Questions have to do with
a.) hepatotoxicity of 17 alpha-substitution
b.) hepatotoxicity of oral steroids both as related to 17aa and steroid
c.) absorption and distribution of 17aa steroids via oral vs. injection methods.
d.) detoxification vs. bioactivation during metabolic process in the liver. (other drugs having hepatotoxicity effects)
Will try to keep it simple.
BOTH the 17 alpha substitution AND the steroid itself are (in different ways) damaging to the liver. However, SOME of the steroids have different levels of absorption and excretion and metabolic transformation in the liver. In other words, SOME oral steroid get pissed out more (not absorbed or transformed). All 17aa ARE hepatotoxic - some more than others (oxandrolone seems to be the least OUT OF the anabolic ones).
Oral administration means that the 17aa steroid must go through the intestinal tract - go through the cell membranes and get transported to the liver via the hepatic artery before undergoing metabolic (biotransformation) changes AND then going into the blood system to the heart, tissues, lungs etc...
17aa administration via injection skips the intestinal tract absorption method -however, it must still be biotransformed (in toxicology it is called DETOXIFICATION) in the liver. So, it is still toxic. Might have improved absorption - so, as someone else said above it "could" be even more toxic only because MORE of the substance makes it to the liver.
Someone else brought up "tylenol" and "other" substances that are liver toxic. There are over 900 medications known to be liver toxic.
When the liver receives said substances it can detoxify them or bioactivate them. Detoxification means metabolites of lower toxicity - bioactivation means metabolites that are more toxic than the parent substance.
Tylenol is a known substance that metabolizes into a MORE TOXIC substance (NAPQi metabolized by P-450 enzymes) above a certain limit intaken. Tylenol causes adverse drug reactions classified as type A (intrinsic or pharmacological) - meaning "we" know when and why and in what quantity they occur.
BOTTOM LINE:
17aa steroids ARE toxic whether taken orally or IM.
17aa steroids in low quantities taken for SHORT periods of time haven't been proven to cause HCC (cancer) but do cause reversible (most of the time) damage.
SOME 17aa steroids are less toxic - like oxandrolone appearing to be the least so.
(for the original "post" - Tbol is toxic to the liver and WILL elevate your liver enzymes - tried it myself this summer - stopped after 4 weeks due to elevated enzymes - oxandrolone at 20mgs/day did NOT elevate enzymes - but this was JUST my experience).
Personally I wouldn't run them unless I knew my liver state prior to - and couldn't monitor during cycle at least weekly. Run vit b-complex (B6, b3, b12) run arginine - run milk thistle ... all prior to, during and after orals.
IF YOU HAVE THE FOLLOWING:
Serum bilirubin level - more that 2 times ULN with associated transaminase rise - this is an ominous sign.
If you want to know WHEN you've caused your liver injury - either (a) ALT level more than three times of upper limit of normal (ULN), (b) ALP level more than twice ULN. This indicates severe hepatotoxicity and is likely to lead to mortality in 10% to 15% of patients, especially if the offending steroid isn't stopped (Hy's Law)
The only diagnostic test to detect HCC is a blood test known as alpha-fetoprotein (AFP). This test is one of the tumor markers (a blood test indicative of, but not diagnostic of, cancer). Normal adult level is less than 20 nanograms per milliliter (ng/ml). If the level in a person’s blood is over 400 ng/ml, then it is pretty safe to say that liver cancer is present. Levels under 400 ng/ml are unclear but I wouldn't want to see them on my result sheet.
MAKE IT A STICKY AND GOOD LUCK .. and if SCARZ's questions are answered I can sleep well - if it's not enough info for Scarz -- tell me and I swear I'll dust of my toxicology manuals in the attic somewhere.