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BioMed Research International
Volume 2014, Article ID 703691, 6 pages
http://dx.doi.org/10.1155/2014/703691
Research Article

Oxytocin Improves Follicular Reserve in a Cisplatin-Induced Gonadotoxicity Model in Rats

1Department of Physiology, Ege University School of Medicine, 35100 Izmir, Turkey
2Department of Obstetrics and Gynecology, Ege University School of Medicine, 35100 Izmir, Turkey
3Department of Histology and Embryology, Ege University School of Medicine, 35100 Izmir, Turkey
4Division of Medical Oncology, Tepecik Educational and Training Hospital, 35100 Izmir, Turkey

Received 23 February 2014; Revised 11 April 2014; Accepted 23 April 2014; Published 15 May 2014

Academic Editor: Christophe Duranton

Copyright © 2014 Oytun Erbaş et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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 () 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, ) or OT (160 μg/kg/day, ) 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 (). OT treatment significantly attenuated CP toxicity in ovaries and increased AMH levels compared to saline group (). Also, administration of OT lessened lipid peroxidation and prevented glutathione depletion in CP-treated rats (). These results indicated that OT could lessen the CP-induced ovarian damage and improve follicular reserve by preventing oxidative damage.