Ok, so, I have been reading about metabolic paths, enzymes, ligands, affinity, biological half life and whatnot and I have a few questions. As I understand (probably incorrectly) ligands are chemicals that bind to receptors like CB1 and 2 (cannabinoid, where THC has its affect{agonistic}) or A2A (adenosine, where caffeine has its affect { antagonisim by blocking adenosine}) and agonise (turn-on) or antagonize (turn-off) the receptor. Thus I’ll be using ligand to refer to things like caffeine and ethanol, please correct me if that’s not right.
My first question is if a chemical has a super high affinity, does that mean it locks into a single receptor for a long time (A), or does that mean it goes along flipping-on every receptor it encounters(obviously of the relevant kind) in a very efficient manner (B)?
Also what determines how long a ligand/chem stays in a receptor? Does the receptor just spit it out once it’s been activated, or does an enzyme have to come along and break it down (metabolize) it in order for it to move-on/ become inactive?
I’m sorry about packing so many questions in, but…What makes certain lingands/chemicals carcinogenic? Does taking a certain metabolic path (i.e epoxygenase) have an implication on a substances’ status as a carcinogen, or does a certain path usually result in the carcinogens? (The cancer enzyme/ path! Lol)
Do chemicals that have less potential for action with enzymes (if they just don’t have the necessary elements in their molecules to react) result in longer biological half lives? (Would a chemical that could take any/every single path/be broken down by any enzyme have a super short half life?) I’m wondering because I smoke MJ and am considering testing out some substituted indoles or other synthetic cannabinoids, but am concerned about (A) how long they may be able to stick around, if the only route out for them is epoxygenase, and (B) if they are carcinogenic, would picking one with a shorter half life be safer due to less opportunity for the flipping of whatever switch there is on a cell that makes it turn cancerous?
Well actually for that matter I have that same question about minimizing the risk of any carcinogens with drug utilization, including that of the legal ones. Wouldn’t the safest ones (yes I know, no drug is safe) have the most possible metabolic path ways (thus the shortest half lives and therefore less time to cause cancer), and the lowest necessary dose to limit the total number of carcinogenic molecules in the body? Does cancer risk equate to:
# of carcinogenic molecules X duration within the body X genetic propensity =risk?
Also when I smoke the herb, it releases some aromatic hydrocarbons (AHCs) right? So am I risking cancer anytime I smoke anything resulting in AHCs, or even drink enough ethanol? Would vaporizing herb eliminate the AHCs, and if so, are any of the other chems in weed carcinogenic that would still be present with vapeing?
Sorry about such a long and scatterbrained post, if my questions don’t get answered because it’s a pain to read, or you think I should just do more reading and am being lazy, I understand. I’ll continue researching this stuff anyway, and hopefully answer my own questions, but if there’s someone out there who could (and wants to) help out/ accelerate the process I’d appreciate it.
Thanks....ncc
My first question is if a chemical has a super high affinity, does that mean it locks into a single receptor for a long time (A), or does that mean it goes along flipping-on every receptor it encounters(obviously of the relevant kind) in a very efficient manner (B)?
Also what determines how long a ligand/chem stays in a receptor? Does the receptor just spit it out once it’s been activated, or does an enzyme have to come along and break it down (metabolize) it in order for it to move-on/ become inactive?
I’m sorry about packing so many questions in, but…What makes certain lingands/chemicals carcinogenic? Does taking a certain metabolic path (i.e epoxygenase) have an implication on a substances’ status as a carcinogen, or does a certain path usually result in the carcinogens? (The cancer enzyme/ path! Lol)
Do chemicals that have less potential for action with enzymes (if they just don’t have the necessary elements in their molecules to react) result in longer biological half lives? (Would a chemical that could take any/every single path/be broken down by any enzyme have a super short half life?) I’m wondering because I smoke MJ and am considering testing out some substituted indoles or other synthetic cannabinoids, but am concerned about (A) how long they may be able to stick around, if the only route out for them is epoxygenase, and (B) if they are carcinogenic, would picking one with a shorter half life be safer due to less opportunity for the flipping of whatever switch there is on a cell that makes it turn cancerous?
Well actually for that matter I have that same question about minimizing the risk of any carcinogens with drug utilization, including that of the legal ones. Wouldn’t the safest ones (yes I know, no drug is safe) have the most possible metabolic path ways (thus the shortest half lives and therefore less time to cause cancer), and the lowest necessary dose to limit the total number of carcinogenic molecules in the body? Does cancer risk equate to:
# of carcinogenic molecules X duration within the body X genetic propensity =risk?
Also when I smoke the herb, it releases some aromatic hydrocarbons (AHCs) right? So am I risking cancer anytime I smoke anything resulting in AHCs, or even drink enough ethanol? Would vaporizing herb eliminate the AHCs, and if so, are any of the other chems in weed carcinogenic that would still be present with vapeing?
Sorry about such a long and scatterbrained post, if my questions don’t get answered because it’s a pain to read, or you think I should just do more reading and am being lazy, I understand. I’ll continue researching this stuff anyway, and hopefully answer my own questions, but if there’s someone out there who could (and wants to) help out/ accelerate the process I’d appreciate it.
Thanks....ncc
