Associated changes of lipid peroxidation and transforming growth factor beta1 levels in human colon cancer during tumour progression.

Background: During neoplastic progression, alterations in transforming growth factor beta1 (TGF-beta1) dependent control of cell growth may be an important mechanism of selective proliferation of transformed cellular clones. Defective regulation of TGF-beta1 receptors has been reported to occur in a number of human malignant tumours while little is known of the actual levels of this growth inhibitory cytokine in cancer. On the basis of the demonstrated ability of major lipid peroxidation products such as 4-hydroxynonenal to modulate TGF-beta1 expression and synthesis, we speculated that decreased lipid oxidation, as frequently observed in neoplastic tissues, would contribute to the selective promotion of tumour growth through decreased expression of the cytokine within the tumour mass.

In vivo potentiation of 1,2-dibromoethane hepatotoxicity by ethanol through inactivation of glutathione-s-transferase.

In the rat, a single ethanol (EtOH) pretreatment (2.5 g/kg b.w.

Rat hepatocytes in single cell suspension: A still suitable system for lipid peroxidation studies.

The investigation of toxic compounds which need a previous metabolic activation often gets advantage by the employment of cell suspensions, in most of the cases rat hepatocytes. In particular, this model system allows the characterization of lipid peroxidation kinetics, the evaluation of its pathogenetic role in the induction of cell death and the analysis of the interaction among different prooxidant compounds in bringing about both oxidative damage and cytolysis.