Toxicity of Arsenic (III) on Isolated Liver Mitochondria: A New Mechanistic Approach

AuthorMir-Jamal Hosseinien
AuthorFatemeh Shakien
AuthorMahmoud Ghazi-Khansarien
AuthorJalal Pourahmaden
Issued Date2013-03-31en
AbstractArsenic exposure mainly through food and water has been shown to be associated with increased incidence of numerous cancers and non-cancer harmful health. It is also used in cancer chemotherapy and treatment of several cancer types due to its apoptogenic effects in the various cancer and normal cell lines. We have already reported that liver is the storage site and important target organ in As (III) toxicity and recently, it has been suggested that hepatic toxicity of arsenic could be resulted from impairment of the liver mitochondria. In this study, interaction of As (III) with freshly isolated rat mitochondria was investigated. We determined different mitochondrial toxicity factors as well as mitochondrial sources of ROS formation using specific substrates and inhibitors following addition of As (III) to the mitochondria. Our results showed that arsenic (III) increased mitochondrial ROS formation, lipid peroxidation and mitochondrial membrane potential collapse, cytochrome c release and mitochondrial swelling in a concentration dependent manner. Addition of As (III) in to the isolated mitochondria, inhibited complexes I and II leading to disruption of mitochondrial electron transfer chain, decreased mitochondrial ATP content and ROS formation.en
DOIhttps://doi.org/10.22037/ijpr.2013.1279en
KeywordArsenic (III)en
Keywordmitochondriaen
KeywordComplex Ien
KeywordComplex IIen
KeywordReactive Oxygen Speciesen
PublisherBrieflandsen
TitleToxicity of Arsenic (III) on Isolated Liver Mitochondria: A New Mechanistic Approachen
TypeOriginal Articleen

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