2009
DOI: 10.1016/j.mito.2009.08.009
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Cadmium and mitochondria

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Cited by 189 publications
(115 citation statements)
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“…Mitochondria are key intracellular targets for Cd due to their ability to accumulate Cd and because of the sensitivity of mitochondrial enzymes to Cd-induced damage (14,48,56,73). Because of the central role of mitochondria in critical cellular processes such as bioenergetics, redox signaling, and cell death, Cdinduced mitochondrial damage has long-ranging consequences for cellular function, energy homeostasis, and whole-organism performance and survival.…”
mentioning
confidence: 99%
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“…Mitochondria are key intracellular targets for Cd due to their ability to accumulate Cd and because of the sensitivity of mitochondrial enzymes to Cd-induced damage (14,48,56,73). Because of the central role of mitochondria in critical cellular processes such as bioenergetics, redox signaling, and cell death, Cdinduced mitochondrial damage has long-ranging consequences for cellular function, energy homeostasis, and whole-organism performance and survival.…”
mentioning
confidence: 99%
“…Because of the central role of mitochondria in critical cellular processes such as bioenergetics, redox signaling, and cell death, Cdinduced mitochondrial damage has long-ranging consequences for cellular function, energy homeostasis, and whole-organism performance and survival. Previous studies have shown that Cd suppresses respiration and leads to the partial uncoupling, as well as elevated rates of reactive oxygen species (ROS) production in animal and plant mitochondria (11,13,14,18,23,35,65, and references therein). Several mechanisms have been proposed to explain effects of Cd on mitochondrial bioenergetics, including inhibition of electron transport chain (ETC), oxidative damage to mitochondrial enzymes and opening of the mitochondrial permeability pore (1,23,52,73).…”
mentioning
confidence: 99%
“…In vitro Cd 2+ inhibited Ca 2+ uptake, but not in vivo, probably it was then bound to SH-groups and did not interfere with Ca 2+ handling [52]. Interaction between Cd 2+ and cells is reviewed in [54]. When Pb 2+ is administrated in vivo, mitochondria seem to be a target [55].…”
Section: +mentioning
confidence: 99%
“…Cadmium, for example, which has been associated with learning impairments and neurological disorders, has been described to cause mitochondrial-dependent apoptosis in oligodendrocytes (Hossain, Liu et al, 2009) and in a skin cell line (Son, Lee et al, 2011). Cadmium accumulation in the kidney involves alteration of mitochondrial function, which results into increased generation of mitochondrial free radicals (Gobe & Crane, 2011), similarly to what occurs in other target organs (Cannino, Ferruggia et al, 2009). As expected, cadmium, similarly to as mercury and copper, induces the MPT, resulting in mitochondrial swelling and activation of basal respiration, as well as in membrane depolarization (Belyaeva, Glazunov et al, 2004).…”
Section: Environmental Pollutantsmentioning
confidence: 99%