Anabolic androgenic steroid-induced hepatotoxicity

Med Hypotheses. 2016 Aug:93:150-3. doi: 10.1016/j.mehy.2016.06.004. Epub 2016 Jun 5.


Anabolic androgenic steroids (AAS) have been abused for decades by both professional and amateur athletes in order to improve physical performance or muscle mass. AAS abuse can cause adverse effects, among which are hepatotoxic effects. These effects include cholestatic icterus and possibly peliosis hepatis and hepatocellular carcinoma or adenoma. In particular, 17α-alkylated AAS appear to be hepatotoxic, whereas nonalkylated AAS appear not to be. The 17α-alkyl substitution retards hepatic metabolism of the AAS rendering it orally bioavailable. The mechanism responsible for the hepatotoxicity induced by 17α-alkylated AAS remains poorly understood. However, oxidative stress has been repeatedly shown to be associated with it. In this manuscript we present a hypothesis which describes a potential mechanism responsible for AAS-induced hepatotoxicity, based on several observations from the literature which suggest oxidative stress being a causal factor.

Keywords: 17α-alkylation; Anabolic androgenic steroids; Androgen receptor; Hepatotoxicity; Oxidative stress; Reactive oxygen species.

MeSH terms

  • Adenoma / chemically induced
  • Administration, Oral
  • Alkylation
  • Anabolic Agents / chemistry
  • Anabolic Agents / toxicity*
  • Androgens / chemistry
  • Androgens / toxicity*
  • Animals
  • Antioxidants / chemistry
  • Carcinoma, Hepatocellular / chemically induced
  • Chemical and Drug Induced Liver Injury / metabolism*
  • Cholestasis / chemically induced
  • Humans
  • Liver / drug effects*
  • Liver / metabolism
  • Liver Neoplasms / chemically induced
  • Models, Theoretical
  • Oxidative Stress / drug effects
  • Oxygen / chemistry
  • Peliosis Hepatis / chemically induced
  • Reactive Oxygen Species / metabolism
  • Receptors, Androgen / metabolism*
  • Substance-Related Disorders / complications*


  • Anabolic Agents
  • Androgens
  • Antioxidants
  • Reactive Oxygen Species
  • Receptors, Androgen
  • Oxygen