol were tested and AC concentrations in mammary tissue, liver and blood were measured at times ranging from 1 to 24 hours. We also determined ADh; AlDh and CYP2E1 activities. Oxidative stress induced hydroperoxides formation; depletion of alpha-tocopherol and GSH contents for the higher dose at different times of exposure. Hydroperoxides levels led to increased values at 6 hours for the higher dose tested also. The obtained results showed that AC concentrations at the three doses tested were always higher than in blood. Limited ADh and AlDh activities in mammary tissue were observed. The microsomal CYP2E1-mediated p-nitrophenol hydroxylase in mammary tissue was several times smaller than in liver. In summary, results suggest that the mutagen AC, either formed in situ or, even in small amounts, arriving via blood, tends to accumulate in mammary tissue as a consequence of a limited capacity of it for detoxification. Supported by ANPCyT (PICT 05-6045) and UNSAM (PIB S05/03).