Cyclosporin A-sensitive permeability transition pore is involved in Cd2+-induced dysfunction of isolated rat liver mitochondria: doubts no more

Belyaeva, E. S.; Glazunov, V. V.; Коротков, С. М.

doi:10.1016/s0003-9861(02)00400-9

Cited by 69 publications

(56 citation statements)

References 73 publications

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“…Thus, GSH depletion may lead to a decrease in GSH-metal interactions, increasing the intracellular concentration of free arsenic and cadmium ions and, hence, their toxicity. In particular, the increase in metal ion concentration could exacerbate mitochondrial dysfunction, since it is known that arsenic and cadmium directly target the mitochondria (48,49). In addition, GSH depletion might potentiate cell death by facilitating the accumulation of reactive oxygen species due to the reduction in glutathione peroxidase activity (50).…”

Section: Resultsmentioning

confidence: 99%

12-O-Tetradecanoylphorbol-13-acetate May Both Potentiate and Decrease the Generation of Apoptosis by the Antileukemic Agent Arsenic Trioxide in Human Promonocytic Cells

Fernández

Ramos

Sancho

et al. 2004

Journal of Biological Chemistry

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Arsenic trioxide (As 2 O 3 ) caused apoptosis in U-937 human promonocytic cells. This effect was potentiated by the simultaneous addition of the glutathione (GSH) synthesis inhibitor DL-buthionine-(R,S)-sulfoximine or the protein kinase C activators 12-O-tetradecanoylphorbol-13-acetate (TPA) and bryostatin 1. In addition TPA decreased the intracellular GSH content, caused ERK activation, and potentiated the As 2 O 3 -provoked activation of p38 and JNK. The addition of N-acetyl-L-cysteine, the PKC inhibitor GF109203X, and the MEK/ERK inhibitors PD98059 and U0126 attenuated both apoptosis induction and GSH decrease, whereas the p38 inhibitor SB203580 and the JNK inhibitor SP600125 were ineffective. TPA also potentiated ERK activation and GSH depletion when added simultaneously to cadmium chloride (CdCl 2 ) and doxorubicin. However, TPA only enhanced apoptosis in the case of CdCl 2 , which is a GSH-sensitive agent, whereas it reduced the toxicity of doxorubicin and other DNA-specific drugs. Finally, preincubation for 14 -24 h with TPA did not potentiate but, instead, attenuated the As 2 O 3 -and CdCl 2 -provoked apoptosis. The same result was obtained by preincubation with bryostatin 1 and other differentiation inducers. It is concluded that TPA increases the apoptotic action of As 2 O 3 , an effect mediated by ERK activation and GSH depletion. However, the increase in apoptosis is only effective in non-differentiated cells.

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Section: Resultsmentioning

confidence: 99%

12-O-Tetradecanoylphorbol-13-acetate May Both Potentiate and Decrease the Generation of Apoptosis by the Antileukemic Agent Arsenic Trioxide in Human Promonocytic Cells

Fernández

Ramos

Sancho

et al. 2004

Journal of Biological Chemistry

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“…Transport of P i in mitochondria was also stimulated by Cd 2+ [28]. State 4 and swelling of mitochondria stimulated by Cd 2+ were substantially increased in the presence of P i [28][29][30]. On the other hand, action of P i on toxic effects of Tl + on mitochondria remains unstudied until now.…”

Section: Introductionmentioning

confidence: 93%

“…Cd 2+ , unlike Tl + , has an extremely high affinity to SH groups and thereby inhibits the enzymes [28,36,40]. Cd 2+ decreased state 3 and DNP-stimulated respiration [29,30,37,41,42] and fast discharged mito [43]. Considering the above data, we can conclude that effects of Tl + on DNP-stimulated respiration are mainly due to massive mitochondrial swelling (Figures 2, 3, and 5) [4], but not to inhibition of respiratory enzymes that takes place only in experiments with Cd 2+ [28,30,37,41].…”

Section: Effects Of Tl + and P I On Mitochondrial Energetics And Mao mentioning

confidence: 99%

Inorganic phosphate stimulates the toxic effects of Tl⁺ in rat liver mitochondria

Коротков

Emelyanova

Yagodina

2008

J Biochem & Molecular Tox

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We studied action of inorganic phosphate (P(i)) on toxic effects of Tl+ in isolated rat liver mitochondria. This is a convenient model to study the toxicity of heavy metals. P(i) markedly retarded contraction of energized mitochondria swollen in the TlNO3 medium and even stronger stimulated swelling and state 4 of succinate-energized mitochondria in the TlNO3 medium. A valinomycin-induced decrease of K+-diffusion potential was also accelerated by Tl+ in the presence of P(i). The mitochondrial permeability transition pore in the medium containing Ca2+, TlNO3, and nitrates of univalent cations was distinctly stimulated by P(i). However, P(i) did not affect both the Tl+-stimulated swelling of nonenergized mitochondria in the TlNO3 medium and swelling of energized mitochondria in the Tl acetate medium. Respiration stimulated by 2,4-dinitrophenol and monoamine oxidase activity of energized mitochondria were not affected by Tl+ regardless of the presence of P(i). We suggested that stimulation by P(i) of toxic action of Tl+ in mitochondria and cells could be due to even greater enhancement of uncoupling of mitochondria as shown by an additional increase of swelling and state 4, and in the greater probability of opening of MPTP in the presence of P(i) and Ca2+.

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“…Mitochondria are regarded as the main target structure of cadmium action on the subcellular level. Damaging the function of mitochondria by cadmium compounds has been confirmed in in vivo [23] and in vitro studies [24]. induced oxidative damage to DNA in cancer cells at concentrations which were relatively higher than those causing lysosome damage (20 uM), which corresponded to lowering the cell viability by 70% [25].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the Toxic Potency of Selected Cadmium Compounds on A549 and CHO-9 Cells

Zapór¹

2014

International Journal of Occupational Safety and Ergonomics

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Cyclosporin A-sensitive permeability transition pore is involved in Cd2+-induced dysfunction of isolated rat liver mitochondria: doubts no more

Cited by 69 publications

References 73 publications

12-O-Tetradecanoylphorbol-13-acetate May Both Potentiate and Decrease the Generation of Apoptosis by the Antileukemic Agent Arsenic Trioxide in Human Promonocytic Cells

12-O-Tetradecanoylphorbol-13-acetate May Both Potentiate and Decrease the Generation of Apoptosis by the Antileukemic Agent Arsenic Trioxide in Human Promonocytic Cells

Inorganic phosphate stimulates the toxic effects of Tl⁺ in rat liver mitochondria

Evaluation of the Toxic Potency of Selected Cadmium Compounds on A549 and CHO-9 Cells

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Cyclosporin A-sensitive permeability transition pore is involved in Cd2+-induced dysfunction of isolated rat liver mitochondria: doubts no more

Cited by 69 publications

References 73 publications

12-O-Tetradecanoylphorbol-13-acetate May Both Potentiate and Decrease the Generation of Apoptosis by the Antileukemic Agent Arsenic Trioxide in Human Promonocytic Cells

12-O-Tetradecanoylphorbol-13-acetate May Both Potentiate and Decrease the Generation of Apoptosis by the Antileukemic Agent Arsenic Trioxide in Human Promonocytic Cells

Inorganic phosphate stimulates the toxic effects of Tl+ in rat liver mitochondria

Evaluation of the Toxic Potency of Selected Cadmium Compounds on A549 and CHO-9 Cells

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Inorganic phosphate stimulates the toxic effects of Tl⁺ in rat liver mitochondria