N-acetylcysteine improves function and follicular survival in mice ovarian grafts through inhibition of oxidative stress. Issue 1 (January 2015)

• Record Type: Journal Article
• Authors: Mahmoodi, Monireh; Soleimani Mehranjani, Malek; Shariatzadeh, Seyed Mohammad Ali; Eimani, Hussein; Shahverdi, Abdulhussein
• Is Part Of: Reproductive biomedicine online. Volume 30:Issue 1(2015)
• Page Start: 101
• Page End: 110
• Publication Date: 2015-01
• Subjects: autotransplantation -- ischaemia reperfusion -- mice -- N-acetylcysteine -- ovary; Human reproductive technology -- Periodicals; Human embryo -- Periodicals; Reproduction -- Periodicals; 616.692
• DOI: 10.1016/j.rbmo.2014.09.013
• Languages: English
• ISSNs: 1472-6483

Abstract

Abstract: The effect of N-acetylcysteine (NAC) on mouse ovary heterotopic autotransplantation was investigated. Mice (age 4–5 weeks) were divided into the following groups: control; autograft plus NAC (150 mg/kg daily intraperitoneal injection) and autograft plus saline ( n = 6 per group). Groups were treated from 1 day before until 7 days after transplantation. After 28 days, ovary compartments were estimated stereologically. Plasma malondialdehyde, progesterone, oestradiol concentrations and the percentage of apoptotic follicles were measured to evaluate the rate of oxidative stress and ovarian graft function. The mean total volume of ovary, cortex and the number of follicles was significantly higher (all P < 0.001) in the autografts plus NAC group compared with the saline group. In the autografts plus NAC group, the mean percentage of apoptotic follicles ( P < 0.001) and malondialdehyde concentration ( P < 0.001 day 7; P < 0.05 day 28) were significantly lower, whereas oestradiol concentration was significantly higher ( P < 0.05) compared with the saline group. Although NAC cannot compensate the above parameters to the control level, it considerably improves follicular survival and development and also the structure and function of transplanted ovaries, through reducing oxidative stress and apoptosis.