Mitochondria, reactive oxygen species and cadmium toxicity in the kidney

Gobe, Glenda and Crane, Denis (2010). Mitochondria, reactive oxygen species and cadmium toxicity in the kidney. In: Proceedings of an International Conference on Cadmium in Food and Human Health. International Conference on Cadmium in Food and Human Health, Phitsanulok, Thailand, (49-55). 15-17 January, 2010. doi:10.1016/j.toxlet.2010.04.013

Attached Files (Some files may be inaccessible until you login with your UQ eSpace credentials)
Name Description MIMEType Size Downloads
UQ216573.pdf UQ216573.pdf application/pdf 87.74KB 2

Author Gobe, Glenda
Crane, Denis
Title of paper Mitochondria, reactive oxygen species and cadmium toxicity in the kidney
Conference name International Conference on Cadmium in Food and Human Health
Conference location Phitsanulok, Thailand
Conference dates 15-17 January, 2010
Proceedings title Proceedings of an International Conference on Cadmium in Food and Human Health   Check publisher's open access policy
Journal name Toxicology Letters   Check publisher's open access policy
Place of Publication Amstedam, The Netherlands
Publisher Elsevier/North-Holland
Publication Year 2010
Sub-type Fully published paper
DOI 10.1016/j.toxlet.2010.04.013
ISSN 0378-4274
Volume 198
Issue 1
Start page 49
End page 55
Total pages 6
Collection year 2011
Language eng
Abstract/Summary The heavy metal cadmium accumulates in kidney cells, particularly those of the proximal tubular epithelium, and the damage this causes is associated with development of chronic kidney disease. One of the causative mechanisms of chronic kidney disease is thought to be oxidative stress. Cadmium induces oxidative stress, but the molecular mechanisms involved in the cell damage from oxidative stress in cadmium-induced chronic kidney disease are not well understood. Mitochondrial damage is likely, given that dysfunctional mitochondria are central to the formation of excess reactive oxygen species (ROS), and are known key intracellular targets for cadmium. Normally, ROS are balanced by natural anti-oxidant enzymes. When mitochondria become dysfunctional, for example, through long term exposure to environmental toxicants like cadmium, they produce less cell energy and more ROS. The imbalance between these ROS and the natural anti-oxidants creates the condition of oxidative stress. The outcomes of mitochondrial injury are manyfold: injured mitochondria perpetuate oxidative stress; the loss of mitochondrial membrane potential causes release of cytochrome-c and activation of caspase pathways that lead to apoptotic deletion of renal cells; and attempts by cells to remove dysfunctional mitochondria through autophagy lead to “autophagic cell death” or apoptosis. Three pathways of mitochondrial regulation (upstream signalling pathways, direct mitochondrial targeting, and downstream cell death effector pathways) are therefore all promising targets for effective anti-oxidant treatment of cadmium toxicity in the kidney.
Subjects E1
1103 Clinical Sciences
Keyword Kidney
Mitochondria
Oxidative stress
Apoptosis
Anti-oxidants
Ischemia-reperfusion Injury
Tubular Epithelial-cells
Oxidative Stress
Vitamin-E
Up-regulation
In-vitro
Nuclear Translocation
Radical Generation
Signaling Pathway
Induced Apoptosis
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 79 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 101 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Sun, 19 Sep 2010, 00:01:02 EST