If you want to answer this question in a nutshell, most drugs theoretically have potential that can harm the liver. Of course, some agents can cause liver damage much more quickly and easily, for example due to their structure or specific changes they undergo (eg paracetamol).
Everything would be good, but … ~ 5% of paracetamol under the influence of cytochrome P450 enzymes (CYP3A4, CYP2E1, CYP2A6, CYP1A2) forms a highly toxic to the liver metabolite N-acetyl-P-benzoquinoline (NAPQI, N-acetyl-p-benzoquinone imine). Glutathione resources have a specific supply and until that time the toxic metabolite is bound (with glutathione) and in the form of mercapturic acid excreted in the urine. Unfortunately, when glutathione is not enough (for various reasons), NAPQI binds to hepatic proteins and leads to hepatocyte necrosis. Symptoms appear after 24-48 h.
Almost all oral SAAs are harmful to the liver, eagerly abused for several decades
To a lesser extent, the problem concerns oral turinabol (dihydrochlormethyltestosterone) and oxandrolone (anavaru). There are examples of substances lacking C17AA – eg testosterone undecanoate – andriol – however it is poorly absorbed (through the lymphatic system), its use by bodybuilders is negligible (it was used by cyclists in the Tour de France).
Very often men using cheering neglect the problem. They claim that in research it has been shown that these are safe means. Yes of course. It’s like comparing the collision with the wall at 30 km / h (tests on drugs) and the same collision at 120 km / h (doses used in doping). In other words, if you use 100 mg oxandrolone or turinabol oral per day it is not said that it will not affect the liver. The issue is complicated by the fact that in some circumstances even massive liver damage does not have to manifest itself in the study, eg ALAT / AsPAT.
Interestingly, protective measures often have the opposite effect than declared. There are serious doubts about ursodeoxycholic acid, essential phospholipids (preparations of phosphatidylcholine from soybeans (Glycine max) (Phospoholipidum essentiale), silymarin. S-adenosyl-L-methionine may be probably used, and GY et al 1 described case 51 a summer man from Puerto Rico who has Class C liver damage (the most advanced liver failure) on the Child-Turcotte-Pugh Scale. The classification was proposed in 1964 by CG Child and JG Turcotte of the University of Michigan to determine mortality The patient with liver damage class C has a 40% chance of survival of the year, and only 20% five years and classified for liver transplantation.The said 51-year-old had jaundice and resistant to diuretics ascites (often Spironolactone and Fu are popular among bodybuilders rosemid). The male also had spontaneous bacterial peritonitis (SBP). And after this very long introduction, I go to the merits.
Well, the man used the supplement containing (D-ribose-L-cysteine). Scientists suspect that the severity of jaundice symptoms and significant deterioration in the man’s condition is associated with the use of such a form of detoxification! Applications should be limited to the use of SAA, PH toxic drugs, medicines containing, for example, paracetamol. Not always an excellent dietary supplement with (according to ads) to protect the liver will fulfill its task when the damage is more serious than you thought. Liver damage is not always manifested through the growth of aspartate aminotransferase or alanine aminotransferase.
You can read also: Disorders of liver test results