Biochemical Mechanisms in Chronic Carbon Disulfide Poisoning

Cohen, Moshe; Scheel, Lester D.; Kopp, John F.; Stockell, R B S Fulton; Keenan, Robert G.; Mountain, John T.; Paulus, Harold J.

doi:10.1080/00028895909343722

Cited by 66 publications

(9 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In rabbits after 16 weeks of exposure to 15 to 2 25 mg/l. CS2, Cohen, Scheel, Kopp, Stockell, Keenan, Mountain & Paulus (1959) found interstitial nephritis, mild fatty degeneration on the liver, meningeal swelling and infiltration, cerebral and cerebellar lesions involving individual nerve cells and also enlarged adrenals. Glomerulosclerosis was observed in rats after exposure for one year to 2 0 mg/l.…”

Section: Discussionmentioning

confidence: 99%

The effects of carbon disulphide exposure on brain catecholamines in rats

Magós

1970

British J Pharmacology

View full text Add to dashboard Cite

Summary1. Rats exposed to 2-0 mg/i. carbon disulphide (CS2) in the inspired air for 2 days, 4 h a day, showed a 13 % decrease in their brain noradrenaline concentration and a 16 % increase in their brain dopamine concentration. 2. After exposure for 5 or 10 days there was a further decrease in the concentration of noradrenaline in the brain, but brain dopamine returned to the control level. 3. In animals treated intraperitoneally with 2 0 mg/kg reserpine and exposed 2 and 3 days later to 20 mg/I. CS2 for 4 h per day, the brain dopamine concentration showed a 770/o increase compared with the unexposed reserpinized animals, but the noradrenaline concentration remained unchanged. 4. The dopamine concentrations in the adrenals after 10 days' exposure to 2-0 mg/I. CS2 were 67% to 100% higher than in the control animals. In reserpinized rats, 2 days' exposure to CS2 nearly trebled the dopamine content of adrenals. 5. Exposure to CS2 had no effect on the tyrosine concentration in the brain, and there was no change in the brain monoamine oxidase (MAO) activity.Tyrosine in the brain showed a 30 to 96% increase in concentration and MAO activity, using kynuramine as substrate, showed an approximately 5% increase 0-5 to 2 h after the subcutaneous administration of 500 mg/kg sodium diethyldithiocarbamate. 6. CS2 at 10-2M or lower concentrations had no inhibitory effect on the brain MAO activity in vitro. Diethyldithiocarbamate inhibited MAO at 10-2M, but not at 10-3M or lower concentrations. IntroductionCarbon disulphide (CS2) exposure can lead to widely different pathological conditions such as mental aberrations, hypertension, extrapyramidal symptoms and atherosclerosis (Quarelli, 1937; Gordy & Trumper, 1938;McDonald, 1938;Lewey, 1941a;Paluch, 1948;Vigliani & Pernis, 1955 ;Weist, 1957;Magos, 1961;Szobor, 1962). Recently, Tiller, Schilling & Morris (1968) have given statistical evidence on the increased frequency of death from coronary heart disease among viscose workers exposed to CS, and other toxic agents in this country.As catecholamines or drugs acting on catecholamine metabolism can influence brain functions and behaviour

show abstract

Section: Discussionmentioning

confidence: 99%

The effects of carbon disulphide exposure on brain catecholamines in rats

Magós

1970

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Rabbits exposed daily-five days a week-for many weeks until a partial loss of control over voluntary movements of the hind legs appeared did not show any pathological changes in the liver (Cohen et al, 1959). An oral dose of 1 mg/kg CS2 given to rats produced only an increase in fat in the periportal zone.…”

mentioning

confidence: 95%

Effect of phenobarbitone and starvation on hepatotoxicity in rats exposed to carbon disulphide vapour

Magós

Butler

1972

Occupational and Environmental Medicine

View full text Add to dashboard Cite

Magos, L., and Butler, W. H. (1972). Brit. J. industr. Med., 29,[95][96][97][98]. Effect of phenobarbitone and starvation on hepatotoxicity in rats exposed to carbon disulphide vapour. Male albino rats given 80 and 50 mg/kg phenobarbitone sodium by intraperitoneal injection 24 and 18 hours before 4-hour exposure to 2-0 mg/l carbon disulphide (CS2) developed hydropic degeneration in the centrilobular zone of the liver. Less marked in some fed animals, this change became general and more severe in rats starved for 24 hours before exposure. On incomplete diets with excess of sucrose or animal fat, the frequency and severity of lesions were somewhat between those observed in starved and fed rats. This observation calls attention to the possibility that in certain circumstances of industrial exposure, such as nutritional deficiency plus drug treatment, CS2 might cause disturbances in liver function.Carbon disulphide (CS2) is not recognized as an hepatotoxic agent. Rabbits exposed daily-five days a week-for many weeks until a partial loss of control over voluntary movements of the hind legs appeared did not show any pathological changes in the liver (Cohen et al., 1959). An oral dose of 1 mg/kg CS2 given to rats produced only an increase in fat in the periportal zone. When the same dose of CS2 was given to rats pretreated with phenobarbitone, extensive centrilobular zone necrosis appeared (Bond, Butler, De Matteis, and Barnes, 1969). However, these animals were subjected not only to phenobarbitone pretreatment but also to starvation as food was withdrawn 24 hours before exposure to avoid the gastric effect of CS2 on food and food consumption.The purpose of the present work was to investigate whether liver damage can be induced in phenobarbitone-pretreated rats by inhalation exposure to CS2. Inhalation exposure also made it possible to study the effect of starvation on liver damage in phenobarbitone-pretreated rats exposed to CS2. Starvation significantly decreased the urinary excretion of both CS2 and its bivalent sulphur metabolites in exposed rats (Magos, 1972) and 95 4 starvation may have contributed to the development of liver necrosis in phenobarbitone-pretreated animals (Bond et al., 1969). As CS2 can be converted in the body to dithiocarbamate type compounds (Soucek, 1957) and dithiocarbamate is partly metabolized to CS2 (Stromme, 1965) the effect of diethyldithiocarbamate on the liver was also investigated in some of the experiments. MethodsMale albino rats of Porton-Wistar strain (200-220 g) bred in this colony were used. Phenobarbitone sodium (BDM) was given intraperitoneally in a dose of 80 mg/kg 24 hours and 50 mg/kg 18 hours before 4-hour exposure to 2 mg/kg CS2 or 18 and 23 hours before the administration of 500 mg/kg sodium diethyldithiocarbamate (DDC; Hopkin and Williams). Animals were exposed to CS2 in a vertical type inhalation chamber

show abstract

“…According to many studies (25,35,38,43,57,61,67,74,81) serum cholesterol, and particularly its beta fraction, is raised among those suffering from exposure. Some results also seem to indicate an elevated trend for beta lipoproteins (12,45,54,56,62,80,81).…”

Section: Biological Mechanismsmentioning

confidence: 95%