Relevancy of bivalent sulphur excretion to carbon disulphide exposure in different metabolic conditions

Abstract

Magos, L. (1972). Brit. J. industr. Med., 29,[90][91][92][93][94]. Relevancy of bivalent sulphur excretion to carbon disulphide exposure in different metabolic conditions. A quantitative spectrophotometric method for the estimation of urinary bivalent sulphur by its catalytic effect on the iodine-azide reaction has been developed for rats exposed to carbon disulphide (CS2). Urinary CS2 was also determined. Exposure to CS2 increased the excretion of bivalent sulphur in both fed and starved animals, but the increase in starved animals was significantly less than in fed animals. Starvation also decreased the urinary excretion of CS2. Phenobarbitone pretreatment, which induced liver damage in animals subsequently exposed to CS2, had no effect on either bivalent sulphur or CS2 excretion. Three dithiocarbamate fungicides, Thiram, Ziram, and Zineb, given by mouth increased the excretion of bivalent sulphur in the following order: Zineb < Ziram < Thiram.After 250 mg/kg sodium diethyldithiocarbamate (DDC) given intraperitoneally the same amount of CS2 was excreted in the urine as after 4 hours' exposure to 2-0 mg/l CS2, but the bivalent sulphur excretion was six times higher. Starvation (Strbmme, 1965). After inhalation of CS2 8 to 30% of the body burden is exhaled and less than 1 % is excreted in the urine of persons exposed to CS2 (Teisinger and Soucek, 1949;Harashima and Masuda, 1962 McKee, 1950;Stromme, 1965). The second group of major metabolites constitutes compounds which retained sulphur in the bivalent form. Their excretion is the best indicator of the level of CS2 exposure when assayed by using their catalytic effect on the reduction of iodine by azide (Vasak,

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

“…Compared with carbon tetrachloride, CS2 is an extremely reactive compound and there is no evidence of the existence of a more reactive metabolite. Furthermore, the urinary excretion of CS2 and its bivalent metabolites is not altered by phenobarbitone treatment but only by starvation (Magos, 1972). Finally, in agreement with the metabolic pathway of DDC, which is mainly detoxified by conjugation with glucuronic acid and to a smaller extent decomposed to CS2 (Stromme, 1965), DDC is able to produce an hepatotoxic effect in fasted phenobarbitone-treated rats, but even a 500 mg/kg dose resulted in only slight changes compared with those observed in rats exposed to CS2.…”

“…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 (Magos, Emery, Lock, and Firmager, 1970). From the starved group, food was withdrawn 24 hours before exposure or before DDC.…”

“…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.…”