title: [Changes in the antioxidant level, cell cycle progression and apoptosis of testicular cells in rats with diet-induced impaired glucose regulation].
abstract: OBJECTIVE
  To detect the changes of the antioxidant level, cell cycle progression, necrosis and apoptosis, calcium ion concentration ([Ca2+] i) and mitochondrial membrane potential (deltapsim) in the model rats of impaired glucose regulation (IGR) induced by long-range high-fat diet, and to explore IGR-induced male reproductive injury and its mechanisms.
  
  
  METHODS
  Forty male Wistar rats were randomly divided into a normal control (n = 10) and an IGR model group (n = 30), and the IGR model was established by 20 weeks of long-range high-fat diet. Pathological changes in the rat spermatogenic cells were detected by HE staining; the content of malondialdehyde (MDA) and activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were measured with biochemical methods; changes in the cell cycle progression, necrosis and apoptosis were determined using flow cytometry with propidium iodide (PI) dyeing and the Annexin V-FITC kit, respectively, and [Ca2+]i and deltapsim were detected by flow cytometry with Fluo-3 and Rhodamine probe labeling, respectively.
  
  
  RESULTS
  After 20 weeks of continuous high-fat diet, fasting blood glucose was kept at 6.1 - 7.0 mmol/L and blood glucose at 7.8 - 11.1 mmol/L after 2 h glucose load in 12 rats, with a 40% success rate of modeling. Lots of dividing spermatocytes and spermatids were seen in the tissue sections of the normal control rats under the microscope, but few or none in the IGR models. Compared with the normal controls, the IGR model rats showed remarkably increased MDA content and decreased SOD, CAT and GSH-Px activities in the testis tissue (P < 0.05 or P < 0.01) , reduced G0/G1 cells and increased G2/M cells (P < 0.05 or P < 0.01), decreased necrotic cells and increased apoptotic cells (P < 0.05 or P < 0.01), increased [Ca2+]i and decreased deltapsim (P < 0.01), but no significant changes in the percentages of S cells and normal cells.
  
  
  CONCLUSIONS
  IGR can cause spermatogenic cell division disorder in rats, which may be attributed to increased oxidative damage, decreased antioxidant enzyme activities, G2/M phase arrest, [Ca2+]i elevation, deltapsim reduction, and apoptosis of testicular cells.
authors.affiliation: Key Laboratory of Radiobiology of the Ministry of Health, Jilin University School of Public Health, Changchun, Jilin 130021, China.
authors.forename: Fang
authors.initials: F
authors.lastname: Fang
authors.forename: Gui-Ying
authors.initials: GY
authors.lastname: Zhang
authors.forename: Tian-Lin
authors.initials: TL
authors.lastname: Gao
authors.forename: Wan-Ning
authors.initials: WN
authors.lastname: Xiao
authors.forename: Yu-Xin
authors.initials: YX
authors.lastname: Liu
authors.forename: Ya
authors.initials: Y
authors.lastname: Liu
authors.forename: Zhi-Cheng
authors.initials: ZC
authors.lastname: Wang
mesh_terms: D000818:Animals; D017209:Apoptosis; D002453:Cell Cycle; D002455:Cell Division; D059305:Diet, High-Fat; D044882:Glucose Metabolism Disorders / Q000378:metabolism*; D005979:Glutathione Peroxidase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D013737:Testis / Q000166:cytology* / Q000378:metabolism*
chemical_list: D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase