A balance between oxidative damage and proliferative potential in experimental carbon tetrachloride-induced cirrhosis: Protective role of adenosine administration
Por:
Chagoya De Sanchez W., Diaz-Munöz M., Löpez V., Löpez Barrera F., Yanez L., Vidrio S., Aranda A., Hernandez-Munöz Y.R.
Publicada:
1 ene 1997
Resumen:
Oxidative stress has been postulated as a major molecular mechanism involved in carbon tetrachloride (CC14) hepatotoxicity. We focused this study on trying to establish a relationship between oxidative stress and the fibrogenic effect induced by chronic treatment of the toxin in the presence or absence of adenosine. The cirrhotic process was validated by histological examination and collagen quantitation. As indicative of oxidative stress a lipid peroxidation (LP) was measured as well as the metabolites and enzymes of the glutathione cycle. As proliferative index thymidine kinase was measured. The experimental animals were injected ip with CC14 (25 ul 1:6 in vegetable oil) and/or adenosine (200 mg/kg b.w.) three times weekly for 4 and 8 weeks. The oxidative damage reflected by an increase in LP and decrease of GSH was prevented by adenosine treatment. A four- to eightfold increase in thymidine kinase was observed in the presence of CC14 and adenosine. The prevention of oxidative damage and the increase of proliferative potential by adenosine might explain partially the beneficial action of the nucleo-side in experimental cirrhosis.
Filiaciones:
Institute de Fisiologia Celular, Universidad National Auto-noma de Mexico, Apartado Postal 70-243, Mexico, D.F., Mexico
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