Tocotrienol preserves ovarian function in cyclophosphamide therapy.

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Tocotrienol preserves ovarian function in cyclophosphamide therapy.

Saleh H, Omar E, Froemming G, Said R. Tocotrienol preserves ovarian function in cyclophosphamide therapy. Hum Exp Toxicol 2015 Jan 13. pii: 0960327114564793.

 
 
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Tocotrienol preserves ovarian function in cyclophosphamide therapy.

March 31, 2015

 
Saleh H1, Omar E2, Froemming G3, Said R4.
Hum Exp Toxicol. 2015 Jan 13. pii: 0960327114564793.

1Faculty of Health Science, Universiti Teknologi MARA, Puncak Alam, Selangor, Malaysia Department of Biology, Faculty of Pure Science Education, Thi-Qar University, Thi-Qar, Iraq.and
2Faculty of Medicine, Institute of Medical Molecular Biotechnology, Universiti Teknologi MARA, Sg Buloh, Selangor, Malaysia Centre for Pathology Diagnostic and Research Laboratories, Universiti Teknologi MARA, Sg Buloh, Selangor, Malaysia effat@salam.uitm.edu.my.and
3Faculty of Medicine, Institute of Medical Molecular Biotechnology, Universiti Teknologi MARA, Sg Buloh, Selangor, Malaysia.and
4Faculty of Health Science, Universiti Teknologi MARA, Puncak Alam, Selangor, Malaysia.

Abstract
INTRODUCTION:
Cyclophosphamide (CPA) chemotherapy leads to ovarian failure and infertility. Tocotrienol (T3) is an antioxidant and anti-inflammatory agent. The role of T3 in ovarian protection throughout chemotherapy remains unclear.
AIM:
To investigate the role of T3 in the preservation of female fertility in CPA treatment.
METHOD:
Sixty female mice were divided into five treatment groups, namely, normal saline, corn oil only, T3 only, CPA and CPA + T3. The treatment was given for 30 days, followed by administration of gonadotrophin to induce ovulation. After killing, both ovaries were collected and examined histologically.
RESULTS:
There was significant reduction in ovarian size in the CPA group compared with the normal group (CPA versus normal, mean area ± SD; 0.118 ± 0.018 vs. 0.423 ± 0.024 cm2; p ≤ 0.005), whilst concurrent administration of T3 with CPA leads to conservation of ovarian size (CPA + T3 vs. CPA, mean area ± SD; 0.285 ± 0.032 vs. 0.118 ± 0.018 cm2; p ≤ 0.005). Ovaries in CPA group showed abnormal folliculogenesis with accompanied reduced ovulation rate, follicular oedema, increased vascularity and inflammatory cell infiltration. These changes were reversed by concurrent T3 administration.
CONCLUSION:
Co-administration of T3 with CPA confers protection of ovarian morphology and function in vivo. These findings contribute to the further elucidation of CPA effect on ovary and suggest the potential of T3 use in preserving fertility in chemotherapy.
© The Author(s) 2015.