جستجوی مقالات مرتبط با کلیدواژه "depleted uranium" در نشریات گروه "پزشکی"

Activity concentrations of (238U series), (226Ra), (232Th) and (40K) in some soil samples in AL-Nahrawan site 52 soil samples were determined and evaluated. The measurements were carried out using high purity germanium (HPGe) detector. The mean activity concentrations in soil samples were (76019.61, 16.634, 11.693 and 147.55) Bq Kg-1 for 238U ,226Ra, 232Th and 40K, respectively. The concentration of 238U more than of accepted limited of clearance level according to IAEA and that mean AL-Nahrawan site is radioactive contaminated site. The risk assessment that calculated for AL-Nahrawan site appear the  most of dose that calculated from different pathways such as ingestion ,inhalation ,drinking water and meat  is  coming from external dose and most of it from 238U than another radio nuclides such as (226R, 232Thand 40K). The total dose for the contaminated area that calculated by RESRAD code (7.2) dose from all nuclides all pathways summed in AL-Nahrawan is (1.46 mSv / year) and that more the accepted limit for dose limit exposure to public (1 mSv/A) according the IAEA and that mean the public have limit use and action for this site. The high purity germanium analysis appears AL-Nahrawan site contaminated with Du depended on the ratio between 235U and 238U radio nuclides. The cancer risk from all nuclides calculated by RESRD code for AL-Nahrawan site is (2.2) ×10-3This value is above the global average of 0.29×10 −3 and 1.16×10 −3 reported by UNSCEAR.

Depleted uranium (DU) is an important by product in uranium enrichment process. Due toits applications in civilian and also military activity, DU emerged as environmental pollutant.The exposure to DU can occur via external or internal pathways. In external exposure, mainlybeta radiation from the decay products contributes to DU toxicity. Internal exposure to DUis more important and can occur through ingestion of DU-contaminated water and food andinhalation of DU aerosols. There is limited information about health effects and mechanism ofDU after environmental exposure. Kidney is reported as the main target organ for the chemicaltoxicity of this metal that was reported in Persian Gulf syndrome. Alterations in behavior,some neurologic adverse effects, immunotoxicity, embryo-toxicity and hepatotoxicity wereobserved in chronic exposure to DU. Also, the increased risk of cancer was revealed inepidemiological and experimental studies. Several mechanisms were suggested for DU toxicitysuch as oxidative stress, mitochondrial toxicity and inflammation. In fact, uranium like othertoxic heavy metals can induce oxidative damage and apoptosis via mitochondrial pathway andinflammatory response. In this review, we have discussed the kinetic of DU including sourceand exposure pathway. In addition, the health effects of DU and also its toxic mechanism havebeen highlighted.

Although the biokinetics, metabolism, and chemical toxicity of uranium are well known, until recently little attention was paid to the potential toxic effects of uranium on reproduction and development in mammals. In recent years, it has been shown that uranium is a developmental toxicant when given orally or subcutaneously (SC) to mice. Decreased fertility, embryo/fetal toxicity including teratogenicity, and reduced growth of the offspring have been observed following uranium exposure at different gestation periods. For investigating the effects of DU on pregnant animals, three groups (control, sham and test) of NMRI mice were chosen. In test group 4mg/kg of DU were administered intraperitonealy at 11 day of gestation, in sham group only normal saline injected to interior peritoneum as indicated in the test group and in Control group which was considered as the comparison base line of our research, no injection was made. Caesarean sections were performed at 15 day of the gestation; and their placentas were examined externally. Base on our results DU caused significant external anomalies, and caused a significant decrease (p<0.05) in the weight and diameter of placentas, the number of the embryos, their body weight and crown-rump length of fetuses.

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.

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 were divided at random into 3 groups. In the first group normal saline was administrated intraperitioneally (i.p), this group served as controls. The second group were i.p injected with uranyl acetate 40 mg/kg. In the third group the rats received 100 mg/kg/day silymarin by i.p injection for 5 days and 1hr after the last injection; animals were injected with a single i.p dose of uranyl acetate (40 mg/kg). Silymarin was tested for its free radical scavenging activity and protective role against mitochondrial dysfunction in uranyl acetate stressed rats. Lipid peroxidation activity was increased and activity of mitochondrial enzymes (cytochrome-coxidases, NADH-dehydrogenase, α-ketoglutarate dehydrogenase and succinate dehydrogenase) and glutathione was decreased in the liver and kidney of rats intoxicated with uranyl acetate when compared to control rats. In traperitoneal administration of silymarin significantly reduced the lipid peroxidation, increased the activity of mitochondrial enzymes and increased glutathione to near control level. These results suggest that the major components in silymarin (including silybin A and B, isosilybin A and B, cis-silybin A and B) play a protective role through their free redical scavenging properties.