Half life of CS2 in rats in relation to its effect on brain catecholamines

Assessment of coronary heart disease risk among viscose rayon workers exposed to carbon disulfide at concentrations of about 30 mg/m3.

“…In previous studies it was possible to demonstrate increased blood lipid levels (ll, 25,27,33,36). Significant increases in the cholesterol triglycerides and low-density lipoprotein cholesterol levels were recently found in a Belgian population of viscose rayon workers exposed to a CS., concentration of about 100 mg/m 3 ; no~ther factor could explain these differences (35).…”

“…These alterations, comparable to mild CHD dysfunction, were interpreted as a consequence of an impaired left ventricular contractility. At least two mechanisms might be involved in the toxic action of CS 2 on the myocardial tissue: {i) interference with the energy metabolism by the inadequate availability of thiamine (1) and nicotine amide {6, 10), or a direct inhibition of cytochrome (6,10) and (ii) interference with the cathecolamine metabolism and defective hormonal control of the energy utilization process (6,24,25).…”

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

“…The interference of CS 2 with catecholamine metabolism (a temporary increase of dopamine level in the brain of CS 2 poisoned rats) has been observed as a consequence of an inhibition of dopamine fJ hydroxylase (26). In addition myocardial lesions caused by subtoxic doses of noradrenaline in CS 2 exposed rats show that CS 2 affects the catecholamine metabolism in the myocardial tissue (9,26).…”

“…In addition myocardial lesions caused by subtoxic doses of noradrenaline in CS 2 exposed rats show that CS 2 affects the catecholamine metabolism in the myocardial tissue (9,26). The increased amount of coronary heart disease among workers exposed to CS 2 might be explained by a der.angement in catecholamine metabolism (25,26). In this way, through an interference with the hormonal control via the adenyl cyclase (11), CS 2 may justify the abnormal myocardial contractility in CS 2 exposed people.…”

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

“…Such an exposure results in approximately 17 jig ml-free plus reversibly bound CS2 in blood (Lam & DiStefano, 1982). The elimination half-life of free and reversibly bound CS2 from the whole body is 35 min (Magos et al, 1974) and in agreement with this fast elimination the conversion ©The Macmillan Press Ltd 1985 of dopamine to NA returns to normal 2 -4 h after a single exposure to CS2 (Caroldi et al, 1984b). However, as at the end of exposure the conversion of dopamine to NA is influenced by the presence of an inhibitor (Caroldi et al, 1984a) and in the adrenals of repeatedly exposed rats the content of D,BH remains high 24 h after exposure to CS2 (Caroldi et al, 1984a), rats were submitted to cold, cold plus immobilization or insulin treatment 24 h after the last of ten exposures to CS2.…”