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Santosh Kumar Karn 《Chemistry and Ecology》2016,32(5):460-471
Microbial arsenite oxidation was observed by Acinetobacter sp. XS21, this strain oxidised arsenite As(III) up to 80?mM within 48–72?h of incubation. The present strain XS21 oxidised As(III) at a very high concentration in a shorter interval of time than any of the previous reported microbes. Further, XS21 was applied to the soil to observe its ability in reducing the mobility of As(III), and we found that Acinetobacter sp. XS21 efficiently removed arsenite from soluble-exchangeable fraction and removed 70% of the arsenite as compared to control. This feature makes it a potential candidate for bioremediation. Arsenic-resistant bacteria with strong As(III)-oxidising ability may have potential to improve bioremediation of As(III)-contaminated sites. To understand their basis of resistance and transformation we found the As(III) oxidase gene using degenerate primer and amplified ~550?bp of aioA gene. Amplified aioA gene sequence exhibiting 52% identity in terms of gene and deduced protein sequence to Uncultured bacterium, and Achromobacter sp. arsenite oxidase of larger subunit. Arsenite oxidase, an enzyme, was also observed in this isolate, which may provide a resistance and transforming ability. This bacterium was identified as Acinetobacter sp., by sequencing 16s rRNA gene sequence analysis. 相似文献
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Jean L. Johnson 《黑龙江环境通报》2003,23(1):6-8
Molybdenum cofactor deficiency and isolated sulfite oxidase deficiency are autosomal recessive inborn errors of metabolism with severe neurological symptoms resulting from a lack of sulfite oxidase activity. The deficiencies can be diagnosed prenatally by monitoring sulfite oxidase activity in chorionic villus sampling (CVS) tissue. In those families in which the specific defects have been identified, diagnosis can be achieved by mutation analysis or linkage studies directed at affected genes. These include MOCS1, MOCS2 or GEPH, in cases of molybdenum cofactor deficiency, or SUOX in patients with isolated sulfite oxidase deficiency. Copyright © 2002 John Wiley & Sons, Ltd. 相似文献
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采用C57BL6小鼠作为模型,SO2(7 mg·m-3)动式吸入染毒28 d,每天染毒6 h;SO2吸入染毒开始后的第1~5 d,每天在SO2吸入染毒结束后对小鼠进行腹腔注射Ba P(40 mg·kg-1(b.w.)),1 d注射1次.吸入染毒结束后,采用荧光定量PCR技术检测小鼠心肌细胞中由核DNA(n DNA)编码的细胞色素C氧化酶亚基CO4和由线粒体DNA(mt DNA)编码的ATP合酶亚基ATP6,以及调控线粒体呼吸链组分的核转录因子PGC1-α、NRF1和mt TFA的mRNA水平;并采用Western blot技术检测上述3种线粒体调控基因的蛋白表达.结果发现,SO2和Ba P复合暴露后,小鼠心肌线粒体氧化磷酸化复合体亚基CO4和ATP6的mRNA表达水平均显著降低,调控基因PGC1-α、NRF1和mt TFA的mRNA和蛋白水平也显著降低.提示小鼠在SO2和Ba P复合暴露后,可能通过降低心肌中NRF1表达,影响其对mt TFA的调控,进一步抑制相关基因组的转录和翻译,最终可能导致小鼠心肌线粒体的氧化磷酸化功能受损,进而引发心血管疾病. 相似文献
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Potassium bromate (KBrO3) is a widely used food additive, a water disinfection by-product and a known nephrotoxic agent. The effect of KBrO3 on rat blood, especially on the anti-oxidant defense system, was studied in this work. Animals were given a single oral dose of KBrO3 (100 mg/kg body weight) and sacrificed 12, 24, 48, 96 and 168 h after this treatment. Blood was collected from the animals and separated into plasma and erythrocytes. KBrO3 administration resulted in increased lipid peroxidation, protein oxidation, hydrogen peroxide levels and decreased the reduced glutathione content indicating the induction of oxidative stress in blood. Methemoglobin levels and methemoglobin reductase activity were significantly increased while the total anti-oxidant power was greatly reduced upon KBrO3 treatment. Nitric oxide levels were enhanced while vitamin C concentration decreased in KBrO3 treated animals. The activities of major anti-oxidant enzymes were also altered upon KBrO3 treatment. The maximum changes in all these parameters were 48 h after the administration of KBrO3 and then recovery took place. These results show for the first time that KBrO3 induces oxidative stress in blood and impairs the anti-oxidant defense system. Thus impairment in the anti-oxidant power and alterations in the activities of major anti-oxidant enzymes may play an important role in mediating the toxic effects of KBrO3 in the rat blood. The study of such biochemical events in blood will help elucidate the molecular mechanism of action of KBrO3 and also for devising methods to overcome its toxic effects. 相似文献
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The effects of alcohol–kola nut interactions on activites of whole brain glucose oxidase, glutamine synthetase, and adenylate deaminase were examined in Wistar rats. Thirty Wistar albino rats were divided into six groups. Control group (1) received a placebo (4 mL of distilled water). Groups 2–6 were treated for a 21-day period with either 10% (v/v) alcohol, kola nut, caffeine, alcohol + kola nut, or alcohol + caffeine at 50 mg per kg in a total volume of 4 mL vehicle via gastric intubation, respectively. One day after the final treatment, the whole brain was harvested and processed to examine for several biochemical parameters, including activities of glucose oxidase, adenylate deaminase, and glutamine synthetase. Results showed that alcohol–kola nut interaction decreased the activities of glucose oxidase, adenylate deaminase, and glutamine synthetase in whole brain, suggesting inhibition of glutamine synthesis, decreased energy (ATP) production, ionic transport and decreased neuronal processes. Data indicates that alcohol–kola nut or alcohol–caffeine interactions modify neuronal processes in rat brain; however, the clinical importance of this is not known. 相似文献
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观察香烟水溶性提取物(CSE)和尼古丁对大鼠心肌线粒体的损伤作用.大鼠心肌线粒体分别与CSE或尼古丁于37℃温孵60min,结果表明,CSE明显降低线粒体细胞色素C氧化酶(COX)活性,呈剂量依赖性.但是ATPase活性不受影响.在线粒体呼吸活性受到抑制的同时,过氧化指标无明显变化.CSE对6.5mmol/L钙离子引起的线粒体肿胀反应具有抑制作用,但可加剧250mmol/L钙离子诱导的线粒体肿胀反应.维生素C对CSE造成的线粒体损伤无保护作用.未见尼古丁对体外大鼠心肌线粒体有毒性.CSE对心肌线粒体的损伤可能是由于它对呼吸酶活性的直接抑制作用而与氧自由基机制无关.尼古丁可能不是CSE损伤大鼠心肌线粒体的毒性成分. 相似文献