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Mechanistic View for Toxic Effects of Arsenic on Isolated Rat Kidney and Brain Mitochondria Publisher



Hassani S1 ; Yaghoubi H2 ; Khosrokhavar R3 ; Jafarian I4, 5 ; Mashayekhi V4, 5 ; Hosseini MJ4, 5 ; Shahraki J6
Authors
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Authors Affiliations
  1. 1. Faculty of Pharmacy and Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Biology, Ardabil Branch, Islamic Azad University, Ardabil, Iran
  3. 3. Food and Drug Laboratory Research Center, Food and Drug Organization, MOH and ME, Tehran, Iran
  4. 4. Zanjan Applied Pharmacology Research Center, Zanjan University of Medical Sciences, Zanjan, Iran
  5. 5. Department of Pharmacology and Toxicology, School of Pharmacy, Zanjan University of Medical Sciences, P. O. Box: 45139-56184, Zanjan, Iran
  6. 6. Department of Pharmacology and Toxicology, Faculty of Pharmacy, Zabol University of Medical Sciences, P. O.Box: 9861663335, Zabol, Iran

Source: Biologia (Poland) Published:2015


Abstract

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. © 2015 Institute of Molecular Biology, Slovak Academy of Sciences.
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