Evaluation of Serum Renin Angiotensin System, Redox Homeostasis and Inflammatory Factors in Aas Abusers

Presentation Number: SUN 530
Date of Presentation: April 2nd, 2017

Luiz Fonte Boa*1, Andrea Jansen DA Silva2, Caroline Coelho de Faria3, Álvaro Leitão4, Denise Pires Carvalho5, José Hamilton Nascimento2 and Rodrigo Fortunato4
1UNIVERSIDADE FEDERAL DO RIO DE JANEIRO, Rio De Janeiro, BRAZIL, 2UNIVERSIDADE FEDERAL DO RIO DE JANEIRO, 3Federal University of Rio de Janeiro, Rio de Janeiro, BRAZIL, 4Federal University of Rio de Janeiro, 5Federal University of Rio de Janeiro, Brazil

Abstract

Cardiovascular system is the most affected by the use of supraphysiological doses of androgenic anabolic steroids (AAS), causing hypertension, cardiac hypertrophy, fibrosis, among others. Previous studies showed that the deleterious cardiovascular effects caused by AAS can be reversed by blocking AT1 and mineralocorticoid receptors, suggesting the participation of Renin Angiotensin System (RAS) in the cardiac changes induced by AAS. Interestingly, RAS increases reactive oxygen species (ROS) generation, which is related to its cardiac effects. Thus, this study examined RAS activity and redox homeostasis in the serum of AAS abusers. For this, blood was collected from AAS abusers and control volunteers for hormonal measurement, antioxidat defense, and oxidative stress and inflammatory biomarkers measurements. Serum levels of renin plasmatic activity (C=1.57 ± 0.24 ng/mL/h, N=18; AAS=2.93 ± 0.46 ng/mL/h N=19), C-Reactive Protein (C=1.06 ± 0.17 mg/L N=14; AAS=2.14 ± 0.41 mg/L N=15), testosterone (C=579.7 ± 45.16 ng/dL n=15; AAS=989.5 ± 145.5 ng/dL n=15,p=0,0119), free testosterone (C=437.6 ± 33.68 pmol/L n=15; AAS=1104 ± 202.2 pmol/L n=13,p=0,0017) and estradiol (C=27.07 ± 2.634 pg/mL n=15; AAS=92.60 ± 25.46 pg/mL n=15,p=0,0161) were higher in AAS group when compared to control group. Besides that, FSH (C=3.26 ± 0.32 mUl/mL, n=15; AAS= 0.70 ± 0.26 mUl/mL n=15, p<0.0001), LH (C=4.69 ± 0.41 mUI/mL, n=15; AAS=1.06 ± 0.50 mUl/mL n=15, p<0.0001) and SHGB (C=33.27 ± 2.37 nmol/L, n=15; AAS=11.42 ± 1.62 nmol/L, n=13, p<0.0001) were lower in AAS group in comparison to control. No significant differences were found for gluthatione peroxidase activity (C=0.45 ± 0.016 nmol NADPH/min/mL, n=15; AAS= 0.46 ± 0.016 nmol NADPH/min/mL n=15, p=0.6032), superoxide dismutase activity (C=184.0 ± 4.37 U SOD/mL, n=15; AAS=192.8 ± 3.91 U SOD/mL, n=15, p=0.1483), Oxidized LDL (C=1347000 ± 110500 pg/mL, n=15; AAS=1291000 ± 69640 pg/mL, n=15, p=0.6710). In conclusion, it seems that AAS activate RAS, without changes in serum oxidative stress.

 

Nothing to Disclose: LF, AJ, CCD, ÁL, DPC, JHN, RF