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Wheat germ oilOxidative stress Estrogen Rats a b s t r a c tThe purpose of this study was to evaluate the effect of sodium nitrate administration on some biochemical parameters and to explore the ability of Wheat germ oil (WGO) as a natural source of antioxidants to minimize the deleterious effects of sodium nitrate.The results showed significant increase in alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP) and significant decrease in butyryl cholinestersea (BChE) content in hepatic tissue in nitrate group as compared to control and wheat germ oil groups through the experimental period. Furthermore, there was a significant increase in thiobarbituric reactive substances (TBARS) accompanied by significant decrease in reduced glutathione (GSH) content in rat renal tissue after 28 and 42 days of treatment with drinking water containing sodium nitrate. Significant decrease was also observed in serum estradiol (E2) in group treated with nitrate through the experimental period. In addition, microscopically examination of renal tissue showed atrophy of glomerular tuft and congestion of renal blood vessels in nitrate treated group. Administration of WGO to rats with sodium nitrate suggesting role of WGO as a natural protective antioxidant agent in hepatic and renal tissues. WGO also stimulates estrogen secretion and inhibits oxidative damage that may be attributed to the presence of biologically active components (unsaturated fatty acids, unsaponifible matters and sterols matters) as antioxidant and cyto-protective activities.It can be concluded that WGO offers a great advantage for therapeutic purpose to minimized sodium nitrate free radical induced cell damage.journal h omepage: http :/ / www .e lsev ie r. co m/ lo cate/ j rras J o u r n a l o f R a d i a t i o n R e s e a r c h a n d A p p l i e d S c i e n c e s 8 ( 2 0 1 5 ) 7 7 e8 3 http://dx.

We aimed in our current study to explore the protective effect of Ginkgo biloba (GB) and magnetized water (MW) against nephrotoxicity associating induced type 2 diabetes mellitus in rat. Here, we induced diabetes by feeding our lab rats on a high fat-containing diet (4 weeks) and after that injecting them with streptozotocin (STZ). We randomly divided forty rats into four different groups: nontreated control (Ctrl), nontreated diabetic (Diabetic), Diabetic+GB (4-week treatment), and Diabetic+MW (4-week treatment). After the experiment was finished, serum and kidney tissue samples were gathered. Blood levels of glucose, triglycerides, cholesterol, creatinine, and urea were markedly elevated in the diabetic group than in the control group. In all animals treated with GB and MW, the levels of urea, creatinine, and glucose were significantly reduced (all P < 0.01). GB and MW attenuated glomerular and tubular injury as well as the histological score. Furthermore, they normalized the contents of glutathione reductase and SOD2. In summary, our data showed that GB and MW treatment protected type 2 diabetic rat kidneys from nephrotoxic damages by reducing the hyperlipidemia, uremia, oxidative stress, and renal dysfunction.