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At least 199 records · Page 11Linked to original sources
PubMed1984

Tissue disposition of carbon disulfide. II. Whole-body autoradiography of 35S- and 14C-labelled carbon disulfide in pregnant mice.

Occupational exposure to carbon disulfide (CS2) has been associated with an increased rate of spontaneous abortions. Animal experiments have shown that CS2 is embryotoxic and teratogenic. In the present study, the embryonal and foetal distribution of CS2 and its metabolites was studied after administration of 35S- or 14C-labelled CS2 to pregnant mice in different stages of gestation. CS2 and its metabolites passed the placenta at all stages of gestation. High levels of metabolites of CS2 were registered in the embryonic neuroepithelium. In mid and late gestation CS2 itself accumulated in the cerebrospinal fluid (CSF) of the brain. 14C-labelled metabolites of CS2 showed affinity for bone and were retained in the liver even at long survival times (24 hours). These localizations may be of significance for some of the reported teratogenic effects of CS2, such as hydrocephalus, ossification defects and foetal liver injury, and support the idea that CS2 and/or its metabolites are embryotoxic and teratogenic by acting directly on embryonal and foetal structures.

Animals↗
PubMed1992

Inhibitory effect of bis(2-aminohexyl) disulfide and bis(2-amino-3-phenylpropyl) disulfide on several mouse inflammations.

The anti-inflammatory profile of the analogues of bis(2-aminopropyl) disulfide dihydrochloride with butyl (compd. II) and phenyl (compd. III) instead of the methyl group was studied in several mouse models related to phagocyte functions. The test samples were administered 2-3 h before the inflammatory stimulation or the peak of inflammation. Subcutaneously administered, compds. II and III significantly inhibited serotonin-induced paw edema in a dose-dependent manner (50% inhibitory dose values: 10 and 5 mg/kg, respectively), when orally administered at 25 mg/kg, these compounds were significantly effective, but their potencies were weaker. Neither compound had any irritant activity when administered at a dose of 12.5 micrograms/5 microliters/paw into the paw. In a sheep red blood cells (SRBC)-induced delayed-type hypersensitivity (DTH) reaction model, compd. II (25 mg/kg, s.c.) significantly inhibited the DTH responses when administered at two different times in relation to the time of challenge. However, there was only slight inhibition by compd. III (25 mg/kg, s.c.) on paw edema formation when administered 14 h after secondary immune response. In a model of experimental acute hepatic failure induced by successive injections of Propionibacterium acnes and lipopolysaccharide, both compounds increased mouse survived, compared with the control mice, and kept the serum levels of components involved in hepatic failure to nearly normal levels. These results demonstrate that compds. II and III possess an inhibitory effect on inflammation related to phagocytes.

Amines↗
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↗
PubMed1986

Improved method for determination of cellular thiols, disulfides and protein mixed disulfides using HPLC with electrochemical detection.

The role of glutathione in cellular responses to toxic insult is well established in the literature and is largely based on chemical determinations of GSH. Although these methods have proved to be adequate to demonstrate the relationships between cellular levels of GSH and xenobiotic toxicity, they may be inadequate for careful investigations regarding the regulation of cellular concentrations of GSH, GSSG and GSSProt. Enzymatic and chromatographic methods provide increased specificity and sensitivity, but the problems of variable accuracy or tedious derivitization steps remain. The HPLC-EC method constitutes a significant improvement over previous methods by satisfying the requirements for selectivity, sensitivity, accuracy and convenience. The utility of the HPLC-EC method has been described in two systems of toxicological interest, particularly with regard to the determination of GSSProt. In further studies, the HPLC-EC method has been useful in investigating the mechanism(s) of alternate nucleophiles, such as cysteamine. The capability to determine various thiols simultaneously in a given biological sample greatly facilitates these investigations. In view of its power as an analytical tool, the HPLC-EC method has the potential for widespread application to the study of cellular thiols.

Animals↗