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  • Title: [Effect of the hypoxia training on the sensitivity of phenylarsineoxide-induced mitochondrial permeability transition pore opening in the rat heart].
    Author: Vavilova HL, Serebrovs'ka TV, Rudyk OV, Bielikova MV, Koliesnikova IeE, Kukoba TV, Sahach VF.
    Journal: Fiziol Zh (1994); 2005; 51(4):3-12. PubMed ID: 16201144.
    Abstract:
    On the mitochondria isolated from the heart tissue of adult rats we studied the sensitivity of mitochondrial permeability transition pore (MPTP) opening to its inductor--phenylarsine oxide (PAO) after mitochondrial swelling, registered by spectrophotometric technique at n = 520 nm. In adult rat under influence of two modes of normobaric intermittent hypoxic training (IHT): i) softer but prolonged one induced by breathing in normobaric chamber with 11% O2 gas mixture, 15 minuets sessions with 15 minuets rest intervals, 5 times daily (first mode) and ii) more severe but shorter one induced by breathing with 8% O2 gas mixture (second mode) were used. The intensity of lipid peroxidation and antioxidant defense mechanisms in rat organism were estimated before and after IHT by measuring malon dialdehyde (MDA) content and enzymatic activity of superoxide dismutase (SOD) and catalase (CAT) in the blood and the liver. It has been shown that IHT in the first mode didn't essentially influence both on PAO induced, cyclosporin A--sensitive mitochondrial swelling and indexes of lipid peroxidation as well as the SOD and CAT enzymatic activity. It was established that IHT in the second mode caused pronounced increase in MDA content both in the blood and the liver by 67% and 32% respectively; considerable augmentation of SOD activity in this tissues (by 49% and 32% respectively) and CAT activity (by 18% and 43% respectively). Moreover, in forty five days the activity of SOD exceeded its initial level in three times in both the blood and the liver. It has been established that IHT in the second mode provoke to twice decrease in PAO-induced mitochondrial swelling as compared with mitochondria of the control group, and even in forty five days after IHT stopping the protective effect on mitochondrial PTP opening was well-preserved. These effects were completely abolished in the presence of an inhibitor--cyclosporin A (10(-5) mol/l) that demonstrated mitochondrial swelling to be due to the mitochondrial PTP opening. Our experiments showed that the influence of IHT in more severe mode decreased the sensitivity of mitochondria to the PAO in rat heart mitochondria. Thus resistance of the mitochondrial membrane to an inductor of PTP opening--PAO increase under the influence of IHT in the second mode.
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