Modulatory role of quercetin against gamma radiation-mediated biochemical and morphological alterations of red blood cells.

PURPOSE: The present work was intended to evaluate the radioprotective effect of quercetin against gamma radiation-induced oxidative stress on red blood cells (RBC). MATERIALS AND METHODS: Swiss albino male mice were treated with quercetin (100 mg/kg body wt) for three consecutive days prior to 5 Gy (60)Co-gamma irradiation. RBC was isolated to estimate the level of intracellular reactive oxygen species (ROS), membrane lipid peroxidation (LPO), intracellular reduced glutathione (GSH), mean corpuscular hemoglobin concentration (MCHC), osmotic fragility and morphological alterations by atomic force microscope (AFM). RESULTS: Irradiation increased intracellular ROS and membrane LPO whereas it decreased the intracellular GSH. Quercetin pretreatment ameliorated these alterations. The MCHC value decreased after irradiation whereas quercetin pretreatment restored it. The average osmotic fragility (H50) and the maximum rate of hemolysis (dH/dC)max increased after irradiation. Quercetin pretreatment decreased the H50 and (dH/dC)max. The AFM study showed that irradiation transformed RBC from biconcave to echinocytes, increased their surface roughness and decreased the vertical distance whereas pretreatment of quercetin significantly prevented both the alterations. CONCLUSIONS: Gamma radiation produced ROS and LPO which rendered oxidative stress and ultimately damaged RBC whereas quercetin ameliorated these changes and protected RBC from radiation-mediated damage.

Leaf extract of Moringa oleifera prevents ionizing radiation-induced oxidative stress in mice.

The present study evaluated the hepatoprotective effect of aqueous ethanolic Moringa oleifera leaf extract (MoLE) against radiation-induced oxidative stress, which is assessed in terms of inflammation and lipid peroxidation. Swiss albino mice were administered MoLE (300 mg/kg of body weight) for 15 consecutive days before exposing them to a single dose of 5 Gy of 6°Co γ-irradiation. Mice were sacrificed at 4 hours after irradiation. Liver was collected for immunoblotting and biochemical tests for the detection of markers of hepatic oxidative stress. Nuclear translocation of nuclear factor kappa B (NF-κB) and lipid peroxidation were augmented, whereas the superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), and ferric reducing antioxidant power (FRAP) values were decreased by radiation exposure. Translocation of NF-κB from cytoplasm to nucleus and lipid peroxidation were found to be inhibited, whereas increases in SOD, CAT, GSH, and FRAP were observed in the mice treated with MoLE prior to irradiation. Therefore pretreatment with MoLE protected against γ-radiation-induced liver damage. The protection may be attributed to the free radical scavenging activity of MoLE, through which it can ameliorate radiation-induced oxidative stress.