The effect of cyclosporin A on Hg2+ -poisoning mitochondria. In vivo and in vitro studies

Chávez, Rita; Corona, N.; Garcı́a, Cruz; Chávez, Edmundo

doi:10.1016/1367-8280(94)90072-8

Cited by 5 publications

(6 citation statements)

References 21 publications

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“…It has been previously reported that the interaction of the heavy metal mercury with mitochondrial membrane increases non-specific membrane permeability [7,26,27]. In agreement, Fig.…”

Section: In Vitro Protective Effect Of Tamoxifen On Hg 2+ -Induced MIsupporting

confidence: 90%

“…As reported previously [27], Fig. 3A, trace a, shows that Hg 2+ induced a rapid fall in the transmembrane electric gradient.…”

Section: In Vitro Protective Effect Of Tamoxifen On Hg 2+ -Induced MIsupporting

confidence: 85%

“…A wide array of drugs and chemicals has been used to remedy mercury poisoning, among them cyclosporin A [27], dpenicillamine [31], diethyldithiocarbamate [32], captopril [3], and EGTA [2]. The present study shows that the estrogen receptor modulator, tamoxifen, effectively prevented renal injury induced by mercury toxicity, both in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 54%

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Protective behavior of tamoxifen against Hg2+-induced toxicity on kidney mitochondria: In vitro and in vivo experiments

Hernández‐Esquivel

Zazueta

Buelna‐Chontal

et al. 2011

The Journal of Steroid Biochemistry and Molecular Biology

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“…It has been previously reported that the interaction of the heavy metal mercury with mitochondrial membrane increases non-specific membrane permeability [7,26,27]. In agreement, Fig.…”

Section: In Vitro Protective Effect Of Tamoxifen On Hg 2+ -Induced MIsupporting

confidence: 90%

“…As reported previously [27], Fig. 3A, trace a, shows that Hg 2+ induced a rapid fall in the transmembrane electric gradient.…”

Section: In Vitro Protective Effect Of Tamoxifen On Hg 2+ -Induced MIsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 54%

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Protective behavior of tamoxifen against Hg2+-induced toxicity on kidney mitochondria: In vitro and in vivo experiments

Hernández‐Esquivel

Zazueta

Buelna‐Chontal

et al. 2011

The Journal of Steroid Biochemistry and Molecular Biology

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“…More recently, it has been proposed that the c subunit of the F1-ATP synthase is the main mPTP constituent and that ANT plays a regulatory role in its open-closed state [ 7 ]. The pore opening is triggered under different experimental settings, i.e., by adding thiol blocking reagents [ 10 ] and heavy metals [ 11 – 13 , 29 ] or by inhibiting the mitochondrial respiratory chain [ 30 , 31 ], and also in physiopathological conditions such as ischemia/reperfusion damage [ 16 ]. Oxidative stress and mPTP opening are “hallmark” of the injury developed during reperfusion [ 9 , 32 , 33 ].…”

Section: Discussionmentioning

confidence: 99%

“…Recently, the interphase between c subunits of the F 1 -ATP synthase dimers has been pointed out as the nonspecific pore, and in this new model, ANT plays a regulatory role [ 7 ]. The pore is opened by a large number of inducers, including carboxyatractyloside [ 8 ], Ca 2+ [ 9 ], thiol-blocking reagents, heavy metals [ 10 – 13 ], and oxidative stress. It is known that oxidative stress is a main factor that promotes mPTP opening in an isolated mitochondria [ 9 , 14 ], in intact cells [ 15 ] and during reperfusion damage [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Interaction of Agaric Acid with the Adenine Nucleotide Translocase Induces Mitochondrial Oxidative Stress

Chávez

Buelna‐Chontal

Macías-López

et al. 2020

Biochemistry Research International

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Mitochondrial permeability transition is characterized by the opening of a transmembranal pore that switches membrane permeability from specific to nonspecific. This structure allows the free traffic of ions, metabolites, and water across the mitochondrial inner membrane. The opening of the permeability transition pore is triggered by oxidative stress along with calcium overload. In this work, we explored if oxidative stress is a consequence, rather than an effector of the pore opening, by evaluating the interaction of agaric acid with the adenine nucleotide translocase, a structural component of the permeability transition pore. We found that agaric acid induces transition pore opening, increases the generation of oxygen-derived reactive species, augments the oxidation of unsaturated fatty acids in the membrane, and promotes the detachment of cytochrome c from the inner membrane. The effect of agaric acid was inhibited by the antioxidant tamoxifen in association with decreased binding of the thiol reagent eosin-3 maleimide to the adenine nucleotide translocase. We conclude that agaric acid promotes the opening of the pore, increasing ROS production that exerts oxidative modification of critical thiols in the adenine nucleotide translocase.

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Octylguanidine ameliorates the damaging effect of mercury on renal functions

Pavón¹,

Franco²,

Correa³

et al. 2010

Journal of Biochemistry

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Mercurials are known to induce morphological and functional modifications in kidney. The protective effect of octylguanidine on the injury induced by Hg(2+) on renal functions was studied. Octylguanidine administered at a dose of 10 mg/kg body weight prevented the damage induced by Hg(2+) administration at a dose of 3 mg/kg body weight. The findings indicate that octylguanidine spared mitochondria from Hg(2+)-poisoning by preserving their ability to retain matrix content, such as accumulated Ca(2+) and pyridine nucleotides. The hydrophobic amine also protected mitochondria from the Hg(2+)-induced loss of the transmembrane potential, and from the oxidative injury of mitochondrial DNA. In addition, octylguanidine maintained renal functions, such as normal values of creatinine clearance and blood urea nitrogen (BUN), and serum creatinine after Hg(2+) administration. It is proposed that octylguanidine protects kidney by inhibiting Hg(2+) uptake to kidney tissue, and in consequence its binding to mitochondrial membrane through a screening phenomenon, in addition to its known action as inhibitor of permeability transition.

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The effect of cyclosporin A on Hg2+ -poisoning mitochondria. In vivo and in vitro studies

Cited by 5 publications

References 21 publications

Protective behavior of tamoxifen against Hg2+-induced toxicity on kidney mitochondria: In vitro and in vivo experiments

Protective behavior of tamoxifen against Hg2+-induced toxicity on kidney mitochondria: In vitro and in vivo experiments

Interaction of Agaric Acid with the Adenine Nucleotide Translocase Induces Mitochondrial Oxidative Stress

Octylguanidine ameliorates the damaging effect of mercury on renal functions

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