Effects of prenatal exposure of N,N-dimethylformamide and the metabolite of N,N-dimethylformamide on male rats reproductive system

• Main Authors: Hung-Chi Hsu, 許弘其
• Other Authors: Ping-Chi Hsu
• Format: Others
• Language: zh-TW
• Published: 2006
• Online Access: http://ndltd.ncl.edu.tw/handle/32008083305555268593

碩士 === 國立高雄第一科技大學 === 環境與安全衛生工程所 === 94 === Abstract The objectives of this study are to determine the effect of postnatal exposure of N,N-dimethylformamide(DMF) on male reproductive system by in vitro and in vivo animal experiment. At in vitro study, the epididymal spermatozoa were exposed of DMF and N-methylformamide(NMF), N-acetyl-S-(N-methylformamide) cystenine (AMCC), the metabolite of DMF, with 0,100,500,2500μM for 1,3,6 hours. There were no significant differences in sperm mitochondrial membrane potential (MMP), reactive oxygen species (ROS) generation, and sperm chromatin DNA integrity between control and treated groups. At in vivo study, Sprague-Dawlye rats received DMF by gavage of 0, 100, 500 and 1000 mg/kg/week from week 7 trough week 16. At the study, significant increases in apoptosis-related protein expression of p53 and Fas were observed in 500 and 1000 mg/kg DMF-tread male rats compared with control rats (p<0.05, respectively). Moreover, protein expression of PARP and caspase-3 were significantly decreased in 500 and 1000 mg/kg DMF-treated groups compared with control rats (p<0.05, respectively). The results revealed that sperm apoptosis might be induced by death receptor pathway. Fas protein expression increases and induce caspase-8 protein activation, then caspase-8 protein induce caspase-3 activation to induce PARP protein hydrolysis, the receptor of caspase-3, and finally induce sperm apoptosis. There were no significant differences in body weights, tissue weight, sperm motility, sperm MMP, ROS generation, DNA content analysis of testis and sperm chromatin DNA integrity between control and treated groups. In conclusion, In vivo exposed of DMF might induce epididymal sperm apoptosis by death receptor pathway at the dose of 500 and 1000 mg/kg/week in rats.