1990
DOI: 10.1016/s0021-9258(17)45467-6
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Membrane protein thiol cross-linking associated with the permeabilization of the inner mitochondrial membrane by Ca2+ plus prooxidants.

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Cited by 190 publications
(45 citation statements)
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“…Reversible permeabilization of the inner mitochondrial membrane induced by Ca 21 ions plus prooxidants is under the regulatory influence of the redox status of both mitochondrial nucleotides, matrix sulfhydryl groups and membrane protein thiols forming cross-linked protein aggregates (Fagian et al, 1990;Petronilli et al, 1994;Bernardi, 1996;Halestrap et al, 1997). In addition to the oxidation of sulfhydryl groups and nucleotides [NAD(P)H], the generation of reactive oxygen species (ROS) within mitochondria (or a decreasing in their detoxification) contributes to the induction of the MPT, as shown by studies with several MPT inducers, including t-BuOOH (Castilho et al, 1996;Nieminen et al, 1995;Kowaltowski et al, 2000) and P i (Kowaltowski et al, 1996(Kowaltowski et al, , 1998.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Reversible permeabilization of the inner mitochondrial membrane induced by Ca 21 ions plus prooxidants is under the regulatory influence of the redox status of both mitochondrial nucleotides, matrix sulfhydryl groups and membrane protein thiols forming cross-linked protein aggregates (Fagian et al, 1990;Petronilli et al, 1994;Bernardi, 1996;Halestrap et al, 1997). In addition to the oxidation of sulfhydryl groups and nucleotides [NAD(P)H], the generation of reactive oxygen species (ROS) within mitochondria (or a decreasing in their detoxification) contributes to the induction of the MPT, as shown by studies with several MPT inducers, including t-BuOOH (Castilho et al, 1996;Nieminen et al, 1995;Kowaltowski et al, 2000) and P i (Kowaltowski et al, 1996(Kowaltowski et al, , 1998.…”
Section: Discussionmentioning
confidence: 99%
“…7A, t-BuOOH), according to what has also been observed by Kushnareva and Sokolove (2000), suggesting that this cation is essential and must act in additional steps in the sequence of events that lead to mitochondrial permeabilization. The binding of Ca 21 to the inner membrane may cause conformational changes to critical proteins that expose thiol groups to the action of oxidants (Fagian et al, 1990;Valle et al, 1993).…”
Section: Discussionmentioning
confidence: 99%
“…Our findings are, at first sight, in contradiction to earlier work reporting a loss of Ca 2+ from the mitochondrial matrix upon exposure to oxidants. In these previous studies, oxidizing agents induced Ca 2+ release from isolated mitochondria secondary to the opening of the transition pore (Crompton et al, 1988;Fagian et al, 1990) or via a selective oxidant-dependent pathway (Schlegel et al, 1992), with a resultant collapse of membrane potential. In the present work, H2O2 and HX-XO did not damage the mitochondria, as demonstrated by preserved ∆ψm, a reliable criterion for functional integrity of mitochondria, as well as normal ATP levels, at least during the first 30 minutes of exposure.…”
Section: Discussionmentioning
confidence: 95%
“…Opening of the pore, referred to as the permeability transition, is regulated by matrix Ca 2+ , but is also enhanced by oxidants and inorganic phosphate (Gunter and Pfeiffer, 1990;Zoratti and Szabò, 1995). Meanwhile, evidence is accumulating that under conditions of oxidative stress, mitochondria rapidly lose their Ca 2+ pool (Vlessis and Mela-Riker, 1989;Fagian et al, 1990;Richter and Kass, 1991;Schlegel et al, 1992) and ∆ψm (Fagian et al, 1990; Schlegel et al, 1992;Nieminen et al, 1995). This is followed by a depletion of cellular ATP content and a loss of cell viability.…”
Section: Introductionmentioning
confidence: 99%
“…Differently from mice mitochondria, which showed a higher susceptibility to PTP when at fasting (Menezes-Filho et al, 2019), nutritional status does not seem to affect the susceptibility to PTP in B. constrictor , as fasting and fed snakes exhibited no differences in mitochondrial Ca 2+ retention. PTP can be sensitized by oxidative stress and oxidized NADPH (NADP + ) (Castilho et al, 1995; Vercesi et al, 1988; Zago et al, 2000), as excess ROS increase oxidation of protein thiols and promotes disulfide bonds and cross-linked protein aggregation in the inner mitochondrial membrane (Castilho et al, 1995; Fagian et al, 1990; Valle et al, 1993; Vercesi, 1984). However, as we will discuss further, we also did not observe changes in NAD(P) redox status, and the increased rate of H 2 O 2 production seems not to be leading to oxidative stress, thus not influencing PTP sensibility.…”
Section: Discussionmentioning
confidence: 99%