Cerebrospinal fluid (CSF) glutamate, hypoxanthine, lactate, xanthine, and uric acid were investigated in neurological patients. In multiple sclerosis, myelopathy, stroke, epilepsy and viral meningitis glutamate, hypoxanthine, xanthine, and uric acid are increased 2-3-fold compared to controls.
This is very interesting as you probably have read that people with multiple sclerosis are found to be LOW in uric acid. I always wondered where the uric acid was, had to be somewhere. It's in the cerebrospinal fluid!
Glutamate-mediated excitotoxicity is associated with adenosine triphosphate (ATP) degradation and generation of oxygen radicals.
I need to know what to do about this. I need to know how to deal with the symptom and also how to reverse whatever damage is causing this.
This study might have some clues. "massive Ca2+ influx induces" "chelation of external calcium"
Xanthine oxidase activation and superoxide (O2.-) production are completely inhibited by concomitant incubation of glutamate with MK-801, a specific NMDA receptor antagonist, or by chelation of external calcium with EGTA. Partial inhibition of both cell death and parallel production of reactive oxygen species is achieved with allopurinol, a xanthine oxidase inhibitor, leupeptin, a protease inhibitor, reducing agents such as glutathione or dithiothreitol, antioxidants such as vitamin E and vitamin C, and externally added superoxide dismutase. It is concluded that glutamate-triggered, NMDA-mediated, massive Ca2+ influx induces rapid conversion of xanthine dehydrogenase into xanthine oxidase with subsequent production of reactive oxygen species that most probably have a causal involvement in the initial steps of the series of intracellular events leading to neuronal degeneration and death.
Kind of sounds similar to mast cell activation.
And I am seeing that hypoxia plays a part in glutamate toxicity. But I won't post any links at this point because I am not sure if I am looking at a tangent or not.