title: [Effect of the microtubule depolymerization on mitochondria damage in rat myocardiocytes early after hypoxia].
abstract: OBJECTIVE
  To investigate the effect of microtubule depolymerization on mitochondria damage in rat myocardiocytes early after hypoxia.
  
  
  METHODS
  Myocardiocytes from Wistar rats were isolated according to routine procedure, and they were randomly divided into control group, depolymerization group (with treatment of 4 micromol/L colchicines in the culture medium), hypoxia group, hypoxia and depolymerization group (with treatment of 4 micromol/L colchicines in the culture medium combined with low oxygen tension). The changes in distribution of the mitochondria were examined with laser confocal microscopy, the morphology and the structure of mitochondria was observed by transmission electron microscope, the respiration control ratio (RCR) was determined by respirometer, and the content of adenosine triphosphate (ATP) in endochylema was detected with liquid chromatograph at 20, 30, 60 post-hypoxia minutes (PHM).
  
  
  RESULTS
  In control group, the mitochondria was in granular form, with regular arrangement, while mild changes were observed in depolymerization group. At 20, 30, and 60 PHM, the disarrangement in distribution and morphologic damage were aggravated in hypoxia depolymerization group, and the RCR (1.58 +/- 0.37, 1.51 +/- 0.32, 1.12 +/- 0.11, respectively) were evidently lower than those in hypoxia group (3.85 +/- 0.56, 2.98 +/- 0.44, 1.79 +/- 0.73, respectively, P < 0.01). The content of ATP showed the same tendency at the same time-points (419 +/- 83, 326 +/- 73, 295 +/- 58 ng/mg) compared with hypoxia depolymerization group [(475 +/- 68, 397 +/- 59, 336 +/- 67 ng/mg) in hypoxia group].
  
  
  CONCLUSIONS
  The disarrangement in distribution of mitochondria, as well as the damage in mitochondrial structure, respiratory, function and energy metabolism, can be aggravated by microtubule depolymerization after hypoxia, which indicates that microtubule depolymerization plays an important role in the mitochondria damage.
authors: Institute of Burn Research, Stale Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University, Chongqing, P. R. China.
authors: Yong
authors: Y
authors: Kuang
authors: Yue-sheng
authors: YS
authors: Huang
mesh_terms: D000818:Animals; D015687:Cell Hypoxia; D002478:Cells, Cultured; D003078:Colchicine / Q000009:adverse effects; D004195:Disease Models, Animal; D000860:Hypoxia / Q000473:pathology*; D008870:Microtubules / Q000473:pathology*; D008929:Mitochondria, Heart / Q000187:drug effects / Q000473:pathology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
chemical_list: D003078:Colchicine