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At least 19 recordsLinked to original sources
PubMed1977

Carbon disulfide. I. The metabolism of inhaled carbon disulfide in the rat.

The pharmacokinetics of inhaled carbon disulfide (CS2) vapor was evaluated in rats. Estimates of free CS2 and its nonvolatile, acid-labile metabolites (AL CS2) were made in a variety of rat tissues after an 8-hour inhalation exposure to CS2 vapor (2 mg/l of air). At the end of the exposure, all tissues examined contained appreciable amounts of the native solvent and AL CS2. Elimination of CS2 from the rat during the postexposure period was rapid and occurred primarily via the lungs. Excretion of AL CL2 occurred primarily via the kidneys and was prolonged with respect to that of free CS2. Accumulation of these metabolites upon repeated exposures and their presence in all tissues examined suggest that they may play a role in the toxicity of CS2.

Animals↗
PubMed1977

[Effect of carbon disulfide on peripheral blood leukocytes. I. Effect of carbon disulfide on in vitro chromosome structure and division capability of leukocytes in man].

The peripheral blood leukocytes in normal subjects were cultured according to Moorhead with addition of CS2 (0,75 microliter/ml of culture). It has been found that CS2 decreases the mitotic index, and in some cultures inhibits totally the cell division. Moreover, it causes structural disturbances of chromosomes being of pre- and postreplicative character as well as their viscous degeneration, lesser spiralization and sometimes pulverization. The presence of greater amount of erythrocytes of the donor's blood in the culture markedly diminished the intensity of these changes.

Adolescent↗
PubMed1977

Serum mineral changes under the effect of carbon disulfide intoxication.

Under the effect of carbon-disulfide intoxication on serum levels of zinc, iron, calcium, magnesium, potassium, and sodium of albino rats, five groups of rats were injected with daily doses of carbon disulfide over a period of 50 days. The extent of regression of the developed biochemical derangement was also studied. A significant decrease was observed in the levels of serum zinc, iron, calcium, and magnesium, while a slight elevation in the level of serum potassium. No definite correlation could be found between the level of serum sodium in control and carbon-disulfide intoxicated rats. By stoppage of dosage at 20 days, most of these derangements started to be normal.

Animals↗
PubMed1976

Systolic time intervals as a measure of left ventricular function in viscose rayon workers exposed to carbon disulfide.

In a group of viscose rayon workers exposed to carbon disulfide the systolic time intervals were calculated. They were determined from the simultaneous recording of an ECG, a phonocardiogram, and arterial pulse tracings. Results indicate a shortened left ventricular ejection time (lvet) and a prolonged isovolumetric contraction time (ICT), together with an increase in the ratio of ICT to LVET. These alterations, which occurred in the absence of any clinical signs or symptoms of heart disease, are interpreted as a consequence of an impaired left ventricular contractility, comparable to mild coronary dysfunction. Literature data support the hypothesis that the biochemical mechanisms involved in the effect of carbon disulfide on myocardial cells are (a) an interference with energy metabolism from the inadequate availability of thiamine and nicotinamide or a direct inhibition of cytochrome or (b) an interference with catecholamine metabolism and defective hormonal control of the energy utilization process. Impaired left ventricular function in rayon viscose workers exposed to carbon disulfide represents an early and highly sensitive sign of carbon disulfide intoxication, and the use of systolic time intervals as a noninvasive measure of myocardial performance may be a useful method for monitoring carbon disulfide exposed people.

Air Pollutants↗
PubMed1977

Disulfiram toxicity and carbon disulfide poisoning.

The author compared the neurotoxic effects of disulfiram with those of carbon disulfide, a disulfiram metabolite. The results suggest that carbon disulfide is responsible for the behavioral and neurological side effects of disulfiram. If this is so, then some other toxic effects of carbon disulfide, including parkinsonism, choreoathetosis, and thalamic syndrome may follow the ingestion of more than 5 g of disulfiram by adults, and individuals receiving as little as 125 mg of disulfiram per day may be at a three- to four-fold greater risk for arteriosclerotic cardiovascular disease than a comparable population not receiving the drug.

Animals↗
PubMed1976

Effects of carbon disulfide and FLA-63 on operant behavior in pigeons.

Carbon disulfide (CS2) and FLA-63 [bis(4-methyl-1-homopiperazinylthiocarbonyl)disulfide] were studied in pigeons working on a differential-reinforcement-of low-rates or a multiple fixed-interval fixed-ratio schedule of food reinforcement. Response rate on both schedules decreased after 8-hour exposures to CS2 (2 mg/1) of administration of FLA-63 (40 and 80 mg/kg). The effects of two successive 8-hour exposures to CS2 were cumulative and ten successive 4-hour exposures produced changes in differential-reinforcement-of-low-rates performance resembling those following acute exposure. Fixed-interval performance was disrupted by exposures to CS2 and doses of FLA-63 that left fixed-ratio performance intact.

Animals↗
PubMed1978

Analysis of charcoal tube samples for carbon disulfide using a photoionization detector.

A gas chromatograph equipped with a photoionization detector was used to detect carbon disulfide eluted from charcoal tubes with acetonitrile. Overall sampling and desorption efficiency for carbon disulfide was found to approach 100 percent when compared to a liquid impingement, colorimetric method. A relative standard deviation of 4.78 percent (sampling plus analysis) was observed when the method was applied to a synthetic test atmosphere of 10 parts per million carbon disulfide. Sensitivity of the proposed method will enable concentrations of 0.10 ppm CS2 to be determined in a 10 liter air sample. The photoionization detector offers several advantages over other detectors, namely ease of operation and greater sensitivity.

Acetonitriles↗
PubMed1979

Behavioral toxicology of carbon disulfide and toluene.

Organic solvents are pervasive in the communal and industrial environments. Although many are potent central nervous system agents, clearly delineated behavioral effects have played only a minor role in the formation of exposure standards. A comprehensive behavioral pharmacology and toxicology of these compounds is one aim of US/USSR collaboration. The current report describes some actions of carbon disulfide and toulene. Earlier data about the actions of carbon disulfide on pigeon operant performance indicated disruption of schedule-controlled key-pecking. Primate data are now described from a situation designed to determine aversive thresholds to electrical stimulation. Effective concentrations of carbon disulfide produced both a rise in the amount of electric shock tolerated and a diminution of the response force exerted by the monkeys. In experiments with toluene, pigeons were shown to elevate key-pecking rate in an operant situation at certain concentrations. Toluene also was studied for its capacity to maintain self-administration in the same way as drugs of abuse. Monkeys worked to gain access to toulene vapor just as they work for opiates or amphetamines. The current experiments demonstrate how comprehensive the range of behavioral toxicology needs to be to deal with environmental health issues.

Animals↗
PubMed1977

Histochemical and electron microscopic observations on the myoneural junctions of rats with carbon disulfide induced polyneuropathy.

Myoneural junctions in the tibialis anterior muscle of rats with clinical signs of polyneuropathy induced with carbon disulfide were studied by light and electron microscopy. Histochemically demonstrable acetylcholinesterase (AChE; E.C. 3.1.1.7) activity was distributed similarly in the myoneural junctions of both the exposed and the control rats. In both groups intense enzyme activity was localized at the level of the post-synaptic membrane of the myoneural junction. The postsynaptic infoldings of the myoneural junctions of the exposed rats appeared normal. No enzyme activity was seen outside the zone of the myoneural junctions. The ultrastructure of the sub-sarcolemmal space, as well as the postsynaptic membranes of the myoneural junctions of the exposed animals, was normal. In the terminal axons signs of various degrees of degeneration were present, e.g., disappearance of the preterminal axoplasmic neurotubules, partial disappearance of synaptic vesicles, appearance of dense bodies, and even total disappearance or destruction of the terminal axons. Synaptic clefts were often widened with Schwann cell interposition. It thus seems that systemic carbon disulfide poisoning primarily alters the presynaptic structures of the myoneural junctions, while the postsynaptic side remains relatively intact, especially since the histochemical distribution of AChE in myoneural junctions was normal.

Acetylcholinesterase↗
PubMedDate not supplied

[Lysosomal and cytoplasmic enzymatic activity under the experimental action of carbon disulfide].

Activity of lysosomal enzymes and content of carbohydrate containing biopolymers (glycosaminoglycans, glycoproteins) were altered in various tissues (liver, kidney, brain, aorta) of experimental animals intoxicated with carbon disulfide. Possible role of the impairments observed, related to neurotropic and hepatotoxic effects, is discussed. Subsequent development of atherogenic and embryotoxic effects of carbon disulfide--one of contaminators of surroundings--are considered.

Animals↗
PubMed1978

Studies on angiopathy due to carbon disulfide. Retinopathy and index of exposure dosages.

The occurrences of retinopathy (microaneurysms/small dot hemorrhages) and the coded resting and postexercise ECG findings suggestive of coronary heart disease (CHD) were studied among 420 Japanese male workers exposed to carbon disulfide and 390 men not exposed to such a solvent. Retinopathy was detected in 24.4% of the exposed group and in 3.8% of the nonexposed group by color fundus photography. Among workers of the former group there was a significant correlation between retinopathy prevalences and the index of exposure dosages (r = 0.925, P less than 0.01). However, correlation between the prevalence of retinopathy and duration of exposure was not so high (r = 0.647, 0.10 less than P less than 0.25). The occurrences of coded resting and postexercise "coronary" ECG findings were not related to the index of exposure dosages. Some risk factors for CHD such as total serum cholesterol, triglycerides, beta-lipoproteins, blood pressure, obesity, and skinfold thickness were simultaneously studied. But these variables did not prove to be important in the development of angiopathy due to carbon disulfide, especially the so-called retinopathia sulfocarbonica.

Adult↗
PubMed1977

Serum and urine amino acid pattern under the effect of carbon disulfide intoxication.

The effect of carbon disulphide intoxication on amino acid pattern was studied. Five groups of rats were treated with carbon disulphide through intramuscular injection of 0.05 ml CS2 in 0.2 mg olive oil/rat/day. A number of rats were sacrificed after receiving 10, 20, 30, 40, and 50 injections. As a result of intoxication, a state of hypoaminoacidemia and hyperaminoacidurea affected all the amino acids investigated, but to variable extent. Of value to add that stoppage of carbon disulphide leads to improvement of the amino-acid pattern in group six, compared to the other groups.

Amino Acids↗
PubMed1979

Ten-year coronary mortality of workers exposed to carbon disulfide.

Two cohorts, one comprising 343 viscose rayon workers exposed for at least five years to carbon disulfide (CS2) and the other made up of 343 nonexposed men, were followed from 1967 to 1977 with respect to coronary heart disease (CHD) mortality. In the examination in 1967 known risk factors of CHD were controlled; only blood pressure was slightly higher in the exposed group. The difference was considered a result of exposure. Five exposed and eight nonexposed men had experienced a previous clinical myocardial infarction. The total mortality was 48 (14%) in the exposed group and 31 (9%) in the compeer group (p congruent to 0.05); 29 exposed and 11 nonexposed men had died from CHD (p less than 0.01), and 5 exposed and 1 nonexposed from other cardiovascular causes (p = 0.1). All coronary deaths occurred in the age interval 40 to 69 years. The estimated risk of death from CHD for this 30-year age span, assuming no competing risks of death, was 31.9% for the exposed cohort against 13.3% for the compeers. A multivariate analysis yielded age, raised blood pressure, and exposure to CS2 as prominent risk factors. The contributory risk caused by past occupational CS2 exposure seemed to increase the already notoriously high risk of CHD mortality among Finnish men.

Adult↗
PubMed1978

Inhibition of 1,2-dimethylhydrazine-induced neoplasia of the large intestine in female CF1 mice by carbon disulfide.

Disulfiram, diethyldithiocarbamate, and bis-(ethylxanthogen) inhibit symmetrical 1,2-dimethylhydrazine dihydrochloride (DMH)-induced neoplasia of the large bowel in female CF1 mice. These three compounds contain a carbon disulfide (CS2) moiety in their structure. In the present study, CS2 itself was found to inhibit DMH-induced neoplasia of the large bowel in female CF1 mice. Thus a relatively simple compound is now available for investigation of the mechanism of inhibition of DMH-induced neoplasia by a group of sulfur-containing inhibitors having common structural features.

Adenocarcinoma↗
PubMed1977

Histological and histochemical studies on the rat brain under conditions of carbon disulfide intoxication.

The brains of 35 male Wistar rats weighing 250 g were histologically and histochemically examined after a chronic intoxication due to five-month exposure to carbon disulfide. Morphologically, myelin sheath disruptions within the longitudinal tract systems of the spinal cord, destructions of individual ganglion cells in all brain regions and elective parenchyma necroses in the frontal and parietal cerebral cortices were found. The histochemical assays for enzyme activities of monoamine oxidase, ATPase, glucose 6-phosphatase, acetylcholine esterase and succinic dehydrogenase in the entire central nervous system revealed values identical to those obtained for control animals. Only succinic dehydrogenase and acetylcholine esterase revealed focal reduction in activities within the elective parenchyma necroses. After twenty-week duration of experiments a moderate decrease in activities of arylsulfatases and glutamic dehydrogenase in the entire central nervous system was found. Eventual causes responsible for these changes are discussed.

Animals↗