Mitochondrial Toxicity of Depleted Uranium: Protection by Beta-Glucan

نویسندگان

  • Fatemeh Shaki 1- Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. 2- Faculty of Pharmacy, Manzandaran University of Medical Sciences, Sari, Iran. 3- Students Research Committee, School of Pharmacy Shahid Beheshti University of Medical Sciences, Tehran, Iran.
  • Jalal Pourahmad 1- Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. 2- Pharmaceutical Sciences Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
چکیده مقاله:

Considerable evidence suggests that mitochondrial dysfunction contributes to the toxicity of uranyl acetate (UA), a soluble salt of depleted uranium (DU). We examined the ability of the two antioxidants, beta-glucan and butylated hydroxyl toluene (BHT), to prevent UA-induced mitochondrial dysfunction using rat-isolated kidney mitochondria. Beta-glucan (150 nM) and BHT (20 nM) attenuated UA-induced mitochondrial reactive oxygen species (ROS) formation, lipid peroxidation and glutathione oxidation. Beta-glucan and BHT also prevented the loss of mitochondrial membrane potential (MMP) and mitochondrial swelling following the UA treatment in isolated mitochondria. Our results show that beta-glucan and BHT prevented UA-induced mitochondrial outer membrane damage as well as release of cytochrome c from mitochondria. UA also decreased the ATP production in isolated mitochondria significantly inhibited with beta-glucan and BHT pre-treatment. Our results showed that beta-glucan may be mitochondria-targeted antioxidant and suggested this compound as a possible drug candidate for prophylaxis and treatment against DU-induced nephrotoxicity.

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mitochondrial toxicity of depleted uranium: protection by beta-glucan

considerable evidence suggests that mitochondrial dysfunction contributes to the toxicity of uranyl acetate (ua), a soluble salt of depleted uranium (du). we examined the ability of the two antioxidants, beta-glucan and butylated hydroxyl toluene (bht), to prevent ua-induced mitochondrial dysfunction using rat-isolated kidney mitochondria. beta-glucan (150 nm) and bht (20 nm) attenuated ua-indu...

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Mitochondrial Toxicity of Depleted Uranium: Protection by Beta-Glucan

Considerable evidence suggests that mitochondrial dysfunction contributes to the toxicity of uranyl acetate (UA), a soluble salt of depleted uranium (DU). We examined the ability of the two antioxidants, beta-glucan and butylated hydroxyl toluene (BHT), to prevent UA-induced mitochondrial dysfunction using rat-isolated kidney mitochondria. Beta-glucan (150 nM) and BHT (20 nM) attenuated UA-indu...

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The Toxicity of Depleted Uranium

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عنوان ژورنال

دوره 12  شماره 1

صفحات  131- 140

تاریخ انتشار 2012-12-12

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