title: [Effects of acrylonitrile on the activities of antioxidant enzymes and levels of lipid peroxidation in rat testes].
abstract: OBJECTIVE
  To explore the mechanism of male reproductive toxicity induced by acrylonitrile (ACN).
  
  
  METHODS
  Male Sprague-Dawley rats were daily administrated ACN by intraperitoneal injection 5 times a week for 13 weeks at the dose of 0, 7.5, 15.0 and 30.0 mg/kg body weight, respectively. The rats were sacrificed and testes were removed at the end of 4, 8, 13 or 15 weeks, respectively. The activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and glutathione S-transferase (GST) and the levels of glutathione (GSH) and malonaldehyde (MDA) were detected in testes.
  
  
  RESULTS
  Following ACN treatment of 4 weeks, the levels of GSH in ACN 15.0 mg/kg and 30.0 mg/kg group were (7.44 +/- 0.77) mg/g pro and (6.95 +/- 0.77) mg/g pro respectively, and the activity of GSH-Px was (70.89 +/- 4.01) U/mg pro in 30.0 mg/kg group, all of which were significantly higher than the control group (P < 0.05, P < 0.01). After 8 weeks, the levels of GSH decreased to (2.50 +/- 0.94) mg/g pro in ACN 30.0 mg/kg group (P < 0.01); the activities of SOD increased to (102.08 +/- 16.08) NU/mg pro and (113.30 +/- 17.20) NU/mg pro in ACN 15.0 mg/kg and 30.0 mg/kg group (P < 0.01). After 13 weeks, the levels of GSH declined in ACN 15.0 mg/kg and 30.0 mg/kg group, and the activities of GST decreased in ACN 30.0 mg/kg group, and of GSH-Px decreased in both doses group. However, the level of MDA [(0.68 +/- 0.16) nmol/mg pro] were significantly higher in 30.0 mg/kg group than that in control group [(0.38 +/- 0.12) nmol/mg pro] (P < 0.01). 2 weeks after stopping ACN treatment, the level of GSH restored to normal but the levels of MDA or the activity of GSH-Px in 30.0 mg/kg group were still higher or lower respectively than those of control (P < 0.05).
  
  
  CONCLUSIONS
  ACN may impair the balance of antioxidant system, thus induce lipid peroxidation damage to rat testes.
authors.affiliation: Jinshan Hospital of Fudan University, Shanghai 200540, China.
authors.forename: Jian-shu
authors.initials: JS
authors.lastname: Huang
authors.forename: Xian-jiu
authors.initials: XJ
authors.lastname: Zhong
authors.forename: Xin
authors.initials: X
authors.lastname: Wu
authors.forename: Tai-yi
authors.initials: TY
authors.lastname: Jin
mesh_terms: D000181:Acrylonitrile / Q000633:toxicity*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D013737:Testis / Q000187:drug effects / Q000378:metabolism*
chemical_list: D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D005978:Glutathione; D000181:Acrylonitrile