Commercial adenochrome pigment samples were evaluated

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Finally, the latest evidence of glutathione S-transferase gene deficiency in patients with schizophrenia is reviewed. This enzyme detoxifies adenochrome.

The adenochrome pigment hypothesis in schizophrenia

This paper reviews the research status of the theory of adenochrome pigment in schizophrenia. An account was first given of all the experiments in which the adenochrome - induced mental simulation effects were reported in normal volunteers. It then presents evidence that adenochrome pigments may actually occur as metabolites of adenochrome in the brain in the C2 group adenochrome neurons of the medulla, and gives an account of the function of these neurons in higher limbic function. Finally, the latest evidence of glutathione S-transferase gene deficiency in patients with schizophrenia is reviewed. This enzyme detoxifies adenochrome.

 

The stability of adenochrome pigment solution in the presence of several inorganic compounds was studied. The purity and stability of several "aged" and commercial adenochrome pigment samples were evaluated. The stability of adenochrome pigment solution in some low aliphatic alcohols was studied.

 

The dose of adenochrome pigment was 10 milligrams. Did not change the EEG of normal volunteers, but at 10,25 and 50 mgm. Bilateral paroxysmal abnormalities of electroencephalogram in epileptic patients with dose increase, but little effect on cortical focusing itself.

 

After niacin was administered orally or intravenously, the EEG frequency shifted slightly to the fast side. In patients with epilepsy, the drug significantly reduced bilateral diffuse paroxysmal abnormalities (except for true idiopathic epilepsy), but had little effect on the lesion itself.

The modes of action of the above-mentioned drugs were discussed.

The causes of paroxysmal electroencephalogram disorder in schizophrenia were preliminarily explained.

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