Some studies might be confounded by meds.
Thanks for the question, made me do more looking.
UC is so complex no wonder they cannot find a cure.
But I have to take a stand at least for my disease, and for now it is oxidation.
genetic defect UC people
down regulated in mouse dss colitis
genotypes,depending on which one, reduced detox of ROS
have not seen this paper before,this one also mentions that our alpha 1-antiprotease inhibitors are destroyed
by ROS, this in itself is a big deal, since using camostat or BBI bowman birk protease inhibitors can put human
UC into remission. see section 4.3 HOCL is causing the problem and that is where taurine would play a protective
role, in addition to its other roles. I also see some indication that peroxide will also deactivate it.
rutin, also when they checked taurine they I guess did not check taucl or br
another good paper
actually not quite sure what to make of the abstract you quoted where the rest of the antioxidant enzymes
are at normal levels. But that was back in 1995. In light of all the ROS going on in the colon, hard to believe
that it is just reduced GST.
We may also have this going on from Pravda patent. So really have to believe there is also a problem
with glutathione peroxidase, whether genetic or some other reason.
On a populational level, ethnic variation of glutathione peroxidase has been recorded with individuals of Jewish or Mediterranean origin exhibiting lower activities (The Metabolic and Molecular Basis of Inherited Disease, 2001, 8th ed., p. 4650). A two to four fold increase in incidence and prevalence of ulcerative colitis has also been reported for these ethnic groups (Roth et al., 1989
here is the patent again, the remission rates are crazy high, looks like oral R-lipoic acid doing much of the work.
Yes they took enemas but 23 were on their standard meds prior to the trial with no remission.
Oxygen-derived free radicals have been implicated in the pathogenesis of ulcerative colitis. Mammalian tissues contain antioxidant systems that offer protection from the damaging effect of these active species. In the present study, the activity of the antioxidant enzymes catalase, glutathione peroxidase, glutathione transferase and glutathione reductase were measured in rectal biopsies from patients with ulcerative colitis and compared with that obtained from normal subjects. A significant decrease in the activity of glutathione transferase was observed in ulcerative colitis (48.32 +/- 6.73 units/mg protein, mean +/- s.e.) compared to normal (68.20 +/- 6.83; P = 0.015). There was no difference in the activity of other antioxidant enzymes between controls and ulcerative colitis. Myeloperoxidase, a marker for neutrophil infiltration, was considerably increased in ulcerative colitis while malonaldehyde, the end product of lipid peroxidation, was not increased. The reduced activity of glutathione transferase in ulcerative colitis may be an additional factor in the pathogenesis of mucosal damage in this disease
Post Edited (Old Mike) : 4/30/2015 9:16:28 AM (GMT-6)