User:McBiophysics/sandbox

== Testosterone, DHT, and Nandrolone conversions to other anabolic steroids ==

Testosterone Derivatives and Reactions
====Testosterone Conversion to DHT, Nandrolone , Dianabol , Turinabol , Halotestin , and Equipoise ====

====DHT Conversion to Winstrol, Primobolan , Anadrol , and Superdrol ====

====Nandrolone Conversion to Trestolone, Trenbolone , Norboletone , and Ethylnandrol ====

Mechanism of action
The pharmacodynamics of AAS are unlike peptide hormones. Water-soluble peptide hormones cannot penetrate the fatty cell membrane and only indirectly affect the nucleus of target cells through their interaction with the cell's surface receptors. However, as fat-soluble hormones, AAS are membrane-permeable and influence the nucleus of cells by direct action. The pharmacodynamic action of AAS begin when the exogenous hormone penetrates the membrane of the target cell and binds to an androgen receptor (AR) located in the cytoplasm of that cell. From there, the compound hormone-receptor diffuses into the nucleus, where it either alters the expression of genes or activates processes that send signals to other parts of the cell. Different types of AAS bind to the AAR with different affinities, depending on their chemical structure.

The effect of AAS on muscle mass is caused in at least two ways: first, they increase the production of proteins; second, they reduce recovery time by blocking the effects of stress hormone cortisol on muscle tissue, so that catabolism of muscle is greatly reduced. It has been hypothesized that this reduction in muscle breakdown may occur through AAS inhibiting the action of other steroid hormones called glucocorticoids that promote the breakdown of muscles. AAS also affect the number of cells that develop into fat-storage cells, by favouring cellular differentiation into muscle cells instead.

Molecular Interaction of AAS with Androgen Receptors
Anabolic steroids interact at a molecular level with ARs across various tissues, including muscle, bone, and reproductive systems. Upon binding to the AR, anabolic steroids trigger a translocation of the hormone-receptor complex to the cell nucleus, where they either alter gene expression or activate cellular signaling pathways; this results in increased protein synthesis, enhanced muscle growth, and reduced muscle catabolism.

Additionally, anabolic steroids influence cellular differentiation, favoring the development of muscle cells over fat-storage cells. Research in this field has shown that the structural modifications in anabolic steroids are critical in determining their binding affinity to ARs and their resulting anabolic and androgenic activities. These modifications affect the steroids' ability to influence gene expression and cellular processes, highlighting the complex biophysical interactions of anabolic steroids at the cellular level.