NDLI: Depleted uranium induces disruption of energy homeostasis and oxidative stress in isolated rat brain mitochondria

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Metallomics Vol - 5 Issue - 5

Metallomics Vol - 5 Issue - 4

Metallomics Vol - 5 Issue - 3

Metallomics Vol - 5 Issue - 2

Depleted uranium induces disruption of energy homeostasis and oxidative stress in isolated rat brain mitochondria

Content Provider	Royal Society of Chemistry (RSC)
Author	Ghazi-Khansari, Mahmoud Hosseini, Mir-Jamal Pourahmad, Jalal Shaki, Fatemeh
Copyright Year	2013
Abstract	Depleted uranium (DU) is emerging as an environmental pollutant primarily due to its military applications. Gulf War veterans with embedded DU showed cognitive disorders that suggest that the central nervous system is a target of DU. Recent evidence has suggested that DU could induce oxidative stress and mitochondrial dysfunction in brain tissue. However, the underlying mechanisms of DU toxicity in brain mitochondria are not yet well understood. Brain mitochondria were obtained using differential centrifugation and were incubated with different concentrations (50, 100 and 200 μM) of uranyl acetate (UA) as a soluble salt of U238 for 1 h. In this research, mitochondrial ROS production, collapse of mitochondrial membrane potential and mitochondrial swelling were examined by flow cytometry following the addition of UA. Meanwhile, mitochondrial sources of ROS formation were determined using specific substrates and inhibitors. Complex II and IV activity and also the extent of lipid peroxidation and glutathione (GSH) oxidation were detected via spectroscopy. Furthermore, we investigated the concentration of ATP and ATP/ADP ratio using luciferase enzyme and cytochrome c release from mitochondria which was detected by ELISA kit. UA caused concentration-dependent elevation of succinate-linked mitochondrial ROS production, lipid peroxidation, GSH oxidation and inhibition of mitochondrial complex II. UA also induced mitochondrial permeability transition, ATP production decrease and increase in cytochrome c release. Pre-treatment with antioxidants significantly inhibited all the above mentioned toxic effects of UA. This study suggests that mitochondrial oxidative stress and impairment of oxidative phosphorylation in brain mitochondria may play a key role in DU neurotoxicity as reported in Gulf War Syndrome.
Starting Page	736
Ending Page	744
Page Count	9
File Format	HTM / HTML PDF
ISSN	17565901
Volume Number	5
Issue Number	6
Journal	Metallomics
DOI	10.1039/c3mt00019b
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Oxidative stress Flow cytometry Spectroscopy Reactive oxygen species Uranyl acetate Gulf War syndrome Enzyme Mitochondrial permeability transition pore Luciferase Lipid peroxidation Urban area UA Mitochondrion Neurotoxicity Oxidative phosphorylation Gulf War Membrane potential ATP Differential centrifugation Depleted uranium Adenosine triphosphate Glutathione
Content Type	Text
Resource Type	Article
Subject	Chemistry Medicine Metals and Alloys Biochemistry Biomaterials Biophysics

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