Ellagic acid protects against arsenic toxicity in isolated rat mitochondria possibly through the maintaining of complex II. (October 2016)

• Record Type: Journal Article
• Authors: Keshtzar, E; Khodayar, MJ; Javadipour, M; Ghaffari, MA; Bolduc, DL; Rezaei, M
• Is Part Of: Human & experimental toxicology. Volume 35:Number 10(2016:Oct.)
• Page Start: 1060
• Page End: 1072
• Publication Date: 2016-10
• Subjects: Mitochondria -- arsenic -- ellagic acid -- reactive oxygen species; Toxicology -- Periodicals; 615.9
• DOI: 10.1177/0960327115618247
• Languages: English
• ISSNs: 0960-3271

Abstract

Chronic arsenic exposure has been linked to many health problems including diabetes and cancer. In the present study, we assessed the protective effect of ellagic acid (EA) against toxicity induced by arsenic in isolated rat liver mitochondria. Reactive oxygen species (ROS) and mitochondrial membrane potential decline were assayed using dichlorofluorescein diacetate and rhodamine 123, respectively, and dehydrogenase activity obtained by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide conversion assay. Arsenic increased ROS levels and mitochondrial dysfunction, which led to a reduction in mitochondrial total dehydrogenase activity. Mitochondria pretreated with EA exposed to arsenic at various concentrations led to a reversal of ROS production and mitochondrial damage. Our results showed that mitochondria were significantly affected when exposed to arsenic, which resulted in excessive ROS production and mitochondrial membrane disruption. Pretreatment with EA, reduced ROS amounts, mitochondrial damage, and restored total dehydrogenase activity specifically associated with mitochondrial complex II. EA protective characteristics may be accomplished particularly throughout the mitochondrial maintenance either directly by its antioxidant property or indirectly through its maintaining of complex II. These findings also suggest a potential role for EA in treating or preventing mitochondria associated disorders.