Y 3+ , La 3+ , and some bivalent metals inhibited the opening of the Tl + -induced permeability transition pore in Ca 2+ -loaded rat liver mitochondria

Коротков, С. М.; Konovalova, Svetlana; Emelyanova, Larisa; Brailovskaya, I. V.

doi:10.1016/j.jinorgbio.2014.08.004

Cited by 16 publications

(4 citation statements)

References 68 publications

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“…Lanthanides have long been identified as potential inhibitors of Ca transporters (Reed and Bygrave 1974; Korotkov et al 2014). They exhibit competitive interactions with protons and major cations including Ca 2+ and Mg 2+ , and they have been shown to interfere with Ca metabolism in cells, presumably because their ionic radii are similar to that of Ca 2+ (González et al 2014).…”

Section: Resultsmentioning

confidence: 99%

Lanthanum and Cerium Toxicity to the Freshwater Green Alga Chlorella fusca: Applicability of the Biotic Ligand Model

Aharchaou

Beaubien

Campbell

et al. 2020

Enviro Toxic and Chemistry

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The environmental risk assessment of rare earth elements (REEs) requires data on their potential toxicity. In the present study, the toxicity of lanthanum (La) and cerium (Ce) was studied in relation to metal speciation in solution. For both La and Ce, the use of organic ligands demonstrated that the calculated free ion concentration was a good indicator of toxicity. Whether in the absence or presence of organic ligands, when based on free ion concentrations, the obtained half‐maximal effective concentrations were similar. When all generated data were pooled, Ce and La showed identical toxicity thresholds after 120 h of exposure with free ion concentration–based median effective concentration values (95% confidence intervals) of 0.48 (0.38–0.60) µM and 0.47 (0.36–0.61) µM for La3+ and Ce3+, respectively. The inhibition of algal growth was also correlated with the intracellular lanthanide concentrations, regardless of the ligand used. Finally, increasing the ambient calcium concentration protected the test algae by reducing the amount of lanthanide internalized into the cells. These results suggest that, at constant pH (5.5), REE accumulation and toxicity are linked to the free ion concentration and ambient calcium concentration, as predicted by the biotic ligand model. Environ Toxicol Chem 2020;39:996–1005. © 2020 SETAC

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Section: Resultsmentioning

confidence: 99%

Lanthanum and Cerium Toxicity to the Freshwater Green Alga Chlorella fusca: Applicability of the Biotic Ligand Model

Aharchaou

Beaubien

Campbell

et al. 2020

Enviro Toxic and Chemistry

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“…We found that such phenomena as mitochondrial swelling, state 3 and 3U DNP decrease, and ∆Ψ mito decline were markedly increased in experiments with energized calcium-loaded mitochondria [121,122]. These effects were completely eliminated or markedly attenuated by MPTP inhibitors (ADP, CsA, bongkrekic acid (BKA), and NEM), mitochondrial Ca 2+ uniporter blockers (RR, Y 3+ , La 3+ , Sr 2+ , and Mn 2+ ), or a Ca 2+ -chelator (EGTA) [115,121,[123][124][125]. Tl + -induced MPTP opening is possible only in the case of calcium-loaded mitochondria, while such loading is not required in similar experiments with heavy bivalent metals.…”

Section: Tl(i) Mitochondrial Researchmentioning

confidence: 99%

Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria

Korotkov

2023

IJMS

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This review analyzes the causes and consequences of apoptosis resulting from oxidative stress that occurs in mitochondria and cells exposed to the toxic effects of different-valence heavy metals (Ag+, Tl+, Hg2+, Cd2+, Pb2+, Al3+, Ga3+, In3+, As3+, Sb3+, Cr6+, and U6+). The problems of the relationship between the integration of these toxic metals into molecular mechanisms with the subsequent development of pathophysiological processes and the appearance of diseases caused by the accumulation of these metals in the body are also addressed in this review. Such apoptosis is characterized by a reduction in cell viability, the activation of caspase-3 and caspase-9, the expression of pro-apoptotic genes (Bax and Bcl-2), and the activation of protein kinases (ERK, JNK, p53, and p38) by mitogens. Moreover, the oxidative stress manifests as the mitochondrial permeability transition pore (MPTP) opening, mitochondrial swelling, an increase in the production of reactive oxygen species (ROS) and H2O2, lipid peroxidation, cytochrome c release, a decline in the inner mitochondrial membrane potential (ΔΨmito), a decrease in ATP synthesis, and reduced glutathione and oxygen consumption as well as cytoplasm and matrix calcium overload due to Ca2+ release from the endoplasmic reticulum (ER). The apoptosis and respiratory dysfunction induced by these metals are discussed regarding their interaction with cellular and mitochondrial thiol groups and Fe2+ metabolism disturbance. Similarities and differences in the toxic effects of Tl+ from those of other heavy metals under review are discussed. Similarities may be due to the increase in the cytoplasmic calcium concentration induced by Tl+ and these metals. One difference discussed is the failure to decrease Tl+ toxicity through metallothionein-dependent mechanisms. Another difference could be the decrease in reduced glutathione in the matrix due to the reversible oxidation of Tl+ to Tl3+ near the centers of ROS generation in the respiratory chain. The latter may explain why thallium toxicity to humans turned out to be higher than the toxicity of mercury, lead, cadmium, copper, and zinc.

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“…We earlier found that a closure of mitochondrial potassium chan nels (mitoK ATP and mitoK Ca ) increased the MPTP opening [46]. However, blocking of the mitochon drial Ca 2+ uniporter by ruthenium red, Y 3+ , La 3+ and Ni 2+ deceased the MPTP opening [15,47].…”

Section: Resultsmentioning

confidence: 94%

Influence of Tl(+) on the Ca(2+) and Na(+) movement across rat neonatal cardiomyocytes and rat heart mitochondria membranes

et al. 2020

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thallium is known to produce one of the most complex and serious patterns of toxicity, involving a wide range of human organs and tissues. the toxic impact on biologic organisms is linked especially to the ability of tl + to disturb calcium homeostasis and to permeate easily the inner mitochondrial membrane (IMM). the aim of this work was to study the effects of Tl + on intracellular Ca 2+ dynamics in rat neonatal cardiomyocytes as well as on sodium penetrability of the IMM and tl + -induced mitochondrial permeability transition pore (MPtP) opening in isolated Ca 2+ -loaded rat heart mitochondria (RHM). The use of the fluorescent calcium indicator Fura 2 aM showed that tl + induced calcium influx across the plasmatic membrane, resulting in calcium ([Ca 2+ ] i ) increase in the cytoplasm. this increase was even more pronounced in experiments with accelerating of tl + -transmembrane fluxes by nonactin. It was nevertheless abolished by the removal of extracellular Ca 2+ ions, but was not inhibited by a calcium-channel blocker (nifedipine). tl + did not release calcium from the intracellular stores. tl + potentiated sodium permeability of the IMM because swelling of nonenergized rhM in medium containing tlNo 3 and NaNo 3 was enhanced at high tl + concentration. the calcium load of rhM induced MPtP opening which was accompanied by the increase of the swelling as well as the decrease of the inner membrane potential and of state 4 0 (basal) and state 3U DNP (2,4-dinitrophenol-uncoupled) respiration. These effects of Tl + were suppressed by MPtP inhibitors (cyclosporine a, aDP and n-ethylmaleimide). the data obtained showed that tl + -stimulated influx of extracellular calcium into cardiomyocytes could cause calcium and sodium rhM overload, which lead to the MPtP opening, thus determining the sensitivity of heart muscle to thallium intoxication. K e y w o r d s: tl + , Ca 2+ , Na + , cardiomyocytes, rat heart mitochondria, mitochondrial permeability transition pore (MPtP).

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Y 3+ , La 3+ , and some bivalent metals inhibited the opening of the Tl + -induced permeability transition pore in Ca 2+ -loaded rat liver mitochondria

Cited by 16 publications

References 68 publications

Lanthanum and Cerium Toxicity to the Freshwater Green Alga Chlorella fusca: Applicability of the Biotic Ligand Model

Lanthanum and Cerium Toxicity to the Freshwater Green Alga Chlorella fusca: Applicability of the Biotic Ligand Model

Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria

Influence of Tl(+) on the Ca(2+) and Na(+) movement across rat neonatal cardiomyocytes and rat heart mitochondria membranes

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