Ali Kurt

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

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.

An investigation about the inhibition of acute ischemia/reperfusion damage by dexmedetomidine in rat ovarian tissue

Reperfusion has always been “the emergency intervention” to ischemic tissue. For a given period of time, tissue injury due to ischemia and reperfusion is more serious than injury due to ischemia only. Groups were as: Group 1: 25 µg/kg dexmedetomidine + ischemia/reperfusion group. Group 2: 10 mg/kg yohimbine +25 µg/kg dexmedetomidine + ischemia/reperfusion group. Group 3: Ischemia/reperfusion (control) group. Group 4: Healthy rats. Rat ovaries were exposed to a 3-hour ischemia and then reperfusion ensured for 2 hours. After ischemia/reperfusion, total glutathione, malondialdehyde, 8-hydroxyguanine levels and histopathological investigation were studied. The highest total glutathione and the lowest malondialdehyde and DNA damage levels were determined in dexmedetomidine group when compared to control group. The difference between yohimbine + dexmedetomidine and the control group was insignificant. Dexmedetomidine protects the ovarian tissue of the rat from I/R injury. It is hypothesized that this protective effect of dexmedetomidine is mediated by the α-2 adrenergic receptors. Dexmedetomidine could be useful for attenuation of tissue damage after I/R and prevention of I/R-related complications.

Leiomyoma of the ovary: report of two cases and review of the literature

Grossly, the hysterectomy material was 16X 12 X 9 cm in size and contained two masses of leiomyoma located within the myometrium and one polipoid submucous leiomyoma in the endometrial cavity. The right ovary was 5X4X4 cm in size and contained a mass 4X 3 X 3 cm in size. The cut surfaces of this formalin fixed tumor exhibited a multicentric nodular or whorled appearence with greyish color. Delineation from the surrounding ovarian cortical investment was usually sharp although the tumor could not be said to be encapsulated (Fig. 1).

Biochemical and histopathological investigation of the protective effect of disulfiram in ischemia-induced ovary damage

It was biochemically and histopathologically investigated whether disulfiram has protective effects on ischemia-induced ovary damage. For this purpose, levels of tGSH, superoxide dismutase (SOD), malondialdehyde (MDA), and 8-OH Gua/Gua were investigated in ischemic rat ovary tissue. Results show that used doses of disulfiram (10, 25, and 50 mg/kg) prevent MDA, a product of ischemia-induced lipid peroxidation, formation in female rat ovary tissue and prevent decrease of enzymatic and non-enzymatic (SOD, GSH) antioxidant parameters. Additionally, all doses of disulfiram significantly prevent DNA damage when compared to control group. Fewer histopathological findings were observed in tissues with higher antioxidant levels and lower oxidant and DNA damage levels.