The body can downregulate or even deactivate the AR signal by a number of means. To illustrate this, one first has to understand what happens when androgen hormones (called ligands) “mate” with the androgen receptor:
- Ligand binds to AR
- AR travels to cell nucleus and triggers transcription (copying) of AR target genes to a copy of those genes called “RNA”
- RNA then travels to a structure within the cell called a ribosome. The ribosome reads the “message” (RNA) and produces a correponding protein. This is called translation.
- This protein often must undergo a finishing step called “posttranslational modification” before it reaches its final, active form. The fully functional protein is what is called a “signal”, because it signals other mechanisms/cells to do something.
- The finished protein (=signal) is what makes androgenic things happen such as keeping the penile structure intact and muscle cells growing, helps give us an erection, helps in producing sperm, keeps our prostate healthy, gives us libido, etc.
So to answer your question, the body “silences” the AR signal mainly by either downregulating step 2 (making less copies of RNA) or step 4 (by modifying the protein in such a way that it’s basically useless = posttranslational modification). Posttranslational modification is actually the most prominent mechanism the AR has at its disposal to completely silence the AR signal if required.
A number of substances can either inhibit or promote transcriptional activity (step 2). Zinc seems to have an effect on transcriptional activity by potentiating AR binding to nuclei [1], which basically means that it increases transcription. This effect could be due to the upregulation of one of the many modulators of transcriptional activity. But the body doesn’t directly influence zinc levels to regulate the AR to my knowledge. That would be an odd way to go about things.