Study On The Spermatogenic Impairment And Toxic Mechanism Of Rats Exposed To Phoxim And Fenvalerate

Pesticides, a major category of environmental pollutant, pervasively exist in the world of production and living. Recently, combined pesticides have become a new trend in the world due to drug-resistance and various hazards of pests, combined use of pesticides can greatly enhance the efficiency as well as the complexity of poisoning prevention and treatment The combination of organophosphorus and pyrethroid pesticides is the most widely used and efficient one at present both home and abroad Data suggest that organophosphorus or pyrethroid pesticides alone can induce spermatogenic impairment However, no report is available to the mechanism of regulation and combined toxicity in spermatogenic impairment This study was aimed to provide scientific basis for the prevention and treatment of poisons and new pesticide development by clarifying the mechanism of joint action of phoxim and fenvalerate on male reproduction function through different doses, and time endpoints.Part I The spermatogenic impairment and toxic mechanism of rats induced by fenvalerateFenvalerate, a type II synthetic pyrethroid, is used widely for the control of various pests in agriculture and indoor. Different doses of fenvalerate (0.0,2.4,12.0,60.0mg/kg bw) were orally treated to the adult male SD rats for 15 days and 30 days, respectively. In order to examine the mechanism of sperrnatogenetic impairment, daily sperm production, activity of testicular marked enzymes, sex hormone level and expression of Fas/Fas-1 gene were investigated No significant changes was noted in rats testis/organ weight analysis; fenvalerate caused dose-dependent reduction in daily sperm production, which markedly reduced at the doses of ?12.0mg/kg bw groups. Activity of acid-phosphatases (ACP) increased in 2.4mg/kg bw group on the 15th day and was restrained in the high dose group(60.0mg/kg bw) on the 30th day, but the activity of gamma-glutamyl transpeptidase ( ? -GT) was arrested with different doses dependentiy in the testis, which significantly decreased in high dose group (60.0mg/kg bw). Lactate dehydrogenase (LDH), obvious changes was examined in the middle dose group(12.0mg/kg bw) on the 30th day. On the 15th day, serum follicle stimulating hormone (FSH) levels markedly increased in rats exposed to ?12.0mg/kg bw group, and levels of luteinizing hormone (LH) increased in 12.0mg/kg bw group. In addition, testosterone (T) levels in testis homogenates decreased after the treatment with the doses of ?12.0mg/kg bw as compared with the control group. On the 30th day, FSH levels were significantly elevated in the groups at doses of 12.0mg/kg bw and over, and homogenate levels of T were diminished in the low dose group (2.4mg/kg bw). It is localized Fas to germ cell and Fas-L to sertoli cell. The expression of these genes was dramatically up-regulated with exposure to 12.0mg/kg bw and over. The number of Fas-positive germ cell markedly increased in the groups treated with fenvalerate at doses of 12.0mg/kg and over. These results suggest that: (1)fenvalerate is of an obvious dose-dependent toxicity tospermatogenesis. (2)fenvalerate could change the function of sertoli cell, disturb the reproductive endocrine regulation and subsequently induce spermatogenetic impairment (3) Injuring the function of sertoli cell and subsequently inducing spermatogenic epithelium impairment, activate the paracrine control of testis by Fas/Fas-L pathway, and suppress spermatogenesis. (4)And expression of Fas is up-regulated with increasing FSH level.