Disease relevance of CARBON DISULFIDE

• The axonal swellings observed in DMHD toxicity are in the proximal axon, as seen in intoxication with beta, beta'-iminodipropionitrile, rather than in the distal axon, where neurofilamentous swellings are observed in n-hexane, carbon disulfide, and acrylamide neurotoxicity [1].
• Heavy metal derivatives of the galactose binding protein of Salmonella typhimurium were obtained by the treatment of crystals with carbon disulfide under anaerobic conditions, followed by exposure to mercury-containing reagents [2].
• Extrapyramidal and other neurologic manifestations associated with carbon disulfide fumigant exposure [3].
• Reactivity of carbon monoxide dehydrogenase from Rhodospirillum rubrum with carbon dioxide, carbonyl sulfide, and carbon disulfide [4].
• Hearing loss in workers exposed to carbon disulfide and noise [5].

Psychiatry related information on CARBON DISULFIDE

• Reaction of glycosyl trimethylphosphinimides with carbon disulfide under mild conditions (room temperature, short reaction time) leads to symmetrical glycosyl carbodiimides [6].
• Psychological tests specific to individual carbon disulfide exposure [7].
• A complete set of recommendations was forwarded to the employer, emphasizing further control of exposure to carbon disulphide, personal protection requirements and a cardiovascular risk reduction programme [8].
• Dietary habits, a non-negligible source of 2-thiothiazolidine-4-carboxylic acid and possible overestimation of carbon disulfide exposure [9].

High impact information on CARBON DISULFIDE

• These three compounds contain a carbon disulfide (CS2) moiety in their structure [10].
• Inhibition of 1,2-dimethylhydrazine-induced neoplasia of the large intestine in female CF1 mice by carbon disulfide [10].
• Glucose tolerance and occupational exposure to carbon disulphide [11].
• (1988) has shown that the observer rat forms an association between two olfactory stimuli on the breath of the demonstrator rat that has eaten the food, the food odor and carbon disulphide, which is normally present in the rat breath [12].
• Two commonly employed solvents, n-hexane and carbon disulfide (CS2), although chemically dissimilar, result in identical neurofilament-filled swellings of the distal axon in both the central and peripheral nervous systems [13].

Chemical compound and disease context of CARBON DISULFIDE

• Disulfiram toxicity and carbon disulfide poisoning [14].
• None of the monkeys developed retinal microaneurysms or hemorrhages, major accepted signs of visual toxicity in CS2 exposed humans; thus, permanent visual loss may result from carbon disulfide exposure even in the absence of retinal vascular effects [15].
• Exposure to a wide variety of neurotoxic compounds, namely, carbon monoxide, carbon disulfide, manganese and MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), are associated with parkinsonism that has a varying neuropathology, which will be discussed [16].
• Protective action of diethyldithiocarbamate and carbon disulfide against acute toxicities induced by 1,1-dichloroethylene in mice [17].
• The toxicity of 1,2-dichloroethane, carbon disulfide, and nitrobenzene on cultured human (KB) and African green monkey kidney (AGMK) cells was studied [18].

Biological context of CARBON DISULFIDE

• Five monkeys were exposed to 256 ppm carbon disulfide (CS2) by inhalation for 6 hr a day, 5 days a week [19].
• Quantitated effects of carbon disulfide exposure, elevated blood pressure and aging on coronary mortality [20].
• Structures of the molecular radical anions were probed to determine whether they undergo cyclization to a cyclohexane-1,4-diyl anion structure by examining chemical reactivity with neutral reagents including carbon dioxide, carbon disulfide, and nitric oxide [21].
• The pharmacokinetics of inhaled carbon disulfide (CS2) vapor was evaluated in rats [22].
• Heart rate variability in workers exposed to carbon disulfide [23].

Anatomical context of CARBON DISULFIDE

• No evidence was found for arteriosclerotic or aneurysmal changes, suggesting that visual system injury in primates induced by carbon disulfide exposure is not dependent on the occurrence of structural changes in retinal blood vessels [19].
• In tests on rabbits, simultaneous neurophysiological and neurochemical analyses were performed on the changes in the functional state of the central nervous system under chronic exposure to carbon bisulfide at various concentrations [24].
• Carbon disulfide hepatoxicity and inhibition of liver microsome calcium pump [25].
• Carbon disulfide-modified LDL markedly stimulates cholesteryl ester formation in macrophages, albeit to a lesser extent than acetylated LDL [26].
• Oxidative metabolism of carbon disulfide by isolated rat hepatocytes and microsomes [27].

Associations of CARBON DISULFIDE with other chemical compounds

• However, alongside this effect, carbon disulphide produces a gradual increase in the adrenal content of dopamine-beta-hydroxylase indicated by the increase of in vitro estimated enzyme activity and by the increased in vivo conversion of dopamine to noradrenaline observed 24 hr after the ninth exposure [28].
• 2-Thiothiazolidine-4-carboxylic acid (TTCA) is the accepted urinary indicator of occupational exposure to carbon disulfide [29].
• As judged by the observation of normal serum GPT, drug metabolism inhibitors such as SKF-525A, piperonyl butoxide, and carbon disulfide prevented the hepatotoxic effect of BHT given in combination with BSO [30].
• The objectives of this study was to establish the kinetics of urinary 2-thiothiazolidine-4-carboxylic acid (U-TTCA) for workers exposed to carbon disulphide (CS2) and to investigate the effects of volume and creatinine adjustment methods for urine measurement [31].
• Activation of the reaction with an equimolar mixture of imidazole and carbon disulfide at the triester formation step permits selective phosphorylation at room temperature [32].

Gene context of CARBON DISULFIDE

• In vivo inhibition of dopamine-beta-hydroxylase in rat adrenals during exposure to carbon disulphide [33].
• The first set of lines are assigned to C=S stretching, O-S stretching, and S-C stretching modes of carbon disulfide S-oxide, OSCS; and the second set of lines are assigned to C=O stretching and OCS bending modes of dithiiranone, O(CS(2)), respectively, based on results of (34)S- and (18)O-isotopic experiments and quantum-chemical calculations [34].
• Loss of 3-methylcholanthrene-inducible form of cytochrome P-450 in liver microsomes following administration of carbon disulfide in C57BL/6 Cr mice [35].
• Inhibition of ammonia monooxygenase in Nitrosomonas europaea by carbon disulfide [36].
• The processing of carbon disulfide-modified LDL through the apo B/E receptor pathway of cultured human fibroblasts is decreased as compared to that of native LDL, depending on the level of modification [26].

Analytical, diagnostic and therapeutic context of CARBON DISULFIDE

• Carbon disulfide effects on the visual system. I. Visual thresholds and ophthalmoscopy [15].
• The components of electrocardiograms (ECG) of 253 workers exposed to carbon disulfide (CDS) and those of 99 controls were quantitatively measured and evaluated [37].
• The effect of carbon disulphide and atherogenic diet on the development of atherosclerotic changes in rabbits [38].
• The effects of carbon disulfide (CS2) on the liver microsomal drug-metabolizing enzyme system and other enzyme activities were studied 1 hr after the oral administration of 3-300 mg/kg of CS2 in mice [39].
• The structure and bonding of the chlorine atom/carbon disulfide (CS(2)/Cl) complex involved in selective photochlorination reactions with alkanes was directly probed using transient resonance Raman spectroscopy [40].

References