The effect of nandrolone treatment with and without enforced swimming on histological and biochemical changes in the heart and coronary artery of male ratsAsghar Tofighi1, Minoo Shirpoor1, Mohammad Hasan Khadem Ansari2, Alireza Shirpoor3, Mitra Zerehpoosh2
1Department of Exercise Physiology, Faculty of Physician Education and Sport Sciences, Urmia University,
2Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences; Urmia-Iran
3Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences; Urmia-Iran
Objective: Chronic anabolic androgenic steroid (AAS) consumption increases incidence of cardiovascular abnormalities in athletes and mechanisms underlying those abnormalities continue to be investigated. This study examines whether nandrolone consumption induced cardiac and coronary artery wall abnormalities via oxidative stress. It was also designed to determine whether enforced swimming augmented possible cardiotoxic effects of nandrolone in rat heart.Keywords: exercise, heart fibrosis, nandrolone, oxidative stress, rat
Methods: Twenty-four male Wistar rats were divided into 3 groups: control, nandrolone, and nandrolone with enforced swimming. Nandrolone group received 10 mg/kg body weight nandrolone 3 times a week for 6 weeks. Nandrolone group with enforced swimming received the same amount of nandrolone and was forced to swim with excess weight of 20% body weight.
Results: After 6 weeks of treatment, results indicated proliferation of heart muscle and coronary smooth muscle cells and lipid peroxidation; significant rise in levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), nicotinamide adenine dinucleotide phosphate oxidase, homocysteine (Hcy), apolipoprotein B, low-density lipoprotein, and cholesterol, as well as severe fibrosis in heart tissue and around coronary arteries of nandrolone and nandrolone with enforced swimming groups compared with control group.
Conclusion: These findings strongly support idea that nandrolone intake by sedentary rats and exercised rats induced heart abnormality mediated by oxidative stress, which was manifest in increased lipid peroxidation, Hcy, and 8-OHdG in heart tissue. (Anatol J Cardiol 2016; 16: 000-00)
Corresponding Author: Alireza Shirpoor, Iran