Mechanistic view for toxic effects of arsenic on isolated rat kidney and brain mitochondria

• Published in: Biológia Vol. 70; no. 5; pp. 683 - 689
• Main Authors: Hassani, Shokoufeh, Hashem Yaghoubi, Roya Khosrokhavar, Iman Jafarian, Vida Mashayekhi, Mir-Jamal Hosseini, Jafar Shahraki
• Format: Journal Article
• Language: English
• Published: Cham De Gruyter Open 01.05.2015; Springer International Publishing; Springer Nature B.V
• Subjects: adenosine triphosphate; Arsenic; ATP; Brain; Carcinogenicity; Cell Biology; Cytochrome; cytochrome c; humans; Kidneys; Life Sciences; liver; males; membrane potential; metals; Microbiology; mitochondria; mitochondrial membrane; oxidation; oxidative phosphorylation; Oxidative stress; permeability; Plant Sciences; rats; reactive oxygen species; reactive oxygen species formation; Risk factors; Toxicity; ultracentrifugation; Zoology; arsenic; cytochrome c; reactive oxygen species formation; mitochondria; oxidative stress
• ISSN: 1336-9563; 0006-3088; 1336-9563
• DOI: 10.1515/biolog-2015-0081

Arsenic is one of the most important risk factors for human health and exhibits carcinogenicity in human. Emerging lines of research indicate that mitochondria are important target organelles for metals toxicity in living cells. In this study male rats were sacrificed and then kidney and brain mitochondria were isolated using ultracentrifugation method. Then, multi-parametric assays including reactive oxygen species (ROS) formation, complex II and IV activity, outer membrane integrity, ATP level and release of cytochrome c release evaluated to predict the biochemical pathways involved in arsenic toxicity. Our results showed that arsenic (25-200 μM) induced significant ROS formation rise and mitochondrial outer membrane damage in kidney and brain mitochondria, mitochondrial membrane potential collapse and mitochondrial ATP levels. Significant decrease in the complex II and IV activity in brain without any change in kidney mitochondria suggests the inevitable role of oxidative stress in mitochondrial permeability transition-mediated cytochrome c release. Therefore, it is supposed that mitochondrial oxidative stress and uncoupling of oxidative phosphorylation may play key roles in arsenic toxicity towards isolated kidney and brain mitochondria. Also, comparison of present study with previous investigations supposed that liver is more susceptible to arsenic exposure and induction of oxidation stress-like condition than kidney and brain tissues.