MDMA, ECGC & COMP inhibition

[SilentRoller]

Greetings everyone,
I have my 'first roll after 3 months' coming up very soon, and I'm wondering about the effect of ECGC (which is a COMT inhibitor) upon the strength of the experience. Obviously, I have heard that ECGC acts as a powerful antioxidant, but considering COMT is one of the metabolic pathways [alongside CYP2D6] in which MDMA is excreted, would it reasonable to assume that ECGC would increase the length/intensity of the MDMA experience?

SR

EDIT- Mistake in title of the thread. I meant COMT not COMP

 

[SilentRoller]

Sorry for double post - If it helps, a MOD can move this to ADD, as I may get more answers there

 

[JWills20]

Moved to ADD because it looks a little out of our league. I don't know what ECGC or COMT stand for.

Fire away ADD'ers!

 

[endotropic]

Greetings everyone,
I have my 'first roll after 3 months' coming up very soon, and I'm wondering about the effect of ECGC (which is a COMT inhibitor) upon the strength of the experience. Obviously, I have heard that ECGC acts as a powerful antioxidant, but considering COMT is one of the metabolic pathways [alongside CYP2D6] in which MDMA is excreted, would it reasonable to assume that ECGC would increase the length/intensity of the MDMA experience?

SR

EDIT- Mistake in title of the thread. I meant COMT not COMP

This is not likely to enhance your experience. COMT is not the first step in MDMA breakdown, meaning that by the time COMT has a chance to act, MDMA has already been degraded. If you inhibit COMT, you're just going to build up that metabolite, which is likely toxic:

Differential roles of phase I and phase II enzymes in 3,4-methylendioxymethamphetamine-induced cytotoxicity.

Metabolism plays an important role in the toxic effects caused by 3,4-methylenedioxymethamphetamine (MDMA). Most research has focused on the involvement of CYP2D6 enzyme in MDMA bioactivation, and less is known about the contribution of other cytochrome P450 (P450) and phase II metabolism. In this study, we researched the differential roles of phase I P450 enzymes CYP1A2, CYP3A4, and CYP2D6 and phase II enzymes glutathione S-transferase (GST) and catechol-O-methyltransferase (COMT) on the toxic potential of MDMA. MDMA acts as inhibitor of its own metabolism with a relative potency of inhibition of CYP2D>CYP3A>> CYP1A in rat liver microsomes and in human liver [immortalized human liver epithelial cells (THLE)] cells transfected with individual CYP1A2, CYP3A4, or CYP2D6. Cytotoxicity measurements [by 3,(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] in THLE cells showed that the inhibition of phase I enzymes CYP1A2 by alpha-naphthoflavone and CYP3A4 by troleandomycin does not affect MDMA-induced cytotoxicity. MDMA metabolism by CYP2D6 significantly increased cytotoxicity, which was counteracted by CYP2D6 inhibition by quinidine. Inhibition of COMT by 2'-fluoro-3,4-dihydroxy-5-nitrobenzophenone (Ro-41-0960) and GST by buthionine sulfoximine showed that COMT is mainly involved in detoxification of CYP2D6-formed MDMA metabolites, whereas glutathione (GSH) is mainly involved in detoxification of CYP3A4-formed MDMA metabolites. Liquid chromatography/tandem mass spectrometry analyses of MDMA-metabolites in the THLE cell culture media confirmed formation of the specific MDMA metabolites and corroborated the observed cytotoxicity. Our data suggest that CYP2D6 as well as CYP3A4 play an important role in MDMA bioactivation. In addition, further studies are needed to address the differential roles of CYP3A4 and GSH/GST in MDMA bioactivation and detoxification.

 

[23536]

ECGC = EGCG (the stuff in green tea)?

 

[sekio]

Yes, I think that's what he's referring to.

Even though EGCG is a good antioxidant, it does not inhibit enzymatic metabolic processes to a significant degree. It's just a radical scavenger, like vitamin C.