1993
DOI: 10.1016/0006-2952(93)90012-l
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Studies on Hg(II)-induced H2O2 formation and oxidative stress in vivo and in vitro in rat kidney mitochondria

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Cited by 285 publications
(151 citation statements)
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“…The toxicologic characteristics of mercury (elemental, inorganic and organic forms) and its ability to react with and deplete free sulfhydryl groups are wellknown [20]. It is demonstrated that the administration of mercury as Hg (II) to rats results in increased hydrogen peroxide formation, glutathione depletion and lipid peroxidation in kidney mitochondria [21].…”
Section: Introductionmentioning
confidence: 99%
“…The toxicologic characteristics of mercury (elemental, inorganic and organic forms) and its ability to react with and deplete free sulfhydryl groups are wellknown [20]. It is demonstrated that the administration of mercury as Hg (II) to rats results in increased hydrogen peroxide formation, glutathione depletion and lipid peroxidation in kidney mitochondria [21].…”
Section: Introductionmentioning
confidence: 99%
“…Hg 2+ also affects mitochondrial transport [12][13][14][15], cytoplasmic enzymes [2,16,17], and the cytoskeleton [18]. Hg 2+ -modification of Na + , K + , and Cl -permeability leads to changes in cell volume and loss of the regulatory volume decrease (RVD) [3,7,19,20].…”
Section: Introductionmentioning
confidence: 99%
“…However, it was later shown that, under physiological conditions in which intracellular thiols are depleted, the NmerA domain binds Hg 2ϩ and transfers it from ligands in cytoplasm to the catalytic core for reduction (12,13). Furthermore, it has been shown that Hg 2ϩ increases H 2 O 2 formation in mitochondria, leading to increased consumption of reduced glutathione (14). Taken together, these results strongly indicate that the pair of cysteines in the NmerA domain of mercuric reductases does have a functional role in vivo, enhancing mercuric ion detoxification by acting as an accessory pathway for delivery of the substrate to the active site (12).…”
mentioning
confidence: 99%