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Re: 5-HTP confirmed to lower Tyrosine stimulation myco

Posted by myco on March 10, 2009, at 11:40:36

In reply to Re: 5-HTP confirmed to lower Tyrosine stimulation desolationrower, posted by myco on March 10, 2009, at 11:24:58

If you were wondering how 5-htp fits into this from what I was going on about earlier....5-htp is given with carbidopa (another AADC - like EGCG from green tea). Carbidopa has been studied well so I was using the studies of 5-htp and AADC's, in general, to develope my idea. Thats all. Not sure if that fits into your confusion on what I was getting at.

----------------


> I'm not sure exactly what your referring to based on what I had posted...I just woke up here lol and bear with me as i'm a pharm noob and still learning
>
> The reason I'm looking at this is a theory I have that i'm investigating regarding increasing bioavailability of nardil.
>
> SULT1A3 (Nagai et al.) catalyzes the sulfation (I think thats the right way to say it) of dopamine and ritodrine in the intestine...inhibiting or acting as a detoxifying enzyme for many compounds of similar structure.
>
> Since EGCG (an aromatic L-amino acid decarboxylase - AADC) from green tea has been shown to inhibit the activity of SULT1A3 in the intestine thus increasing bioavailability (inhibiting peripheral formation) of dopamine and ritodrine (Natai et al.) in the CNS, it could be possible that it could also increase bioavailability of Nardil. Not many studies have looked at phenelzine in this way that I know of.
>
> If you look at the general structure of dopamine and ritodrine you will see that they are very similar to phenelzine (pointed out to me by Larry Hoover). It's quite possible that SULT1A3 has an unknown effect on the breakdown of phenelzine (recall all the complaints of the "new" nardil and it's "subpar" effect - I believe issues with absorption and bioavailability). Larry also confirmed the possibility of this theory actually working.
>
> I'm struggling a lil bit with the idea of totally understanding this, have emailed some research docs and still no response yet, but I think there is something here to be looked at.
>
> Myco
>
>
>
>
> ------------------
>
>
>
> > Absorption and distribution of tea catechin, (-)-epigallocatechin-3-gallate, in the rat.
> >
> > Nakagawa K, Miyazawa T.
> >
> > Food Chemistry Laboratory, Faculty of Agriculture, Tohoku University, Sendai, Japan.
> >
> > To investigate the absorption and metabolism of an anticarcinogenic tea catechin, (-)-epigallocatechin-3-gallate (EGCg), in rats, a newly developed chemiluminescence-detection high-performance liquid chromatography (CL-HPLC) method was employed and the EGCg concentrations in blood plasma, liver, brain, small intestinal mucosa and colon mucosa were determined before and after EGCg administration. The recovery of EGCg, extracted consecutively with ethyl acetate and methanol, was 86.1% from plasma and 64.5-74.2% from the tissue samples. The EGCg concentrations of plasma and tissue samples from the control rat (before EGCg administration) were all below the detection limit (< 0.002 nmol/mL, 0.002 nmol/g), but 60 min after a single oral administration of EGCg (500 mg/kg body weight), the levels increased, reaching 12.3 nmol/mL in plasma, 48.4 nmol/g in liver, 0.5 nmol/g in brain, 565 nmol/g in small intestinal mucosa and 68.6 nmol/g in colon mucosa. The EGCg levels found in the tissues corresponded to 0.0003-0.45% of ingested EGCg. The results indicate that tea catechin, EGCg, is absorbed from the digestive tract, with the intestinal mucosa the most enriched of the organelles. This may explain the potent antioxidant function of EGCg in inhibiting colon mucosal phospholipid hydroperoxidation in the prevention of rat colonic carcinogenesis.
> >
> > Neuroprotection and neurorescue against A&#946;toxicity and PKC-dependent release of non-amyloidogenic soluble precursor protein by green tea polyphenol (-)- epigallocatechin-3-gallate
> > Yona Levites, Tamar Amit, Silvia Mandel, and Moussa B. H. Youdim
> >
> > E-mail contact: Youdim{at}Tx.Technion.ac.il
> >
> > Green tea extract and its main polyphenol constituent (-)-epigallocatechin-3-gallate (EGCG) possess potent neuroprotective activity in cell culture and mice model of Parkinsons disease. The central hypothesis guiding this study is that EGCG may play an important role in amyloid precursor protein (APP) secretion and protection against toxicity induced by &#946;-amyloid (A&#946;). The present study shows that EGCG enhances (~6-fold) the release of the non-amyloidogenic soluble form of the amyloid precursor protein (sAPP&#945;) into the conditioned media of human SH-SY5Y neuroblastoma and rat pheochromocytoma PC12 cells. sAPP&#945; release was blocked by the hydroxamic acid-based metalloprotease inhibitor Ro319790, which indicated mediation via &#945;-secretase activity. Inhibition of protein kinase C (PKC) with the inhibitor GF109203X, or by down-regulation of PKC, blocked the EGCG-induced sAPP&#945; secretion, suggesting the involvement of PKC. Indeed, EGCG induced the phosphorylation of PKC, thus identifying a novel PKC-dependent mechanism of EGCG action by activation of the non-amyloidogenic pathway. EGCG is not only able to protect, but it can rescue PC12 cells against the &#946;-amyloid (A&#946;) toxicity in a dose-dependent manner. In addition, administration of EGCG (2 mg/kg) to mice for 7 or 14 days significantly decreased membrane-bound holoprotein APP levels, with a concomitant increase in sAPP&#945; levels in the hippocampus. Consistently, EGCG markedly increased PKC&#945; and PKC&#949; in the membrane and the cytosolic fractions of mice hippocampus. Thus, EGCG has protective effects against A&#946;-induced neurotoxicity and regulates secretory processing of non-amyloidogenic APP via PKC pathway.
> >
> > Wide distribution of [3H](-)-epigallocatechin gallate, a cancer preventive tea polyphenol, in mouse tissue
> >
> > M Suganuma, S Okabe, M Oniyama, Y Tada, H Ito and H Fujiki
> > Saitama Cancer Center Research Institute, Japan. masami@saitama-cc.go.jp
> >
> > The increasing recognition of green tea and tea polyphenols as cancer preventives has created a need for a study of their bioavailability. For this purpose, we synthesized [3H] (-)-epigallocatechin gallate ([3H]EGCG) with a specific activity of 48.1 GBq/mmol and directly administered the solution into the stomachs of CD-1 female or male mice. Radioactivity in the digestive tract, various organs, blood, urine and feces was measured with an oxidizer at various times after administration and significant radioactivity was found in the previously reported target organs of EGCG and green tea extract (digestive tract, liver, lung, pancreas, mammary gland and skin), as well as other organs (brain, kidney, uterus and ovary and testes) in both sexes. Incorporation of radioactivity in the cells was confirmed by microautoradiography. Within 24 h, 6.6 (females) and 6.4% (males) of total administered radioactivity was excreted in the urine and 37.7 and 33.1% in feces. HPLC analysis of urine from both sexes revealed that 0.03-0.59% of administered [3H]EGCG, along with at least five metabolites, was excreted. In addition, we found that a second, equal administration to female mice after a 6 h interval enhanced tissue levels of radioactivity in blood, brain, liver, pancreas, bladder and bone 4-6 times above those after a single administration. These results suggest that frequent consumption of green tea enables the body to maintain a high level of tea polyphenols and this paper is the first pharmacological evidence of a wide distribution of [3H]EGCG in mouse organs, indicating a similar wide range of target organs for cancer prevention in humans.
> >
> > I don't see any mention of EGCG/green tea in the first study, and the second on is in reference to some phase II enzyme affecting Dopamine, which is not the same as l-dopa/5-htp. And, theres like a million studies on green tea improving outcomes of various measure of brain health.
> >
> > -d/r
>
>


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