- Joined
- Jul 9, 2018
- Messages
- 1,067
'Abstract
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.'
link: https://www.ncbi.nlm.nih.gov/pubmed/27372877
I've gotten the green light from the man himself to post the full text in PDF too. EDIT: File too big, sen dme a PM if you're interested.
On his instagram( https://www.instagram.com/p/BiCn5tMhrw6/) he posted something pretty interesting:
'The combination of metabolic resistance as well as the potency to induce AR transactivation also seems to be in line with what is seen in practice (oxandrolone hardly hepatotoxic, oxymetholone a bit hepatotoxic, methandienone quite hepatotoxic, methyltrienolone very hepatotoxic on a mg per mg basis).'
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.'
link: https://www.ncbi.nlm.nih.gov/pubmed/27372877
I've gotten the green light from the man himself to post the full text in PDF too. EDIT: File too big, sen dme a PM if you're interested.
On his instagram( https://www.instagram.com/p/BiCn5tMhrw6/) he posted something pretty interesting:
'The combination of metabolic resistance as well as the potency to induce AR transactivation also seems to be in line with what is seen in practice (oxandrolone hardly hepatotoxic, oxymetholone a bit hepatotoxic, methandienone quite hepatotoxic, methyltrienolone very hepatotoxic on a mg per mg basis).'
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