The effect of nandrolone treatment with and without enforced swimming on histological and biochemical changes in the heart and coronary artery of male rats

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.
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 2017; 17: 176-83)
Keywords: exercise, heart fibrosis, nandrolone, oxidative stress, rat