phase_dancer
Bluelight Crew
- Joined
- Mar 12, 2001
- Messages
- 6,179
thanks babydoc.
My concern stems from the fact that 5HTP is a direct precursor to serotonin and there is no rate limiting step, apart from perhaps vesicle limited 5HTP diffusion. Serotonin and its many receptors are distributed throughout the body, and because of the abundance of aromatic amino acid decarboxylase, wouldn't that mean 5HTP can be decaboxylated to serotonin anywhere cells have this enzyme (which is everywhere)?
What regulating mechanisms would be likely to prevent this? Could the excess be taken up by the pineal gland and converted to melatonin or would MAOA be able to handle such high amounts? If so, could this affect NE deamination?
I also wonder which would be the favoured excretory metabolite, and would these pathways be affected by other drugs, particularly alcohol which uses the same reductase and dehydrogenase as for 5-hydroxyindole aldehyde catabolism?
My concern stems from the fact that 5HTP is a direct precursor to serotonin and there is no rate limiting step, apart from perhaps vesicle limited 5HTP diffusion. Serotonin and its many receptors are distributed throughout the body, and because of the abundance of aromatic amino acid decarboxylase, wouldn't that mean 5HTP can be decaboxylated to serotonin anywhere cells have this enzyme (which is everywhere)?
What regulating mechanisms would be likely to prevent this? Could the excess be taken up by the pineal gland and converted to melatonin or would MAOA be able to handle such high amounts? If so, could this affect NE deamination?
I also wonder which would be the favoured excretory metabolite, and would these pathways be affected by other drugs, particularly alcohol which uses the same reductase and dehydrogenase as for 5-hydroxyindole aldehyde catabolism?