Archaeal Porphyrins, Regulation of Cell Function and Neuroimmunoendocrine Integration

Ravikumar Kurup A., Parameswara Achutha Kurup


Objectives: Actinidic archaea have been related to the pathogenesis of schizophrenia, malignancy, metabolic syndrome x, autoimmune disease and neuronal degeneration[1-8]. An actinide dependent shadow biosphere of archaea and viroids in the above mentioned disease states is described[7, 9]. Actinidic archaea have a mevalonate pathway and are cholesterol catabolizing. They can use cholesterol as a carbon and energy source. Archaeal cholesterol catabolism can generate porphyrins via the cholesterol ring oxidase generated pyruvate and GABA shunt pathway. Porphyrins have been related to schizophrenia, metabolic syndrome x, malignancy, systemic lupus erythematosis, multiple sclerosis and alzheimer’s diseases. The role of archaeal porphyrins in regulation of cell functions and neuroimmunoendocrine integration is discussed. Methodology: Plasma from fasting heparinised blood was used and the experimental protocol was as follows (I) Plasma+phosphate buffered saline, (II) same as I+cholesterol substrate, (III) same as II+rutile 0.1 mg/ml, (IV) same as II+ciprofloxacine and doxycycline each in a concentration of 1 mg/ml. The following estimations were carried out:- Cytochrome F420, free RNA, free DNA, polycyclic aromatic hydrocarbon, hydrogen peroxide, pyruvate, ammonia, glutamate, succinate, glycine, delta aminolevulinic acid and digoxin. Results: Plasma of control subjects showed increased levels of the above mentioned parameters with after incubation for 1 hour and addition of cholesterol substrate resulted in still further significant increase in these parameters. The plasma of patients showed similar results but the extent of increase was more. The addition of antibiotics to the control plasma caused a decrease in all the parameters while addition of rutile increased their levels. The addition of antibiotics and rutile to the patient’s plasma produced the same changes but the extent of change was more in patient’s sera as compared to controls. There was upregulated archaeal porphyrin synthesis in the patient population which was archaeal in origin as indicated by actinide catalysis of the reactions. The cholesterol oxidase pathway generated pyruvate which entered the GABA shunt pathway. This resulted in synthesis of succinate and glycine which are substrates for ALA synthase. Conclusion: An actinide dependent shadow biosphere of archaea and viroids in the above mentioned disease states is described. Thus the archaeal porphyrins can contribute to the pathgenesis of metabolic syndrome x, malignancy, psychiatric disorders, autoimmune disease, AIDS, prion disease, neuronal degeneration and epileptogenesis. Archaeal porphyrin synthesis is crucial in the pathogenesis of these disorders. Porphyrins may serve as regulatory molecules modulating immune, neural, endocrine, metabolic and genetic systems. The porphyrins photo-oxidation generated free radicals can produce immune activation, produce cell death, activate cell proliferation, produce insulin resistance and modulate conscious/quantal perception. The archaeal porphyrins functions as key regulatory molecules with mitochondrial benzodiazepine receptors playing an important role.

Key words: Actinide; Archaea; Porphyrins; GABA Shunt; Peripheral benzodiazepine receptor; Delta aminolevulinic acid


Actinide; Archaea; Porphyrins; GABA Shunt; Peripheral benzodiazepine receptor; Delta aminolevulinic acid



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