title: [Effect of NO and Fas pathway on T-2 induced apoptosis in chondrocytes].
abstract: OBJECTIVE
  To investigate the relationship of T-2 toxin-induced chondrocytes apoptosis with nitric oxide(NO) and Fas apoptosis pathway.
  
  
  METHODS
  Human chondrocytes cultured in vitro were treated with different concentrations of T-2 toxin at different time (1-5 d). Cell viability of the treated cells was measured by MTT assay. Apoptotic ultrostructural changes of the treated cells were observed with electron microscopy. Biological changes of apoptosis were detected by annexin V/PI Flow cytometer (FCM). The levels of NO in culture media were detected by colorimetric method of Griess assay. Nitric oxide synthase (iNOS) and Fas protein were measured by Western blot.
  
  
  RESULTS
  In this study the results shown the dose-dependent and time-dependent effects of T-2 toxin, within a range of concentration (1-2000 ng/mL) and a period of time (1-5 d), on the T-2 toxin-treated chondrocytes. Apoptotic body was found in T-2 toxin-treated chondrocytes by electron microscopy. Early-stage apoptosis rate and late-stage apoptosis rate were both increased in T-2 toxin-treated cells when compared with non-treated cells in a dose-dependent manner. The levels of NO in T-2 toxin-treated culture media were higher than that of normal control. Over-expressions of iNOS and Fas protein were detected in T-2 toxin-treated cells. T-2 toxin-induced apoptosis was noted to be significtnly correlated with the level of NO production and the levels of iNOS and Fas protein expression.
  
  
  CONCLUSIONS
  T-2 toxin can enhance NO production and upregulate the expression of iNOS and Fas protein. Both NO and Fas signaling pathway are involved in T-2 toxin-induced apoptosis.
authors.affiliation: Institute of Endemic Diseases, Environment and Diseases-related Gene of Key Laboratory of Education Ministry, Medical School of Xi'an Jiaotong University, Xi'an 710061, China.
authors.forename: Jing-hong
authors.initials: JH
authors.lastname: Chen
authors.forename: Yong-lie
authors.initials: YL
authors.lastname: Chu
authors.forename: Jun-ling
authors.initials: JL
authors.lastname: Cao
authors.forename: Zhan-tian
authors.initials: ZT
authors.lastname: Yang
authors.forename: Zhong-li
authors.initials: ZL
authors.lastname: Shi
authors.forename: Xiong
authors.initials: X
authors.lastname: Guo
authors.forename: Zhi-lun
authors.initials: ZL
authors.lastname: Wang
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D002478:Cells, Cultured; D019902:Chondrocytes / Q000166:cytology* / Q000378:metabolism; D006801:Humans; D009569:Nitric Oxide / Q000096:biosynthesis*; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis; D013605:T-2 Toxin / Q000633:toxicity*; D019014:fas Receptor / Q000096:biosynthesis*
chemical_list: C491901:FAS protein, human; D019014:fas Receptor; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D013605:T-2 Toxin