Mitochondrial Toxicity of Depleted Uranium: Protection by Beta-Glucan
| Author | Fatemeh Shaki | en |
| Author | Jalal Pourahmad | en |
| Issued Date | 2013-01-31 | en |
| Abstract | 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. | en |
| DOI | https://doi.org/10.22037/ijpr.2012.1220 | en |
| Keyword | Depleted uranium | en |
| Keyword | Beta-glucan | en |
| Keyword | Mitochondria | en |
| Keyword | Nephrotoxicity | en |
| Keyword | Protection | en |
| Keyword | Antioxidant | en |
| Publisher | Brieflands | en |
| Title | Mitochondrial Toxicity of Depleted Uranium: Protection by Beta-Glucan | en |
| Type | Original Article | en |
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