Continued from:

Carbon Disulfide – CS2 Intro

Hypo thesis: The Etiology of Schizophrenia 1

Hypo thesis: The Etiology of Schizophrenia II

The pathomorphology of CS2 neuropathy resembles much like other samples orginating from an impaired energy metabolism. (1) A studie in rats shows the oxidative effects of CS2 exposure, a marked increase in cerebral cortex hippocampus, spinal cord and serum. Reactive oxygen species, Malondialdehyd. Ca2+ and Calmodulin levels increased in in Cerebral Cortex, hippocampus and spinal cord. (2) Carbon disulfide is used in viscose rayon plants as a solvent in the spinning process. It is known to have central and peripheral neurotoxic effects, and among the pleiotrophic conditions it causes are atherosclerotic change, diabetes mellitus, and coronary heart disease (3-6). In previous studies, the radiologic findings of carbon disulfide poisoning were diffuse or focal brain atrophy, infarcts in the basal ganglia, subcortial white matter and gray matter, and central demyelination (7-11). A few case reports have described the computed tomographic (CT) (7-10) or magnetic resonance imaging (MRI) findings (10, 11 )

Continued from:

Carbon Disulfide – CS2 Intro

Hypo thesis: The Etiology of Schizophrenia 1

Continues:

Hypo Thesis: The Etiology of Schizophrenia III

… It has been reported that the glucose and lipid metabolism is disturbed by carbon disulfide both in experimental animals and in exposed workers, but not to conclusive. There is a large body of indirect information associating abnormal energy metabolism in peripheral neuropathies caused by CS2.

Acetyl-CoA

In Clostridium thermoaceticum Carbon monoxide dehydrogenase CODH has three paramagnetic centers iron-nickel-sulfur, labeled A,B and C.  CS2 mimics CO at centre A, competively, thereby most probably alternating parts of it’s enzymologic timing and functionality. (BB)  The function of CS2 in the human Acetyl-CoA, remains to be elucidated.