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Purpose; The current study aimed to investigate the oxidative stress in diabetic rat liver as well as the protective effects of N-acetylcysteine (NAC)on irisin expression. Methods; Twenty-eight male Wistar rats were divided into four groups, 7 rats in each group and 30-d regimens of experimental or control groups. NAC treated group: 100mg/kg once daily was administered intraperitoneally (i.p.). Diabetes-induced group: Single dose intraperitoneal injection of streptozotocin (STZ) (50mg/kg B.W.) was used to induce diabetes mellitus in overnight fasting Wistar rats. By determining blood glucose concentration in STZ-induced rats 72 hours after injection of STZ, diabetes was assessed. DM+NAC group: STZ-induced DM plus NAC as described previously. Serial and liver samples were collected on the 30-day and after overnight fasting. Biochemical analyses were performed to measure total antioxidant status (TAS), total oxidant status (TOS), and Malondialdehyde (MDA)levels. Each liver sample was weighed, then prepared for histopathologic evaluation by light microscopy. Results; There was a statistically significant decrease in TAS levels and an increase in TOS and MDA levels in the DM group compared to the control group. In contrast, TOS and MDA levels were found significantly decreased, and TAS levels increased in the serum and liver tissues of the DM+NAC group compared to the DM group. Liver samples were also used for histopathological examination using hematoxylin-eosin and immunohistochemical staining. STZ-induced liver injury via increasing oxidative stress, sinusoidal dilatation, degeneration of hepatocytes, and in irisin, and immunoreactivity. NAC significantly reduced the STZ-induced hepatotoxicity. Conclusion; In the early period of diabetes, due to the antioxidant properties of irisin related to the sudden response of liver tissue to oxidative stress, it is thought that the immunoreactivity in the tissue increases in the early period. As a result, NAC in diabetic rat liver tissue was found to suppress oxidative damage and irisin immunoreactivity.

Background. Endometriosis is a chronic inflammatory pathology that can cause persistent pelvic pain and infertility by affecting women of reproductive age. It is defined as the placement of endometrial tissue outside the uterine cavity. Hormonal, genetic and immunological factors have an effect on the development of endometriotic implants. Adalimumab is a monoclonal antibody specific for tumor necrosis factor alpha (TNF-α), used in the treatment of autoimmune diseases.Objectives. To investigate the effectiveness of adalimumab on histopathological and biochemical values in rats with experimental endometriosis. Materials and methods.This study is a comparative, prospective, experimental rat study. Wistar albino female rats were divided into 4 groups. Group 1 was separated as the control group. Endometriotic implants were simultaneously induced in group 2 and group 3. After 4 weeks, developing endometriotic foci were measured. Adalimumab (5 mg/kg) was simultaneously intraperitoneally (ip.) administered to group 3 and group 4 for 4 weeks. At the end of the study, histopathological scoring and fibrillin-1 scoring were performed. Total antioxidant status (TAS), total oxidant status (TOS) and malondialdehyde (MDA) values were measured. Findings in all groups were compared. Results.When group 1 and group 2 were compared, the histopathological score, as well as MDA and TOS levels increased, while TAS levels decreased in group 2 (p < 0.001). After adalimumab treatment, the average endometriotic implant size in group 3 (0.32 ±0.002 mm) decreased compared to group 2 (0.77 ±0.04 mm) (p = 0.032). While fibrillin-1 score increased in group 2 and group 3 compared to group 1, it decreased in group 3 compared to group 2 (p < 0.001). Histopathological score decreased, TAS levels increased and MDA levels decreased in group 3 compared to group 2 (p < 0.001). Conclusions.Adalimumab may play a role in the regression of endometrial implants by showing antioxidant and anti-inflammatory effects on histopathological damage and fibrosis.

Objective: The aim of this study is to investigate the histopathological and biochemical efficacy of vitamin D on oxidative damage and fibrosis in rat ovaries induced by experimental hyperthyroidism. Methods: This study is a comparative, prospective experimental rat study. Sprague-Dawley female rats were divided into four groups. Only distilled water was given to the rats in group 1 for 25 days. In group 2, 100 μg/day L-thyroxine was given to rats for 25 days. In Group 3, 100 μg/day L-thyroxine and 200 IU/day vitamin D were given to rats for 25 days. In group 4, only 200 IU/day vitamin D was administered for 25 days.Results: This study is the first to demonstrate the protective effect of vitamin D against ovarian damage caused by experimental hyperthyroidism. Hyperthyroidism caused fibrotic degenerative changes in the ovaries and an increase in the fibrillin 1 score. It caused serum follicle-stimulating hormone (FSH) levels to increase and serum E2 levels to decrease. In addition, malondialdehyde (MDA) and total oxidant status (TOS) levels increased in rats with hyperthyroidism. Vitamin D decreased MDA and TOS values and increased total antioxidant status (TAS) values in rats with hyperthyroidism. It also increased TSH values by causing a decrease in TT3 and TT4 values. It decreased fibrosis, follicle degeneration, stromal degeneration, and fibrillin 1 score in ovarian tissue. Conclusion: Vitamin D has positive histopathological and biochemical effects on the oxidative stress and follicle damage caused by hyperthyroidism in ovarian tissue. Human studies with larger case populations should be conducted to evaluate the effects and clinical applications of vitamin D.