CS2

All posts tagged CS2

Is Schizopherenia caused by a substance or lack of a substance?

Posted by gdnf on March 14, 2011
Posted in: CO2 Reactivity, Neuroscience, Schizophrenia, Science. Tagged: , , , , , , .

1

To little or to much of a substance?

Some of the theories of Schizophrenia etiology mention the drug induced hallucinations as a raw-model for Schizophrenia but there is a problem with that – Persons with Schizophrenia doesn’t have these substances in their blood while hallucinating. Some drugs and some medicines might create states that remind of Schizophrenia: Ketamine and Phencyclidine (PCP) are the most mentioned. But the substances are not identified in the blood of the persons having the problem.

Here will in show the signs of lacking Oxygen and that there actually is a substance that can cause some of the symptoms and that persons with schizophrenia have it in their exhaled breath.

2

Lacking essentials as cause of Schizophrenia?

Probably, as much as 50% of the genes involved in the disease could be changed due to hypoxia. And seeing the BOLD results really tells me that they don’t get the oxygen needed.  Can we really get a much stronger evidence of hypoxia?

The CO2 reactivity or the driving reaction to breath is also changed…

3

A substance that can give the symptoms is detected in the populations having the disease

We will show that there is in fact, a substance that by itself can create most of the symptomatology panorama and that this very substance also is detected in the individuals having disease. The substance is Carbon Sulfide or CS2. One of the most active metabolites are H2S (Hydrogen Sulfide) or more likely – H2S is the mother-substance and CS2 the metabolite.

Schizophrenia H2S and Carbonic Anhydrase

Posted by gdnf on June 22, 2010
Posted in: Neuroscience, Schizophrenia. Tagged: , , , , , , , , , , .

After the updates of the new page: The Etiology of Schizophrenia – CS2. The work now continues by following the metabolism from CS2 to H2S in what could be and the reactive core in the etiology of Schizophrenia. Up next are the effects of H2S.

But first of all let us see that the CAC-hålet theory shows that the reactive substance CS2 which in itself can cause some of the symptoms in Schizophrenia and is metabolized to Hydrogen Sulfide – H2S in the body, by a new route.  CS2 is also detected in the exhaled air from persons with Schizophrenia.

Aspiration and Respiration

The core function in aspiration is gas exchange with the biosphere and to regulate the breathing to the needs of the cellular respiration. In schizophrenia the Carbonic Anhydrase Catalysis – CAC is slower than normally resulting in a prolonged hypoxia in the mitochondria after increases in the O2 consumption, part of these fundamentals are later shown in the BOLD fMRI where the blood oxygenation levels curve are steeper in persons with schizophrenia.

CS2 and the metabolites dithiocarbamates and H2S are potent inhibitors of CAC, this will result in a further decrease in the function of Carbonic Anhydrase and the CO2 reactivity will get even slower. Or the other way around, H2S is the mother-substance to the reaction.

—

Refrenences
Carbonic anhydrase inhibitors. Inhibition of cytosolic isoforms I, II, III, VII and XIII with less investigated inorganic anions
Alessio Innocentia, Andrea Scozzafavaa and Claudiu T. SupuranCorresponding Author Contact Information, a, E-mail The Corresponding Author
Università degli Studi di Firenze, Laboratorio di Chimica Bioinorganica, Rm. 188, Via della Lastruccia 3, I-50019 Sesto Fiorentino, Firenze, Italy
2009.

Chengelis, C. P. and Neal, R. A., Studies of carbonyl sulfide toxicity: metabolism by carbonic anhydrase,
Towicol. Appl. Pharmacol., 55, 198, 1980

Baird, T.T., A. Waheed, T. Okuyama, W.S. Sly, & C.A. Fierke (1997) Catalysis and Inhibition
of Human Carbonic Anhydrase IV, Biochemistry, 36: 2669 – 2678.

The possible role of CO2 in producing a post-stimulus CBF
and BOLD undershoot
Meryem A. Yücel1,2, Anna Devor2,3, Ata Akın1 and David A. Boas2*
1 Institute of Biomedical Engineering, Bogˇ aziçi University, Istanbul, Turkey

CS2 Protease inhibitors and Schizophrenia

Posted by gdnf on May 26, 2010
Posted in: Schizophrenia. Tagged: , , , , , , , , , , .

Disassociative states like Schizophrenia or psychosis seems to have a plethora of dysregulated organic pathways. Today we take a look at the Ubiquitin proteasome system. The Ubiquitin proteasome system is tagging unwanted or abnormal proteins. Dysfunction of these systems results in a buildup of malfunctioning proteins and is emerging as an important factor in neurodegenerative diseases.

New research show that the ubiquitin proteasome pathway was listed in the top ten canonical pathways for Bipolar Disorder and psychosis diagnostic groups across both samples with a considerably low likelihood of a chance occurrence
Preliminary evidence of ubiquitin proteasome system dysregulation in schizophrenia and bipolar disorder: convergent pathway analysis findings from two independent samples.

Why the interest in Ubiquitin protease?
Well the reactive agent in CAC-Hålet theory results in protease inhibitors, CS2 is known to metabolize to dithiocarbamate complexes and they tend to be strong protease inhibitors. This could in fact be an explanation to why the ubiquitin protease system is disturbed in Schizophrenia since the group already is known to have CS2 in their systems.

This pathway can possibly also explain why persons with Schizophrenia tends to have a lower rate of cancer when  the risk factors are calculated, since protease inhibitors is probably the mothers of anticancer therapies.
Disulfiram’s anticancer effects are getting interesting and its main
metabolite is CS2 – The same agent that the CAC-Hålet theory hypothesizes as a possible reactive factor in the etiology of Schizophrenia.

Targeting of Nuclear Factor-kB andproteasome by Dithiocarbamate.

The Etiology of Schizophrenia CAC-hålet Theory

Posted by gdnf on May 25, 2010
Posted in: CO2 Reactivity, Schizophrenia. Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , .

Manuscript Draft part 1,  part 2

Just like a dream, you entering this world and take your first breath

The Hypo-Thesis of cognition – A Central command in emergency light

In this hypothesis I will show a possible reactive agent in the etiology of Schizophrenia  This first step is showing a map of what CS2 are capable of. The next step will look into earlier steps in the etiological map of the etiology of Schizophrenia, the preconditioning.

Corresponding Author: POW Pär-Olof Wassén,
Corresponding Author’s Institution: CAC-Hålet Theory
First Author: Pär-Olof Wassén

CAC-Hålet theory The reactive agent
-Showing what hypotetically could be a reactive factor in the etiology of Schizophrenia

The thermodynamics of Homo Sapiens largely rely on old CODH/ACS constructions for TCA, carbon to carbon transfer, glucose and lipid metabolism. It is shown in bacterial CODH/ACS that CS2 can alter the thermodynamics of the process by tunnel gating in centre A. (9) Themechanisms in Homo Sapiens enzymology still remains to be elucidated.

CS2 exposure can give symptoms of Schizophrenia. (1) People with Schizophrenia have CS2 in their breath (2) other persons usually don’t. Persons with Schizophrenia appears to react differently and have different partial arterial pressure on CO2 than others (3), (4). The very ground-level carbon to carbon transfer used in CO2 fixation is done by constructions relying on the CODH/ ACS. The distribution of cerebral blood flow is highly sensitive to changes in the arterial CO2. (5) The CO2 regulations during sleep might be more vulnerable. (6) When the CS2 reactivity where measured between groups exposed to CS2 and not exposed to CS2, a remarkable difference was noted in the reactivity to CO2. (7) It has been shown in rats that low PaCO2 inhibits NMDA receptors. (8) The Thermodynamic backbone of human Neural transmittance is dependent on lipid and glucose metabolism, both is altered by the gating in the CODH/ACS tunnel A. One study suggests that the effect of CS2 on learning and memory ability in rats is related to the activity of NOS and the expression of nNOS in the hippocampus. (10)

B-vitamin metabolism disturbance
Exposure to carbon bisulfide results in an increased turnover of the B-vitamin complex (16, 17, 18, 19, 20) CS2 induced elevated serum lipid levels and decreased cholesterol synthesis ( on rat, 176 ppm, inh) are reportedly blocked by feeding nicotinic acid at a dose of 40 mg/kg/da (20) Nicotinic acid has protective effects against CS2 poisoning. CS2 reduces the levels of Nicotinic Acid. (21 22 23 24 25)


Chelating effects on various essential trace metals
Carbon disulfide reacts with the amino groups of amino acids and proteins to form thiocarbamate in blood and tissues (36) thiocarbamates, possessing sulfhydryl groups, may chelate polyvalent inorganic ions. CS2 reacts with endogenous amines to form dithiocarbamates.(26) which could be metabolized back to CS2. An implication is the formation of acid labile CS2 (AL CS2) that will continue to increase, even at steady-state concentrations of CS2, as long as free CS2 is available to the tissue and adequate amine substrates are available. (26) An additional important finding was the slow elimination of AL CS2, suggesting that AL CS2 may accumulate in the body after repeated exposure to CS2. (26) Dithiocarbamates are capable of chelating several polyvalent inorganic ions such as copper and zinc, and
thus may inactivate numerous enzymes in which these ions are essential for activity. (27) The hypothesis of a chelating effect has been supported by the results of some studies (28), Reports of increase in zinc and copper excretion in exposed rats, but also increased copper levels in peripheral nervous tissue of exposed rats (28) (29). Copper and zinc ions are essential for the prosthetic groups of many enzymes. The neurotoxic action of carbon disulfide and its interference with the activity of many enzymes could partly be explained by chelating effects. Zinc is required for the activity of enzymes such as lactic acid dehydrogenase a, carbonic anhydrase, glutamate dehydrogenase, and alcohol dehydrogenase. Copper, represents a cofactor of pyridoxol, a form of vitamin B6. Copper is required for the proper functioning of enzymes such as cytochrome c oxidase, the coenzyme A dehydrogenase system, eg. dopamine ß hydroxylase. The loss of copper from the spinal cord is accompanied by cellular damage, producing tissue degeneration. Disturbances of the central and peripheral nervous systems,
resulting from carbon disulfide exposure, could be connected with the loss of copper due to chelation and consequent inhibitory effects on enzyme systems (30) like Tyrosinase and the very core carbon to carbon transfer.

LOX, Lysyl oxidase is copperdependent. The LOX activity are essential for the mechanical stability of the fibers and other supramolecular assemblies formed by these proteins and the elasticity of elastin. Because collagens and elastin are important components of the extracellular matrix, abnormalities in their modification can be expected to affect many tissues, as seen in lathyrism, a connective tissue disorder caused by the administration of ß-aminopropionitrile, an irreversible inhibitor of lysyl oxidases. (31)
Extracellular copper enzymes initiate the formation of the lysine and hydroxylysine derived crosslinks in collagens and lysine-derived crosslinks in elastin. (32) CS2-mediated protein cross-linking occurs in vivo through the generation of Lys-Lys thiourea and that diethyldithiocarbamate can, through in vivo release of CS2, produce the same cross-linking structure. This observation supports the utility of cross-linking of peripheral proteins as a specific dosimeter of internal exposure for CS2 and provides a biomechanistic explanation to account for the high-molecular-weight neurofilament protein species isolated from rats exposed to CS2 or N, N-diethyldithiocarbamate. (33) High levels of homocysteine will irreversibly inhibit LOX. (34) One study suggest that LDL downregulation of LOX could contribute to the endothelial dysfunction caused by hypercholesterolemia, thus contributing to atherosclerotic plaque formation. (35) 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.


The energy depletion

The pathomorphology of CS2 neuropathy resembles much like other samples originating from an impaired energy metabolism. (37) A study 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. (38) 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 (39-42). 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 (43-47). A few case reports have described the computed tomographic (CT) (43-47) or magnetic resonance imaging (MRI) findings (46, 47) Finding of decrease in the GSH contents and GSH-Px, CAT activities in cerebral cortex, hippocampus, spinal cord and serum. The activities of T-AOC also decreased in all three nerve tissues and serum, as time went on and symptom developed. Furthermore, significant correlations between LPO and gait abnormality were observed as symptom developed. Oxidation stress also resulted in increased Ca (2+) concentrations and calmodulin (CaM) levels increases in cerebral cortex, hippocampus and spinal cord. (48) Carbon disulfide intoxication results in alternations of microtubule and microfilament expression, and the alternations might be related to its neurotoxicity. fast changes in beta-tubulin and beta-actin in rats
exposed to CS2 could indicate a rapid change in the cytoskeleton metabolism: The beta-tubulin mRNA increased 207% and beta-actin 94% which might give insights in the metabokinetic prosperities of CS2 on a cytoskeletal level. (49) Many electrophiles toxicants cause synaptic dysfunction by unknown mechanisms. It is recognized that synaptic activity is regulated by the redox state of certain cysteine sulfhydryl groups on proteins. Research indicates that thiolates are receptors for the endogenous nitric oxide (NO) pathway and that subsequent reversible S-nitrosylation finely regulates a broad spectrum of synaptic activities. Electrophilic neurotoxicants like CS2 might, according to a hypothesized mechanism (16) produce synaptic toxicity by modifying these thiols. SNAP-25, NMDA, GAP-43, Methionine adenosyl transferases, v-ATPase are thiol-regulated proteins and protein complexes targeted by NO which further might explains the action of CS2 toxicity. One study suggests that the effect of CS2 on learning and memory ability in rats is related to the activity of NOS and the expression of nNOS in the hippocampus. (17)

Cancer and p53
The p53 gene has been proposed as tumour suppressor and a candidate susceptibility gene in schizophrenia. (52) results of one study indicate that occupational exposure results in a significant increase in P53 CGT>CTT transversions. (53) identified occupational exposure in combination with smoking as a significant risk factor for the mutation. It was concluded that AS-PCR of the P53 273rd codon transversions is a suitable technique for studying the effects of occupational exposure to CS2. (53), (57).

The CAC-Hålet Swedish site ADHD och ADD.

The Etiology of Schizophrenia CAC-Hålet Theory

Posted by gdnf on May 25, 2010
Posted in: CO2 Reactivity, Schizophrenia. Tagged: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , .

From Part 1

part II the CAC-hålet theory

The etiology of Schizophrenia could be linked to endogenous Carbon disulfide CS2 production. The manufacture and exposure to endogenous CS2, could probably act in months after months before showing some of the symptoms of high CS2 exposure (Hallucinations, Psychosis and personality changes)

Suggestions

To ensure a proper analysis of earlier undetectable biomarkers one might consider gas-analysis from skin and breath as an biomarker and emission source, since the CS2 otherwise could leave undetected through the biggest organ –  the skin. I propose analysis of total air content in a closed chamber with subjects naked to avoid contamination with techniques for gas detection (59), (60) to reveal the biometrics of human endogenous CS2 production. Which has not been done to my knowledge.

By practising these suggestions it might be easier to understand and prevent the disease by detecting the prodromal and active  systems conditions besides the genetic vulnerability and map out what role CS2 play in the etiology of Schizophrenia.

References:

(1)
Wien Klin Wochenschr. 1958 Jun 13;70(24):445-6.
[Schizophreniform reactions in chronic carbon disulfide poisoning.]
[Article in German]
Petran V
(2)
Clin Pathol 1993;46:861-864
Increased pentane and carbon disulfide in the
breath of patients with schizophrenia
M Phillips, M Sabas, J Greenberg
(3)
Respiration. 1987;52(1):34-41.Links
Respiratory sensitivity to carbon dioxide in schizophrenia.
Verma R, Dewan M, Ashutosh K.
(4)
Acta Psychiatr Scand. 1990 Jun;81(6):497-506.
Cerebral blood flow responses to inhaled carbon dioxide in schizophrenia.
Mathew RJ, Wilson WH.
Department of Psychiatry, Duke University Medical Center, Durham, North Carolina 27710.
(5)
Am J Physiol Regul Integr Comp Physiol. 2009 May;296(5):R1473-95.
Integration of cerebrovascular CO2 reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation.
(6)
Adv Exp Med Biol. 2006;588:65-73
Control of cerebral blood flow during sleep and the effects of hypoxia.
Corfield DR, Meadows GE
(7)
J Korean Med Sci. 1998 Dec;13(6):645-51. Cerebral vasoreactivity by transcranial Doppler in carbon disulfide poisoning cases in Korea. Lee E, Kim MH.
(8)
Br J Anaesth. 2008 Nov;101(5):673-9. Epub 2008 Sep 12.
Carbon dioxide negatively modulates N-methyl-D-aspartate receptors.
Brosnan RJ, Pham TL.
(9)
1994: Kumar M; Lu W P; Ragsdale S W
Binding of carbon disulfide to the site of acetyl-CoA synthesis by the nickel-iron-sulfur protein, carbon monoxide dehydrogenase, from Clostridium thermoaceticum.
Biochemistry 1994;33(32):9769-77.
(10)
Chin Med J (Engl). 2008 Dec 20;121(24):2553-6.
Effects of carbon disulfide on the expression and activity of nitric oxide synthase in rat hippocampus.
Guo XM, Tang RH, Qin XY,Yang J, Chen GY.
(11)
Yang KS, Choi HR, Kim JJ, et al. Study of carbon disulfide intoxication.
Seoul: Korean Ministry of Labor Press, 1999
(12)
Lee E, Kim MH. Cerebral vasoreactivity by transcranial Doppler in carbon disulfide poisoning cases in Korea. J Korean
Med Sci 1998;13:645-651
(13)
J Korean Med Sci. 1998 Dec;13(6):645-51. Cerebral vasoreactivity by transcranial Doppler in carbon disulfide poisoning cases in Korea. Lee E, Kim MH.
(14)
Biochem. J. (1980) 188, 107-1 12 107
The Effects of Carbon Disulphide on Rat Liver Microsomal Mixed-Function
Oxidases, in vivo and in vitro
Maria J. OBREBSKA,* Peter KENTISH and Dennis V. PARKE
(15)
Journal of Ncurochcmistru. 1971, Vol. 18, pp. 177 to 182. Pergamon Press.
Oxidation and phosphorylation processes in brain mithochondria of rats exposed to carbon disulfide.
S. Tarkowski Hanna Sobczak
(16)
Lefaux, R. 1968. Carbon disulphide. Pp. 117-119 in Practical Toxicology of Plastics. Cleveland, OH: Chemical Rubber Company
(17)
Gorny, R., Carbon disulfide-induced vitamin 96 deficiency in rats fed diets with different vitamin B6 contents, Bromarol. Chem. Toksykol., 13(3), 299, 1980.
(18)
Washuettl, J., Winker, N., and Steiner, I.,The effects of carbon disulfide on the vitamin BI content in the serum of exposed workers, Munch. Med. Wochenschr., 121(24), 819, 1979.
(19)
165. Miyagawa, K., Carbon disulfide poisoning – Effects of L-methionine and L-methionine
combined with vitamin B12 on carbon disulfide poisoning, Shikoku Acra Med., 6(3), I, 1955.
(20)
Wronska-Nofer,. T., Nofer, J., and Stanislaw, T., Disorders in excretion of niacin metabolites in carbon disulfide-poisoned animals, Med. Pr., 16, 77, 1965.
(21)
Wronska-Nofer, T., The influence of low doses of nicotinic acid upon the development
of lipid disturbances in rats chronically exposed to carbon disulphide, hi. Arch. Arbeitsmed., 29(4), 285, 1972.
(22)
Knobloch, K., Effect of nicotinamide on excitability of the vestibular nerve and some motor nerves in chronic carbon disulfide poisoning in guinea pigs, Med. Pr., 12, 355, 1961.
(23)
Kuljak, S. and Stern, P., Protective effect of glutathione and xanthinol nicotinate against carbon disulfide poisoning in the mouse, Arh. Hig. Rada Toksikol., 22(2), 137, 1971
(24)
Paine, A. J., Williams, L., and Legg, R. F., Apparent maintenance of cytochrome P450 by
nicotinamides in primary cultures of rat hepatocytes, Life Sci., 24, 2185, 1979.
(25)
Silvestroni, A. and Rimiani, R., Microcirculation in chronic experimental intoxication with carbon disulfide. Effects of nicotinic acid, Folia Med., 53, 1, 1970.
(26)
McKenna, M. J. and DiStefano, V., Carbon disulfide. I. The metabolism of inhaled carbon disulfide in the rat, J. Pharmacol. Exp. Ther., 202(2), 245, 1977
Reaction of carbon disulfide with blood in vitro, Prac. Lek., 6, 11, 1954.
(27)
Brieger, H., Carbon disulfide in the living organism-retention, biotransformation and
pathophysiologic effects, in Toxicology of Carbon Disulfide, Brieger, H., Ed., Excerpta Medica Foundation,
Amsterdam, 27, 1967.
(28)
Gadaskina, I. D. and Andreeva, N. B., Biochemical shifts occurring in the organism
following carbon disulfide poisoning (free SH groups and blood ceruloplasmin; copper and zinc metabolism), Gig. Tr. Prof. Zabol.. 13, 28, 1969.
(29)
Kotas, P., Obrusnik, I., Lukas, E., and Krivanek, M., Determination of zinc and copper in the
periphera nerves of rats with carbon disulfide-induced neuropathy, J. Radioanal. Chem., 19(2), 263, 1974.

(30)
(Scheel, 1967). ISBN 92 4 154070 2, World Health Organization 1979
COHEN AE, SCHEEL LD, KOPP JF, STOCKELL FR, Jr, KEENAN RG, MOUNTAIN JT, PAULUS HJ.
Biochemical mechanisms in chronic carbon disulfide poisoning. Am Ind Hyg Assoc J. 1959
Aug;20(4):303–323.
(31)
Wilmarth KR, Froines JR (November 1992). “In vitro and in vivo inhibition of lysyl oxidase by aminopropionitriles”. J Toxicol Environ Health 37 (3): 411–23. PMID 1359158
(32)
Csiszar K. Lysyl oxidases: a novel multifunctional amine oxidase family. Prog Nucleic Acid Res Mol Biol.
2001; 70: 1–32.
(33)
Chem Res Toxicol. 1998 May;(5):544-9.
Carbon disulfide and N,N-diethyldithiocarbamate generate thiourea cross-links on erythrocyte spectrin in vivo.
Erve JC, Amarnath V, Graham DG, Sills RC, Morgan AL, Valentine WM.
(34)
Volume 272, Number 51, Issue of December 19, 1997 pp. 32370-32377
Irreversible Inhibition of Lysyl Oxidase by Homocysteine Thiolactone and Its Selenium and Oxygen Analogues Implications for Homocystinuria
(35)
Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1409-1414
Low Density Lipoproteins Downregulate Lysyl Oxidase in Vascular Endothelial Cells and the Arterial Wall Cristina Rodríguez ; Berta Raposo ; José Martínez-González ; Laura Casaní ; and Lina Badimon
(36)
Madlo, Z. and Soucek, B., Absorption, metabolism, and action of carbon disulfide in the organism. VII. Inhibition of serum cholinesterase by carbon disulfide, Prac. Lek., 6, 312, 1953
Soucek, B. and Madlo, Z., Absorption metabolism, and action of carbon disulfide in the organism. VIII.
(37)
Acta Neuropathol. 1984;63(3):255-63.Links
Ultrastructure of carbon disulphie neuropathy.
Jirmanová I, Lukás E.
(38)
Ca2+ Calmodulin levels was increased in cerebral cortex, hippocampus and spinal cord. Volume 179, Issues 2-3, 15 May 2009, Pages 110-117 Changes of lipid peroxidation in carbon disulfide-treated rat nerve tissues and serum Da-Qing Suna, b Ai-Wu Lic, , Ju Lid, Dian-Guo Lib, Yi-Xin Lib, Hao-Fengb and
Ming-Zhi Gongb, Chemico-Biological Interactions.
(39).
Davidson M, Feinleib M. Carbon disulfide poisoning: A review.
Am Heart J 1972;83:100-114
(40).
Lee KB, Byoun HJ, Choi TS, Kim SS, Cho WY, Kim HK.
Clinical manifestation of chronic carbon disulfide intoxication.
Korean J Int Med 1990;39:245-251
(41).
Choi JW, Jang SH. A review of the carbon disulfide poisoning
experience in Korea. Korean J Occup Med 1991;3:11-20
(42).
Yang KS, Choi HR, Kim JJ, et al. Study of carbon disulfide intoxication.
Seoul: Korean Ministry of Labor Press, 1999
(43)
Aaserud O, Gierstad L, Nakstad P, et al. Neurological examination,
computerized tomography, cerebral blood flow and neurophysiological
examination in workers with long-term exposure
to carbon disulfide. Toxicology 1988;49:277-28
(44)
Aaserud O, Hommeren OJ, Tvedt B, et al. Carbon disulfide exposure
and neurotoxic sequelae among viscose rayon workers.
Am J Ind Med 1990;18:23-37
(45)
Sugimura K, Kabashima K, Tatetsu S. Computerized tomography
in chronic carbon disulfide poisoning. No to Shinkei 1979;
31:1245-1253
(46)
Huang CC, Chu CC, Chen RS, et al. Chronic carbon disulfide
encephalopathy. Eur Neurol 1996;36:364-368
(47)
Peters HA, Levine RL, Matthews CGM et al. Extrapyramidal
and other neurologic manifestations associated with carbon
disulfide fumigant exposure. Arch Neurol 1988;45:537-540
(48)
Ca2+ Calmodulin levels was increased in cerebral cortex, hippocampus and spinal cord. Volume 179, Issues 2-3, 15 May 2009, Pages 110-117 Changes of lipid peroxidation in carbon disulfide-treated rat nerve tissues and serum Da-Qing Suna, b Ai-Wu Lic, , Ju Lid, Dian-Guo Lib, Yi-Xin Lib, Hao-Fengb and
Ming-Zhi Gongb, Chemico-Biological Interactions.
(49)
Alterations of microtubule and microfilament expression in spinal cord of carbon disulfide intoxicated rats. Chinese journal of industrial hygiene and occupational diseases. Original title: Zhonghua lao dong wei sheng zhi ye bing za zhi Zhonghua laodong weisheng zhiyebing zazhi. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2007 Mar;25(3):148-51 Pan GB, Song FY, Zhao XL, Yu LH, Zhou GZ, Xie KQ.
(50)
Toxicological Sciences 94(2), 240–255. Richard M. LoPachin. David S. Barber
doi:10.1093/toxsci/k?066 Advance Access publication July 31, 2006
(51)
Chin Med J (Engl). 2008 Dec 20;121(24):2553-6.
Effects of carbon disulfide on the expression and activity of nitric oxide synthase in rat hippocampus.
Guo XM, Tang RH, Qin XY, Yang J, Chen GY.
(52)
Schizophr Res. 2000 Feb 14;41(3):405-15
Apoptosis and schizophrenia: is the tumour suppressor gene, p53, a candidate susceptibility gene?
Catts VS, Catts SV.
Schizophrenia Research Unit, South Western Sydney Area Health Service, Liverpool Hospital, Liverpool, NSW, Australia.
(53)
Int J Hyg Environ Health. 2007 Jan;210(1):69-77. Epub 2006 Sep 1.
Use of genotypic selection to detect P53 codon 273 CGT>CTT transversion: application to an
occupationally exposed population.
Carton T, Tan XD, Hartemann P, Joyeux M.
(54)
Forensic Sci Int. 2005 Oct 29;153(2-3):147-55. Epub 2004 Nov 25.
A study of volatile organic compounds evolved from the decaying human body.
Statheropoulos M, Spiliopoulou C, Agapiou A.
School of Chemical Engineering, National Technical University of Athens (NTUA)
(55)
(Purdon et al., 2002; Purdon and Rapoport, 2007).
(56)
Bartonicek V. The distribution of carbon disulfide in whole blood, the brain and the suprarenal gland over a given period in parenteral administration in white mice. Prac Lek 1957; 9:28-30.
(57)
The modification of genetic expression after CS2 exposure have been shown in humans with p53. Chem Biol Interact. 2009 May 15;179(2-3):110-7. Epub 2008 Nov 25.
Changes of lipid peroxidation in carbon disulfide-treated rat nerve tissues and serum.
Sun DQ, Li AW, Li J, Li DG, Li YX, Hao-Feng, Gong MZ.
Shandong University, Jinan, Shandong, China.
(58)
Schizophrenia Research Volume 62, Issue 3, 1 August 2003.
The niacin skin flush test in schizophrenia- a combined a quantitative dose–response study
(59)
MCCANN Patrick, NAMJOU Khosrow, ROLLER Chad, MCMILLEN Gina, KAMAT Pratyuma. IV-VI Semiconductor Lasers for Gas Phase Biomarker Detection
Proceedings of SPIE, the International Society for Optical Engineering ISSN 0277-786X
(60)
Mater. Res. Soc. Symp. Proc. Vol. 891 © 2006 Materials Research Society
Patrick J. McCann1 and Yurii Selivanov2 1 School of Electrical and Computer Engineering, University of Oklahoma, Norman, OK 73019 2 P. N. Lebedev Physical Institute, Russian Academy of Sciences, Leninskii Pr. 53, 119991, Moscow, Russia
(61)
Br J Anaesth. 2008 Nov;101(5):673-9. Epub 2008 Sep 12.
Carbon dioxide negatively modulates N-methyl-D-aspartate receptors. Brosnan RJ, Pham TL.
(62)
Am J Physiol Regul Integr Comp Physiol. 2009 May;296(5):R1473-95.
Integration of cerebrovascular CO2 reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation.
(63)
Adv Exp Med Biol. 2006;588:65-73
Control of cerebral blood flow during sleep and the effects of hypoxia.
Corfield DR, Meadows GE
(64)
Activity of glutamate decarboxylase in the brain of rats exposed to carbon disulfide
International Archives of Occupational and Environmental Health Volume 33, Number 1 / March, 1974
Stanislstrokaw Tarkowski
(65)
Tarkowski S, Cremer JE. 1972. Metabolism of glucose and free amino acids in brain, studied with C-labelled glucose and butyrate in rats intoxicated with carbon disulfide. J Neurochem
19:2631-2640.
(66)
The Journal of Neuroscience, 1999, 19:RC16:1-9
RAPID COMMUNICATION Novel Injury Mechanism in Anoxia and Trauma of Spinal Cord White Matter: Glutamate Release via Reverse Na+-dependent Glutamate Transport Shuxin Li1, Geoff A. R. Mealing2, Paul Morley2, and Peter K. Stys1

The etiology of Schizophrenia

Posted by gdnf on May 19, 2010
Posted in: Schizophrenia. Tagged: , , , , , , , .

PCP, LSD, Ketamine and ….  have been used as models for the state of schizophrenia, the problem with that models is very simplified, that the person with schizophrenia usually don’t have them in their blood.

However there is a substance that can cause some of the phenomenological effects of Schizophrenia – personality changes, paranoia, mania and alternations in the transient receptor potential – TRPV secondary to environmental exposure. This effect has been known since the late 1800.  To make a complex story very short, we present the CAC-Hålet theory about-

The etiology of Schizophrenia in 3 very easy steps

1/ There is a substance known to cause some of the symptoms in Schizophrenia

2/The group of persons with Schizophrenia does have it, other usually don’t

3/ There might be a connection with, the reactive phase of Schizophrenia etiology and the substance.

The Substance is: Carbon Disulfide or CS2

Since  Carbon disulfide is a known neurotoxin one might think that we just have to remove the external source of CS2 exposure in order to eliminate the problem. But the source is not external it is internal. And this endogenous production of Carbon Disulfide is continuously taken it’s toll on the system. I conclude that Carbon Disulfide could be a reactive factor that trigger but don’t predispose for the etiology of Schizophrenia.

Ref:

Clin Pathol 1993;46:861-864
Increased pentane and carbon disulfide in the
breath of patients with schizophrenia

A part of the CAC-hålet theory is now moving to GDNF – BDNF from The Etiology of Schizophrenia @ Co2reactivity.