Tl+ induces both cationic and transition pore permeability in the inner membrane of rat heart mitochondria

Abstract

Effects of Tl(+) were studied in experiments with isolated rat heart mitochondria (RHM) injected into 400 mOsm medium containing TlNO3 and a nitrate salt (KNO3 or NH4NO3) or TlNO3 and sucrose. Tl(+) increased permeability of the inner membrane of the RHM to K(+) and H(+). This manifested as an increase of the non-energized RHM swelling, in the order of sucrose < K(+) < NH4 (+), respectively. After succinate administration, the swollen RHM contracted. The Tl(+)-induced opening of the mitochondrial permeability pore (MPTP) in Ca(2+)-loaded rat heart mitochondria increased both the swelling and the inner membrane potential dissipation, as well as decreased basal state and 2,4-dinitrophenol-stimulated respiration. These effects of Tl(+) were suppressed by the MPTP inhibitors (cyclosporine A, ADP, bongkrekic acid, and n-ethylmaleimide), activated in the presence of the MPTP inducer (carboxyatractyloside) or mitoKATP inhibitor (5-hydroxydecanoate), but were not altered in the presence of mitoKATP agonists (diazoxide or pinacidil). We suggest that the greater sensitivity of heart and striated muscles, versus liver, to thallium salts in vivo can result in more vigorous Tl(+) effects on muscle cell mitochondria.

Allicin Decreases Lipopolysaccharide-Induced Oxidative Stress and Inflammation in Human Umbilical Vein Endothelial Cells through Suppression of Mitochondrial Dysfunction and Activation of Nrf2

“…However, these organelles are extremely susceptible to oxidative stress, which triggers mutations in the mtDNA and regulates the membrane permeability [34]. Furthermore, past studies have also supported the involvement of mitochondrial dysfunction in AS development [35-37].…”

Retracted: AT1R knockdown confers cardioprotection against sepsis‐induced myocardial injury by inhibiting the MAPK signaling pathway in rats

“…The heart apex of rats in the AT1R-shRNA group was injected with 0.1 mL of Ad5-AT1R-shRNA and the NC group with 0.1 mL of Ad5-EGFP, whereas the sham group and the model group with 0.1 mL of diluted phosphate-buffered saline (PBS) containing recombinant virus. 23 During 10-s blocking circulation, the mice presented with gradually decreasing heart rate and decreased ventricular wall motion without ventricular fibrillation.…”

“…Finally, the cells were stained with 4′,6-diamidino-2-phenylindole, incubated at room temperature for 15 minutes and observed under a fluorescence microscope. 23 2.10 | Extraction of myocardial mitochondria and analysis of swelling and membrane potential in rats After the rats were killed, about 100-mg myocardial tissue blocks were placed on ice, sliced into pieces, and added with a precooled homogenate medium A solution (including 250 mmol/L of sucrose, 0.1 mmol/L of ethylene glycol tetraacetic acid (EGTA), 2 mmol/L of 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid (HEPES), and 5 mg/L of calf serum protein, pH 7.2) to make 10% tissue homogenate on ice using a homogenizer using a 1:9 ratio. Next, the homogenate was centrifuged at 1500 rpm for 10 minutes at 4°C, and the precipitate was discarded.…”

“…The mitochondrial membrane potential was expressed by the ratio of the average fluorescence intensity between the second channel and the first channel. 23…”

The Nrf-2/HO-1 Signaling Axis: A Ray of Hope in Cardiovascular Diseases

“…Chen et al showed that the potential of the mitochondrial membrane is higher than normal levels, and the mitochondrial ROS level is abruptly reduced during ischemia-reperfusion injuries [7]. Under the influence of oxidative stress, mtDNA mutations easily occur in the mitochondria, thus altering the permeability of the cell membrane [11]. Experimental studies conducted by Zhang et al have shown that the activation of Nrf2 can reduce the degree of oxidative stress in the mitochondria and can reduce the oxidative stress and inflammatory response of vascular endothelial cells [12].…”