High-dose testosterone supplementation disturbs liver pro-oxidant/antioxidant balance and function in adolescent male Wistar rats undergoing moderate-intensity endurance training.

In some countries, anabolic-androgenic steroid abuse is rampant among adolescent boys and young men, including some of those seeking physical fitness and/or pleasing appearance through various exercise types. This tactic carries the risk of severe harmful health effects, including liver injury. Most anabolic-androgenic steroid stacking protocols employed are based on the use of the 'prototypic' anabolic-androgenic steroid testosterone and/or its esters.

The effect of endurance training and testosterone supplementation on the expression of blood spinal cord barrier proteins in rats.

The present study aimed to estimate the effect of endurance training, two doses of testosterone, and the combination of these stimuli on the level of the endothelial proteins claudin, occludin, JAM-1, VE-cadherin, ZO-1, ZO-2, and P-glycoprotein in rat spinal cords. Adult male Wistar rats were trained using a motor-driven treadmill for 6 weeks (40-60 min, 5 times per week) and/or were treated for 6 weeks with two doses of testosterone (i.m.

High-dose testosterone enanthate supplementation boosts oxidative stress, but exerts little effect on the antioxidant barrier in sedentary adolescent male rat liver.

Background: Anabolic-androgenic steroids abuse is on the rise among adolescent boys and young men, mostly in those seeking a 'shortcut' to an improved body image. This approach is associated with the risk of severe adverse health effects, some of which involve the liver and are linked to hepatic oxidative stress. Testosterone and its esters is a cornerstone of most anabolic-androgenic steroid stacking protocols.

High-dose testosterone propionate treatment reverses the effects of endurance training on myocardial antioxidant defenses in adolescent male rats.

This study was aimed at evaluation of changes in activities of selected antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) and contents of key nonenzymatic antioxidants (glutathione, protein thiol groups, and α- and γ-tocopherols) in the left heart ventricle of young male Wistar rats subjected to endurance training (treadmill running, 1 h daily, 5 days a week, for 6 weeks) or/and testosterone propionate treatment (8 or 80 mg/kg body weight, intramuscularly, once a week, for 6 weeks) during adolescence. The training alone increased the activities of key antioxidant enzymes, but lowered the pool of nonenzymatic antioxidants and enhanced myocardial oxidative stress as evidenced by elevation of the lipid peroxidation biomarker malondialdehyde. The lower-dose testosterone treatment showed mixed effects on the individual components of the antioxidant defense system, but markedly enhanced lipid peroxidation.

Testosterone affects hormone-sensitive lipase (HSL) activity and lipid metabolism in the left ventricle.

Fatty acids, which are the major cardiac fuel, are derived from lipid droplets stored in cardiomyocytes, among other sources. The heart expresses hormone-sensitive lipase (HSL), which regulates triglycerides (TG) breakdown, and the enzyme is under hormonal control. Evidence obtained from adipose tissue suggests that testosterone regulates HSL activity.

Short-term effects of electrically induced tachycardia on antioxidant defenses in the normal and hypertrophied rat left ventricle.

Increased oxidative stress resulting from enhanced production of reactive oxygen species and/or inadequate mechanisms of antioxidant defenses has been recognized as an important factor contributing to the initiation and progression of cardiac dysfunction under a wide variety of pathophysiological conditions. The main objective of this study was to examine the effect of electrically induced tachycardia on oxidative stress and the capacity of antioxidant defenses in the normal and hypertrophied left ventricle (LV) in the rat. Left ventricular hypertrophy (LVH) was produced by banding the descending abdominal aorta.