Enhanced deleterious effects of carbon tetrachloride on nuclear and microsomal components from livers of animals chronically exposed to alcohol

DÍAZ GÓMEZ M.I., FANELLI S.L. AND CASTRO J.A.

San Carlos de Bariloche

Congreso; XXXIX Annual Meeting Sociedad Argentina de Investigación en bioquímica y Biología Molecular (SAIB). XXXII Annual Meeting Sociedad argentina de Biofísica (SAB).; 2003

Sociedad Argentina de Investigación en bioquímica y Biología Molecular (SAIB).

It is known that chronic alcohol consumption induces CYP2E1-mediated liver microsomal metabolism of some xenobiotics. Our laboratory reported a CYP2E1 dependent ethanol metabolizing system in highly purified liver nuclei, leading to acetaldehyde and free radicals and inducible by chronic ethanol drinking. This could change to toxic and carcinogenic response of other environmental chemicals bioactivated by CYP2E1, such as CCl4. We found that, liver microsomes and nuclei from animals chronically exposed to alcohol showed enhanced protein carbonyl formation when these subcellular fractions were activating CCL4 in either the presence or absence of NADPH. The microsomal and nuclear protein sulphydryl groups content from alcohol treated animals was decreased in incubation mixtures bioactivating CCl4 in the absence of NADPH and this effect was partially reversed by NADPH. Liver microsomal and nuclear proteins from alcohol treated animals showed increased formation of CCl4 altered proteins in the presence of NADPH but no enhancing effects in the content of their altered lipids was observed. Results suggest that chronic exposure to alcohol might enhance the liver carcinogenic effects of CCl4.