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alt.support.food-allergies |
Thanks, I'll try glutamine next for the burning tongue syndrome that I Per your advice, I recently added carnitine and alpha lipoic acid But I am wondering if I have the OCTN1 vs OCTN2 defect which would Recent I experimented with cooked vs raw bananas and strawberries. For Have you noticed that an apple or potato turns brown when cut or In humans, a similar process is used to produce melanin. Here tyrosine Does anyone have links that describe the metabolism of dietary Background Info: Various members in my family have suffered Crohn's --------- > Given that supplemental carnitine in liposomes has alleviated TNBS colitis in mice when TNBS downregulates OCTN2, I'd say it's causative
[PMID 17065219]. The other limiting factor might be glutamine (via
the
Atb0+ transporter).
have been experiencing for the last 8 years. In the last two years it
has reduced mostly by avoiding trigger foods of which there are many
including organic fruits and veggies.
(ALA) and they both reduce the tongue burn. And of the two, ALA seems
to be more effective. It also seems my "food allergies" which manifest
itself as itching, sharp intermittent shooting pains and hand
numbness have been reduced, at least for black pepper and raw
hazelnuts. And I can ingest more beans before incurring a heartburn.
prevent the plant derived antioxidant, ergothioniene, from being
accumulated in related tissues (ie skin, gut, endothelial lining,
eyes, joints, immune cells, nervous system). OCTN1 variants are also
linked to CD, RA, lupus, psoriasis and leukemia.
some reason cooked cause less tongue burn than raw ones. Anyone else
experience this? What might be the reason?
bruised. Supposedly, the enzyme tyrosinase converts some polyphenols
into quinones. Quinones are quite reactive and apparently have anti-
viral, bacterial, insect and worm properties.
is oxidized by tyrosinase into quinones and then further into melanin.
Supposedly ingested dietary polyphenols are also oxidized into
quinones. And neurotransmitters (ie adrenaline) are also oxidized into
quinones. Coincedentally, I get bloating and nerve pain from elevated
stress. And according to some abstracts, vitiligo (white skin) may be
related to quinones also.
polyphenols and if it involves carnitine or ergothioniene? Also can
anyone suggest some low molecular weight, non-phenolic based,
antioxidants effective against quinones and hydrogen peroxide (H2O2)?
Thx
Disease, Psoriasis, Dermatitis, Breast Cancer, Leukemia, Cataracts,
etc. Starting 2001, I also experienced gut inflammation, rhoids/
fissures, pain near terminal ileum, IBS, CFS, neuropathy, CTS, RLS,
sciatica, heartburns, sore joints and food allergies that peaked in
late 2007. About half a year ago I starting developing vitiligo on my
hands.
Catechin metabolism: glutathione conjugate formation catalyzed by
tyrosinase, peroxidase, and cytochrome p450.
The metabolic pathways of dietary flavonoids are still largely
unknown. In the present work, mass spectrometry and UV-vis
spectroscopy studies were used to show that the naturally occurring
flavonoid catechin underwent enzymatic oxidation by tyrosinase in the
presence of glutathione (GSH) to form mono-, bi-, and tri-glutathione
conjugates of catechin and mono- and bi-glutathione conjugates of a
catechin dimer. A hydroxylated catechin adduct was also detected.
Using UV spectroscopy, it was shown that the catechol B-ring of
catechin was oxidized by tyrosinase to form an o-quinone which could
be reduced back to catechin with potassium borohydride or reacted with
GSH to form glutathione conjugates. The catechin-glutathione
conjugates formed had much lower distribution coefficient values than
catechin itself. When peroxidase and hydrogen peroxide were used
instead of tyrosinase, only mono-glutathione conjugates were formed
but not bi-glutathione conjugates or hydroxylated adducts. (1)H NMR
evidence showed that three different mono-glutathione conjugates on
ring B of catechin were formed by peroxidase and hydrogen peroxide.
Rat liver microsomes and NADPH or cumene hydroperoxide also catalyzed
catechin-glutathione conjugate formation which was prevented by
benzylimidazole, a P450 2E1 inhibitor. Catechin cytotoxicity toward
isolated hepatocytes was also markedly enhanced by hydrogen peroxide
or cumene hydroperoxide and was prevented by benzylimidazole,
suggesting that catechin could be metabolically activated by P450
peroxidase activity to form cytotoxic quinoid species. PMID: 11453730