Biochemical and histological investigation of famotidine effect on postischemic reperfusion injury in the rat ovary.

ABSTRACT

BACKGROUND/PURPOSE: In this study, an investigation was performed on the ovarian tissue of rats subjected to ischemia-reperfusion for the effect of famotidine on certain parameters of oxidation-antioxidation, cell DNA damage, and histological appearance. METHODS: The effects of famotidine on certain parameters of oxidation-antioxidation (total glutathione [tGSH], superoxide dismutase [SOD], malondialdehyde) and cellular DNA injury in the ovarian tissue of rats subjected to ischemia-reperfusion were investigated and underwent histological examination. RESULTS: The results show levels of 5.2 ± 0.6 nmol/g protein for tGSH, 8.3 ± 0.8 U/g for SOD activity, and 7.7 ± 0.9 µmol/g protein for malondialdehyde (P < .0001 when compared with controls) in ovarian tissue subjected to ischemia-reperfusion following famotidine treatment. The tGSH levels in control rats and in a healthy animal group were, respectively, 1.76 ± 0.7 and 5.5 ± 0.3 nmol/g protein (P < .0001). The SOD activity was 3.2 ± 0.9 U/g in control and 9.2 ± 0.6 U/g in healthy animal tissues. The differences between the values in the treatment and the control group, and between the healthy animal group and the control group were both highly significant (P < .0001). It was also observed that famotidine prevented, to a significant extent, an increase in the level of 8-hydroxy-2-deoxyguanine/guanine, a DNA damage product, as compared with the control group. CONCLUSION: These biochemical and histological results show that famotidine protects the ovarian tissue from ischemia-reperfusion injury.