The anabolic androgenic steroid nandrolone decanoate disrupts redox homeostasis in liver, heart and kidney of male Wistar rats

PLoS One. 2014 Sep 16;9(9):e102699. doi: 10.1371/journal.pone.0102699. eCollection 2014.

Abstract

The abuse of anabolic androgenic steroids (AAS) may cause side effects in several tissues. Oxidative stress is linked to the pathophysiology of most of these alterations, being involved in fibrosis, cellular proliferation, tumorigenesis, amongst others. Thus, the aim of this study was to determine the impact of supraphysiological doses of nandrolone decanoate (DECA) on the redox balance of liver, heart and kidney. Wistar male rats were treated with intramuscular injections of vehicle or DECA (1 mg.100 g(-1) body weight) once a week for 8 weeks. The activity and mRNA levels of NADPH Oxidase (NOX), and the activity of catalase, glutathione peroxidase (GPx) and total superoxide dismutase (SOD), as well as the reduced thiol and carbonyl residue proteins, were measured in liver, heart and kidney. DECA treatment increased NOX activity in heart and liver, but NOX2 mRNA levels were only increased in heart. Liver catalase and SOD activities were decreased in the DECA-treated group, but only catalase activity was decreased in the kidney. No differences were detected in GPx activity. Thiol residues were decreased in the liver and kidney of treated animals in comparison to the control group, while carbonyl residues were increased in the kidney after the treatment. Taken together, our results show that chronically administered DECA is able to disrupt the cellular redox balance, leading to an oxidative stress state.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anabolic Agents / administration & dosage
  • Anabolic Agents / pharmacology*
  • Animals
  • Antioxidants / metabolism
  • Biomarkers
  • Enzyme Activation
  • Gene Expression
  • Heart / drug effects
  • Homeostasis / drug effects*
  • Homeostasis / physiology*
  • Kidney / drug effects
  • Kidney / metabolism
  • Liver / drug effects
  • Liver / metabolism
  • Male
  • NADPH Oxidases / genetics
  • NADPH Oxidases / metabolism
  • Nandrolone / administration & dosage
  • Nandrolone / analogs & derivatives*
  • Nandrolone / pharmacology
  • Nandrolone Decanoate
  • Oxidation-Reduction / drug effects*
  • Oxidative Stress / drug effects
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Transaminases / blood

Substances

  • Anabolic Agents
  • Antioxidants
  • Biomarkers
  • RNA, Messenger
  • Nandrolone
  • NADPH Oxidases
  • Transaminases
  • Nandrolone Decanoate

Grant support

This work was supported by grants from Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), and Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.