Melatonin ameliorates oxidative stress and reproductive toxicity induced by cyclophosphamide in male mice

Human and Experimental Toxicology - Tập 33 Số 2 - Trang 185-195 - 2014
Aroona Chabra1, Mohammad Shokrzadeh2,3, Farshad Naghshvar4, Fatemeh Salehi4, Amirhossein Ahmadi3
1Student Research Committee, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Islamic Republic of Iran
2Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Islamic Republic of Iran
3Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Islamic Republic of Iran
4Department of Pathology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Islamic Republic of Iran

Tóm tắt

The present study evaluated the efficacy of melatonin in cyclophosphamide (CP)-induced testicular injury, lipid peroxidative damage, and antioxidant enzymes status of the mice testis on the basis of biochemical and histological studies. Mice were pretreated with four different doses of melatonin (2.5, 5, 10, and, 20 mg/kg by body weight (b.w.)) via intraperitoneal injection for five consecutive days followed by injection with CP (200 mg/kg b.w.) 1 h after the last injection of melatonin on the 5th day. After 24 h, mice were euthanized, testes were immediately removed, and biochemical and histological studies were conducted. Treatment with melatonin significantly mitigates lipid peroxidation, superoxide dismutase, and catalase activity and the level of reduced glutathione content abnormality induced by CP in mice testis. Histological examination clearly demonstrates that pretreatment of melatonin prevented CP-induced spermatogenesis toxicity and spermatogenic cells reduction in mice testis. The protective effect of melatonin is likely due to the antioxidative properties of the indolamine existed in the chemical structure. Because melatonin is a safe, natural compound, it could be used concomitantly as a supplement to protect people undergoing chemotherapy against reproductive toxicity.

Từ khóa


Tài liệu tham khảo

Turner AJ, 1986, Biochem Educ, 14, 93

Marinello AJ, 1984, Cancer Res, 44, 4615

10.2165/00003495-199142050-00005

10.1016/S0959-437X(02)00014-X

10.1053/j.ajkd.2004.01.008

10.1016/0027-5107(95)00039-L

Kaur F, 1997, Indian J Exp Biol, 35, 771

Meistrich ML, 1995, J Androl, 16, 334, 10.1002/j.1939-4640.1995.tb00538.x

Das UB, 2002, Asian J Androl, 4, 201

10.1081/DCT-120005891

10.1191/096032701718890568

10.1191/0960327102ht304oa

10.1016/j.reprotox.2004.06.015

10.1016/j.cca.2005.11.034

10.1093/toxsci/kfi333

10.1080/1071576021000016472

Reiter RJ, 1993, Braz J Med Biol Res, 26, 1141

10.1016/S0024-3205(97)00030-1

10.1111/j.1600-079X.1995.tb00163.x

10.1016/0891-5849(96)00046-9

10.1016/0024-3205(94)00666-0

10.1006/phrs.2001.0828

10.1016/0003-2697(76)90527-3

10.1016/0076-6879(90)86134-H

10.1111/j.1745-4522.2002.tb00208.x

10.1016/S0021-9258(19)45228-9

10.1016/0003-9861(72)90080-X

10.1016/0003-9861(59)90090-6

10.1079/BJN20031066

Fawcett DW, 1994, Bloom and Fawcett: a textbook of histology, 12

10.1023/B:CBTO.0000013342.17370.16

Gul M, 2000, Indian J Exp Biol, 38, 625

10.1016/S0300-483X(00)00307-3

10.1016/j.foodchem.2011.05.075

10.1016/j.fertnstert.2008.07.1758

10.1016/j.tox.2006.01.027

10.1016/j.tox.2008.03.015

10.2164/jandrol.106.002428

10.1093/molehr/4.3.235

10.1016/j.tox.2008.11.005

10.1016/0024-3205(94)00417-Q

10.1016/0926-6917(95)90052-7

10.1111/j.1600-079X.1997.tb00334.x

10.1016/0014-2999(96)00241-5

10.1096/fasebj.9.12.7672513

10.1111/j.1600-079X.1997.tb00333.x

10.1016/0006-2952(96)00055-X

10.2174/1568026023394443

10.1046/j.1439-0272.2002.00522.x

10.1007/s11010-008-9907-1

10.1042/bj2640527

10.1007/s12272-001-1228-z

10.1177/1534735409360361