[Effect of the microtubule depolymerization on mitochondria damage in rat myocardiocytes early after hypoxia]

To investigate the effect of microtubule depolymerization on mitochondria damage in rat myocardiocytes early after hypoxia.

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).

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].

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.