| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5849010 | Environmental Toxicology and Pharmacology | 2012 | 9 Pages |
This study investigated nitric oxide (NO) mediation of carbon disulfide (CS2) toxicity that compromised male rat spermatogenesis and endocrine function. Rats were exposed to multiple levels of CS2 concentration (0, 50, 250, 1250Â mg/m3). A 1250Â mg/m3 CS2Â +Â sodium nitroprusside (SNP) group and a 1250Â mg/m3 CS2Â +Â NG-monomethyl-l-arginine (l-NMMA) group were established to explore the role of NO in mediating CS2 toxicity. NO concentrations, NO synthase (NOS) activity, and sex hormone levels were measured, and sperm characteristics were observed and analyzed. Our data show that CS2 exposure decreased: NOS activity; tissue NO concentrations; serum levels of gonadotropin-releasing hormones, luteinizing hormones, and testosterone; and sperm count and activity. In contrast, increased serum follicle-stimulating hormone concentrations and teratospermia were observed with CS2 exposure. SNP reduced some of the toxic effects of CS2, while l-NMMA treatment showed no effect. The results suggests that NO mediates compromised reproductive system function caused by CS2 exposure.
⺠NOS activity, NO concentrations, and rat reproductive parameters were affected by CS2 exposure. ⺠The effects of CS2 on NOS activity and NO concentration were greater for the pituitary than for other tissues. ⺠Increasing doses of CS2 resulted in decreased numbers and motility of sperm, and increased rates of teratospermia.
