Abstract: AIM: To preliminarily study the molecular mechanism for the cardiac injury in rat by adriamycin and the mechanism for the acuterepair in the body.METHODS: The male Sprague-Dawley rats were randomly dividedintofour groups (n =10 in each):The first group was kept without treament and served as the control;the second, the thirdand the fourth received ADR in different doses (10, 20, 40 mg·kg^-1, respectively) by injection of adriamycin.The content of malondialdehyde (MDA) in the serum was estimated with thiobarbituric acid.Cu-Zn-SOD was measured by its reaction with xanthine oxidase.GSH was measured by its reaction with 5, 5-nitrobenzoic acid. Using semi-quantitativereverse transcription-polymerase chain reaction (RT-PCR), we analyzed the expression of the associated gene.RESULTS: MDA contents in the medium and high ADR dose groups were higher than that in the control group (P<0.05, P<0.01).FN mRNA and P105 mRNA had different extents higher expression in different doses groups compared to normal rats.The enzymeactivities of copper, zinc-superoxide dismutase (Cu-Zn-SOD) and glutathione peroxidase(GSH-Px) in the medium and high ADR dose groups were lower than that in control group respectively (P<0.01), and were positively correlated with the expression of their gene.CONCLUSION: The changes of the expression of Cu-Zn-SOD and GSH-Px may be one of the molecular mechanism for the cardiotoxicity by adriamycin, andit is supposed that FNand P105 are involvedin the acuterepair after the cardiac injury induced by ADR in the body through a serial of signal pathways.

Key words: adriamycin, Cu-Zn-SOD, GSH-Px, fibronectin, P105, gene expression, heart, rats