Mitochondrial Toxicity of Depleted Uranium: Protection by Beta-Glucan

Authors

  • 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.
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.

Upgrade to premium to download articles

Sign up to access the full text

Already have an account?login

similar resources

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...

full text

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...

full text

The Toxicity of Depleted Uranium

Depleted uranium (DU) is an emerging environmental pollutant that is introduced into the environment primarily by military activity. While depleted uranium is less radioactive than natural uranium, it still retains all the chemical toxicity associated with the original element. In large doses the kidney is the target organ for the acute chemical toxicity of this metal, producing potentially let...

full text

Free Radical Scavenging Activity of Silymarin with Refrence to Depleted Uranium Induced Mitochondrial Dysfunction

Introduction: Recently depleted uranium is being widely used as anti-armour ammunition and at very high temperature, results in information of an aerosol of very small uranium oxide particles, which may be inhaled. It is alleged that these particles represent a new battlefield hazard because of the chemical toxicology and/or radioactivity. Method & materials: Male Wistar strain albino rats ...

full text

My Resources

Save resource for easier access later

Save to my library Already added to my library

{@ msg_add @}


Journal title

volume 12  issue 1

pages  131- 140

publication date 2012-12-12

By following a journal you will be notified via email when a new issue of this journal is published.

Hosted on Doprax cloud platform doprax.com

copyright © 2015-2023