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21.08.2012

Trenbolone users who smoke more likely to get cancer

In the good old days steroids users lived the life of a monk. They didn't drink and they didn't smoke. The only thing they put in their body that didn't count as 'food' was steroids. If you use trenbolone – or a similar steroid – this may be the sensible way to go, according to a Korean study. It suggests that trenbolone users who smoke are more likely to develop lung cancer than non steroid-taking smokers.

The Koreans did experiments with cells in test tubes. They were searching for mechanisms whereby steroids may increase the risk of cancer. In their article, which will soon be published in Toxicology in Vitro, they show that some steroids can do this via the aryl hydrocarbon receptor. This is the same receptor as the one that dioxins and PCBs interact with.

Nearly all animal cells have an aryl hydrocarbon receptor. It probably detects substances that do not belong in the body. If liver cells notice compounds via this receptor, they start to produce the enzyme CYP1A1.

In a healthy body this enzyme works as a detoxifier, but in people with high levels of PAKs or who are smokers increased activity of CYP1A1 often goes wrong. For example, the enzyme converts toxic substances in cigarette smoke into compounds that are even more dangerous than their precursors. That's why people who naturally produce high amounts of CYP1A1 are 700 percent as likely to develop lung cancer if they smoke than smokers who produce normal amounts of the enzyme. And don’t forget: smokers are 1000 percent more likely to develop lung cancer than non-smokers. In smokers who also drink the chance is actually 2000 percent higher.

The Koreans studied drostanolone, oxandrolone, fluoxymesterone, androstatrienedione, nandrolone decanoate, nandrolone, DHT, methandrostenolone, oxymetholone, stanozolol, epitestosterone, testosterone and the designer steroid THG, a 17-alpha-ethyl-analogue of trenbolone. The figures above show, from top to bottom, the structural formulas of testosterone, trenbolone and THG.

The researchers put their steroids into test tubes containing genetically manipulated liver cells, which fluoresce when their aryl hydrocarbon receptors are activated. You can see in the figure above that THG activated the receptor. Testosterone – and the other steroids – didn't do that. At high concentrations THG had almost the same effect as the 'ultimate dioxin' TCDD.

When the researchers exposed liver cells to THG, the production of the enzyme CYP1A1 rose. Testosterone had no effect.

To make sure, the Koreans repeated their tests with the fluorescent liver cells again, using CH-223191, which blocks the aryl hydrocarbon receptor. As you can see above, this compound undermined the effect of THG.

It's probably the trenbolone-like structure with three double bonds in the A, B and C ring which enable THG to interact with the aryl hydrocarbon receptor. If this is the case, then the combination of smoking and taking trenbolone or methyl trenbolone is even more risky. THG isn't available on the market, but trenbolone and methyl trenbolone are.

Animal research has shown that trenbolone reduces the concentration of thyroid hormone in the body. [Br Vet J. 1980 Mar-Apr; 136(2): 168-74.] The Korean research may explain why this happens. Stimulation of the aryl hydrocarbon receptor reduces the concentration of thyroid hormone. [Environ Health Perspect. 2007 Aug; 115(8): 1197-203.]

"The results of this in vitro study could represent the result of prolonged exposure to THG or other synthetic AASs that may cause adverse effects through dioxin-activating pathways", the researchers conclude.

Source:
Toxicol In Vitro. 2012 Jun 1. [Epub ahead of print].