Abstract
Cisplatin (CP), an antitumor agent, has been shown to cause ovarian injury and dysfunction in both animal and human studies. The present study was conducted to investigate the protective effect of oxytocin (OT) on CP-induced ovarian toxicity in rats. Twenty-one adult female rats were included in the study. Fourteen rats were administered intraperitoneally CP (2 mg/kg/day) twice a week for 5 weeks. Control group (n = 7) did not receive any treatment. Following treatment, CP-received rats were randomly divided into two groups and treated with either saline (1 mL/kg/day, n = 7) or OT (160 μg/kg/day, n = 7) for 5 weeks. Then, ovarian toxicity and effects of OT were evaluated by histomorphological and biochemical analysis. Our findings revealed a significant reduction in the number of follicles at each grade in saline-treated group. AMH level was significantly lower in saline group compared to control (P < 0.0005). OT treatment significantly attenuated CP toxicity in ovaries and increased AMH levels compared to saline group (P < 0.005). Also, administration of OT lessened lipid peroxidation and prevented glutathione depletion in CP-treated rats (P < 0.05). These results indicated that OT could lessen the CP-induced ovarian damage and improve follicular reserve by preventing oxidative damage.
Highlights
Cytotoxic chemotherapy is used for treating cancers, autoimmune diseases, or hematologic diseases and potentially causes ovarian damage
Ovarian primordial follicular cells have no ability to regenerate, and destruction of these cells leads to ovarian dysfunction, which manifests as premature ovarian failure and infertility [2]
Perez et al reported that mice exposed to chemotherapeutic agents showed apoptosis of granulosa cells in primordial follicles [21]
Summary
Cytotoxic chemotherapy is used for treating cancers, autoimmune diseases, or hematologic diseases and potentially causes ovarian damage. For women of reproductive age, chemotherapy-induced gonadotoxicity may cause premature ovarian failure resulting from depletion of ovarian reserve [1]. Repetitive treatment with CP is associated with numerous side effects such as nephrotoxicity, neurotoxicity, and reproductive toxicity [3] In both animal and human studies, CP has been shown to cause ovarian injury, leading to ovarian dysfunction, changes in the estrous cycle, increased follicular apoptosis, and a reduction in the number of antiMullerian hormone- (AMH-) secreting follicles [4]. Several studies have demonstrated the protective role of OT in various types of tissue injury, there is still lack of data with regard to beneficial effects of this peptide in chemotherapy-induced ovarian gonadotoxicity. We conducted the present study to explore whether OT has protective effects on follicle reserve in a CP-induced gonadotoxicity model in rats by evaluating histopathological alterations, plasma AMH levels, and ovary malondialdehyde (MDA) and glutathione (GSH) levels as markers of oxidative stress
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