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

CDP‐choline circumvents mercury‐induced mitochondrial damage and renal dysfunction

“…Furthermore, provided Ca 2+ was added, mitochondria underwent a fast and extensive swelling, which is characteristic of the membrane permeability transition. In agreement with our previously published work (Hernández‐Esquivel et al, ), Hg 2+ accumulation induces the enzyme activity inhibition of aconitase and the detachment of membrane cytochrome c. Oxidative stress caused by the generation of hydrogen peroxide is also reflected in the oxidative damage found in mitochondrial DNA and in the increased generation of TBARS. The mechanism by which Hg 2+ induces a massive production of ROS could be related to both the inhibition on the respiratory chain (Lund et al, )—which could explain the loss of oxidative phosphorylation—and the depletion of superoxide dismutase.…”

“…Several reports have established that the accumulation of Hg 2+ in kidney tissue induces mitochondrial oxidative membrane damage (Southard and Nitisewojo, ; Ambudkar et al, ; Hernández‐Esquivel et al, ; Pavón et al, ). Conversely, citicoline protects heart mitochondria from reperfusion‐stimulated oxidative injury (Hernández‐Esquivel et al, ).…”

Tamoxifen inhibits mitochondrial oxidative stress damage induced by copper orthophenanthroline

“…The equilibration of H + across the inner membrane and the consequent collapse of the μH + gradient conduce to the uncoupling of oxidative phosphorylation. In addition to Ca 2+ matrix overload, a number of agents have been employed in order to induce membrane permeability transition, for instance, carboxyatractyloside (Halestrap, ; García et al, ), heavy metals (Chávez and Holguín, ; Hernández‐Esquivel et al, ), fatty acids (Wi et al, ; García et al, ; Oyanagi et al, ), and inhibitors of the respiratory chain (Fontaine et al, ). Experimental results from our laboratory and others have established that permeability transition may occur by oxidative stress (Halestrap and Woodfield, ; Pavón et al, ), which in turn evokes the modification of thiol groups of membrane proteins (Harris et al, ; Hernández‐Esquivel et al, ; Pavón et al, ).…”

“…The equilibration of H þ across the inner membrane and the consequent collapse of the mH þ gradient conduce to the uncoupling of oxidative phosphorylation. In addition to Ca 2þ matrix overload, a number of agents have been employed in order to induce membrane permeability transition, for instance, carboxyatractyloside (Halestrap, 1999;Garc ıa et al, 2008), heavy metals (Ch avez and Holgu ın, 1988;Hern andez-Esquivel et al, 2011), fatty acids (Wi et al, 2000;Garc ıa et al, 2008;Oyanagi et al, 2015), and inhibitors of the respiratory chain (Fontaine et al, 1998).…”

“…Experimental results from our laboratory and others have established that permeability transition may occur by oxidative stress (Halestrap and Woodfield, 1997;Pav on et al, 2014), which in turn evokes the modification of thiol groups of membrane proteins (Harris et al, 1979;Hern andez-Esquivel et al, 2011;Pav on et al, 2014). Inhibition of pore opening can be achieved by different types of compounds; one of the most effective is the immunosuppressant cyclosporin A (CSA).…”