Studies on the ameliorative potential of dietary supplemented different dose of selenium on doxorubicin-induced ovarian damage in rat.

Doxorubicin (Dox) may induce loss of follicles, resulting in the depletion of ovarian reserve and consequent premature ovarian failure. Selenium (Se) is an oligoelement with fundamental biological features and is among the most common chemical inhibitor compounds. The present study describes the curative effects of dietary supplementation with different Se doses on Dox-induced ovarian damage in rats. In this study, 64 adult female Wistar rats were randomly separated into eight groups: Control group, Dox group (5 mg/kg intraperitoneal [i.p.]), low-dose Se (0.5 mg/kg i.p.), middle dose Se (1 mg/kg i.p.), high dose (Se 2 mg/kg i.p.), Dox + low-dose Se group (0.5 mg/kg i.p.), Dox + middle dose Se (1 mg/kg i.p.), and Dox + high-dose Se group (2 mg/kg i.p.). After the experiment, ovarian follicles were counted, and Antimüllerian hormone, interleukin 1 beta, tumor necrosis factor alpha, and caspase-3 expression were determined. Levels of malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase were biochemically measured in ovarian tissue. Dox caused ovarian injury, as evidenced by significant changes in ovarian markers, histological abnormalities, and the debilitation of antioxidant defense mechanisms. Furthermore, Dox therapy significantly changed the expression of inflammatory and apoptotic markers. Dox + 1 mg Se with various saturations was studied, and this study demonstrated both histopathological and follicular reserve and more protective features. 1 mg Se pretreatment improved Dox-induced ovarian toxicity through alleviating the antioxidant mechanism, decreasing inflammation and apoptosis, and restoring ovarian architecture. As a result, our findings indicate that 1 mg Se is a promising therapeutic agent for the prevention of ovarian damage associated with Dox.

The effect of different doses of nonylphenol on the blood-testicular barrier integrity, hormone level, and DNA damage in the testes of rats.

Determining the molecular characteristics of the damage caused by NP exposure in the testis is very important for understanding the source of the damage and developing treatment methods accordingly. Therefore, in this study, it is aimed to evaluate the toxic effects that different doses of NP may cause in the testis, including blood-testicular barrier integrity and sperm DNA damage. For this purpose, 50 adult male Wistar albino rats were used in the study. Low, medium, and high-dose NP groups and the corn oil group were formed. After NP administration at determined doses for 15 days, the testis tissue taken under anesthesia was fixed in formaldehyde. Paraffin blocks were embedded using the routine histological tissue follow-up method. Histopathological and immunohistochemical analyses were performed by taking 5 µm thick sections from paraffin blocks. The other testicular tissue was taken for the Western blot, Elisa, and comet methods, and the findings of sperm DNA analysis and the blood-testicular barrier were examined. NP caused the seminiferous epithelium to be disorganized and have significantly fewer cells in the testes of rats in different dose NP-induced groups. Compared with the control group, mTOR, Cx43, SCF, and HSP70 protein levels were decreased, while the expression of MMP-9 levels was increased in the different NP dose groups. Furthermore, tissue testosterone and inhibin B levels and SF-1 immunoreactivity intensity gradually decreased depending on the dose increase of NP. DNA damage of testicular tissues were increased in NP groups depending on NP dose. These results suggest that it is evident that NP, a commonly used industrial chemical, is an endocrine disrupting chemical (EDC) with estrogenic activity exerting adverse effects on health and that urgent measures are needed regarding the use.