Reference

The effects of diethyldithiocarbamate and carbon disulfide on acute nephrotoxicity induced by furan, bromobenzene and cephaloridine in mice

The effects of diethyldithiocarbamate and carbon disulfide on acute nephrotoxicity induced by furan, bromobenzene and cephaloridine in mice. Masuda, Yasusuke; Nakayama, Nobue; Yamaguchi, Atsuko; Murohashi, Masatomo (Dep. Toxicol., Niigata Coll. Pharm., Niigata 950-21, Japan). Jpn. J. Pharmacol., 34(2), 221-9 (English) 1984. CODEN: JJPAAZ. ISSN: 0021-5198. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Section cross-reference(s): 1 Diethyldithiocarbamate (DTC) [147-84-2] and CS2 [75-15-0] prevented mice from renal injury induced by furan (I) [110-00-9] and bromobenzene [108-86-1] as evidenced by suppression of elevations in plasma urea N concn. and kidney Ca content and of morphol. alterations. 110-00-9 and 147-84-2 are also in the experiment. Cephaloridine [50-59-9] nephrotoxicity, however, was not prevented. In CCl4-poisoned mice, I nephrotoxicity was augmented, whereas bromobenzene and cephaloridine nephrotoxicity was suppressed. The augmented I nephrotoxicity was also prevented by DTC or CS2. Thus, I may exert nephrotoxicity through active metabolites formed in the kidney. For bromobenzene and cephaloridine nephrotoxicity, a renal bioactivation mechanism is suspected. DTC and CS2 also protected against hepatotoxicity induced by I and thiophene. .

An evaluation of the copulatory, endocrinologic, and spermatotoxic effects of carbon disulfide in the rat

An evaluation of the copulatory, endocrinologic, and spermatotoxic effects of carbon disulfide in the rat. Zenick, Harold; Blackburn, Karen; Hope, Esther; Baldwin, David (Med. Cent., Univ. Cincinnati, Cincinnati, OH 45267, USA). Toxicol. Appl. Pharmacol., 73(2), 275-83 (English) 1984. CODEN: TXAPA9. ISSN: 0041-008X. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) The endocrinol. and spermatogenic effects of CS2 [75-15-0] exposure was studied in the rat. Adult, male rats were exposed to either 600 ppm CS2 or filtered air for 6 h/day for 5 days/wk for 10 wk. One wk prior to exposure and then at wk 1, 4, 7, and 10, males were placed with ovariectomized, hormonally primed females, and copulatory behaviors were scored. Fifteen min postcopulation, the female was killed and the ejaculate was recovered from the excised uterine tract along with the semen plug. Sperm counts, sperm motility, and morphol. were detd. A blood sample was obtained for analyses of testosterone [58-22-0], FSH [9002-68-0] and LH [9002-67-9]. At the end of the 10th wk, 5 animals in each group were challenged with either human chorionic gonadotropin (50 IU/animal, i.v.) or gonadotropin-releasing hormone (100 ng/animal, i. 9002-68-0 and 9002-67-9 which are cas registry numbers of chemicals are mentioned.v.), and the testosterone or gonadotropin responses were monitored over time. CS2 exposure produced significant alterations in copulatory behavior and a decrease in ejaculated sperm counts by the 4th and 7th wks of exposure, resp. No endocrinol. alterations were obsd. Moreover, caudal epididymal sperm counts were not depressed and the testes appeared histol. normal. Thus, CS2 does not seem to exert a direct effect on the testes, but rather may interfere with the process regulating sperm transport and ejaculation. .