The relationship between oxidative stress markers and endometrial hyperplasia: A case-control study

Objective: Endometrial hyperplasia (EH) is considered an endometrial cancer precursor. This study aimed to determine the role of oxidative stress and thiol groups with antioxidant properties in EH pathogenesis. Materials and Methods: In our prospective case-control study, participants were washed with 5 mL of saline before the endometrial biopsy. Endometrial washing fluid was taken into microtubules, and thiol and disulfide levels were analyzed using the Ellman reagent. Results: A total of 108 patients were in the EH group and 84 patients in the control group. The total and native thiol levels were higher values in the control group (p<0.001, for both). Disulfide levels were higher in the EH group (p<0.001). Native/total thiol ratio and disulfide/total thiol ratio were higher in the EH group (p<0.001, for both). The analysis performed in the control group revealed a significant positive correlation between estradiol and disulfide levels (r=0.322, p=0.033). No significant correlation was found between estradiol and disulfide in the EH group. Conclusion: Oxidative stress level was higher in the washing fluids of patients with EH and this stress plays a role in the EH etiology.

An antibody of TNF-alpha did not prevent thioacetamide-induced hepatotoxicity in rats.

Tumor necrosis factor (TNF)-α antibodies have been shown to reduce liver damage in different models. We investigated the effects of infliximab (a TNF-α antibody) on liver damage in thioacetamide (TAA)-induced hepatotoxicity in rats. Group 1 (n = 8) was the control group. In group 2 (n = 8), the TAA group, the rats received 300 mg/kg intraperitoneal (ip) TAA daily for 2 days. In group 3 (n = 8), the TAA + Infliximab (INF) group, infliximab (5 mg/kg ip daily) was administered 48 hours before the first dose of TAA daily for 2 days and was maintained for 4 consecutive days. In group 4 (n = 8), the INF group, the rats received only ip infliximab (5 mg/kg) daily. Livers were excised for histopathological and biochemical tests (thiobarbituric-acid-reactive substances [TBARS], and myeloperoxidase [MPO]). Serum ammonia, aspartate transaminase (AST), alanine transaminase (ALT), TNF-α, liver TBARS and MPO levels, and liver necrosis and inflammation scores in the TAA group were significantly higher than in the control and INF groups (all p < 0.01). All parameters except AST were not significantly different between TAA and TAA + INF. In conclusion, our results suggest that oxidative stress plays an important role in TAA-induced hepatotoxicity, and infliximab does not improve oxidative liver damage.