The effects of carbon disulphide exposure on brain catecholamines in rats

Abstract

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

Vascular effects of carbon disulfide: a review.

“…Elevation of blood pressure (28,33,64,72): Although the exact nature of this finding 'is still far from being clarified, one of the many hypotheses advanced can be supported by the studies of Magos et al (40,41) that are summarized in no. 5.…”

“…The interference of carbon disulfide with catecholamine metabolism seems to have been well-established in studies on rats (40,41), although these results are not, as such, applicable to human responses in the viscose rayon industry.…”

“…A toxic effect upon the myocardium: Exposure to carbon disulfide results in small areas of myocardial fibrosis and necrosis in rats (9). Carbon disulfide may also affect the heart and the vessels through interference with the catecholamine metabolism (40,41). Toxicological studies have indicated that carbon disulfide probably inhibits dopamine-fJ -hydroxylase, the enzyme which converts dopamine to noradrenaline.…”

Parkinson`s disease and occupational exposure to organic solvents, agricultural chemicals and mercury--a case-referent study.

“…Furthermore, it has been observed in rats that this solvent can influence the activity, in general, of neural transmittors in the brain (10). The mental disturbances caused by exposure to organic solvents, including carbon disulfide (2), and the possibility of an influence on the dopamine metabolism in the substantia nigra seemed to justify the hypothesis that occupational exposure to other organic solvents might contribute to an increased risk of contracting Parkinson's disease.…”

Carbon disulphide exposure affects the response of rat adrenal medulla to hypothermia and hypoglycaemia

“…Exposure to carbon disulphide (CS2), which inhibits DPH, (Caroldi et al, 1984b) shares some of the short and long term stress-induced effects on adrenal catecholamines. CS2 depresses the concentration of hydroxylated amines more in the brain than in the adrenals (Magos & Jarvis, 1970) and after repeated exposure induces adrenal DPiH (Caroldi et al, 1984a).…”