Abstract:

The aim of the present study was to investigate the relationship between liver damage induced by carbon tetrachloride (CCl4) and adenosine deaminase (ADA), 5'-nucleotidase (5'NT), xanthine oxidase (XO) enzyme activities, and malondialdehyde (MDA) levels. The effect of stobadine on purine metabolism was also evaluated. Materials and methods: This study measured the effect of CCl4 on ADA, 5'NT, XO enzyme activities, and MDA levels, and measured the histopathologic changes in liver cells. Results: Our research found that ADA, XO activities, and MDA levels increased in the CCl4 group when compared with the control group. This was also supported by the histopathological changes in the CCl4 and CCl4+stobadine group found when compared with the control group. Stobadine could not protect cells against CCl4 damage. Conclusion: The present study helps explain the biochemical mechanisms of liver injury formed by CCl4 and shows the relationship between the purine degradation pathway and CCl4induced cellular toxic effect. Cellular damage is dependent upon the biochemical response to increased purine degradation pathway enzyme activities, which also may be responsible for decreasing liver cellular adenosine levels and S-adenosyl-methionine and increasing superoxide anion and hydrogen peroxide levels. It is suggested that the inhibition of key enzymes of the purine degradation pathway (particularly ADA and XO) may prevent liver damage.

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