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首页> 外文期刊>Biological Rhythm Research >Effect of melatonin on arsenic-induced oxidative stress and expression of MT1 and MT2 receptors in the kidney of laboratory mice
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Effect of melatonin on arsenic-induced oxidative stress and expression of MT1 and MT2 receptors in the kidney of laboratory mice

机译:褪黑素对实验室小鼠肾脏诱导砷诱导的氧化胁迫和MT1和MT2受体表达的影响

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摘要

Arsenic is a ubiquitous element of the environment present in both inorganic and organic forms. Arsenic exposure leads to oxidative stress and tissue damages in living organisms. Kidney is one of the major target organs that are affected by arsenic exposure. Besides its chronobiotic and immunomodulatory properties, melatonin plays an important role as an antioxidant and protects cells and tissues from oxidative damages. The aim of this study was to look over the effects of melatonin on arsenic-induced toxicity and MT1 and MT2 receptor expression in the kidney of mice. Healthy Swiss albino mice were used for this study. Experimental mice were received sodium arsenate (7 mg/kg B.wt./day) and melatonin (25 mu g/100 g B.wt./day) alone and in combination for consecutive 30 days. Arsenic treatment increased malondialdehyde (MDA) level and suppressed the SOD and catalase activity in kidney tissue. Melatonin treatment to arsenic-treated mice suppressed the MDA level and restored the SOD and catalase activity in kidney tissues. Arsenic stress caused an increase in MT1 and MT2 receptor expression in kidney tissue. Melatonin supplementation to arsenic-treated mice maintained the increased expression of MT1 and MT2 receptors in kidney tissue. This finding may suggest the protective effect of melatonin and responsiveness of melatonin receptors during the arsenic-induced oxidative stress in kidney tissues of experimental mice.
机译:砷是无机和有机形式存在的环境的无处不存在的环境。砷暴露导致生物体中的氧化应激和组织损伤。肾是受砷暴露影响的主要目标器官之一。除了其计时和免疫调节性质之外,褪黑激素还发挥着重要作用作为抗氧化剂,保护来自氧化损伤的细胞和组织。该研究的目的是浏览褪黑素对小鼠肾脏诱导毒毒性和MT1和MT1和MT2受体表达的影响。健康的瑞士白化小鼠用于这项研究。将实验小鼠接受砷酸钠(7mg / kg B.wt./day)和褪黑激素(25μg/ 100g b.wt./day),并且组合连续30天。砷治疗较常见的丙二醛(MDA)水平,并抑制肾组织中的SOD和过氧化氢酶活性。将褪黑素处理到砷处理的小鼠抑制了MDA水平并恢复了肾组织中的SOD和过氧化氢酶活性。砷应激导致肾组织中MT1和MT2受体表达的增加。对砷处理的小鼠的褪黑激素补充剂保持了肾组织中MT1和MT2受体的表达增加。该发现可能表明在实验小鼠肾组织中砷诱导的氧化胁迫期间褪黑激素和褪黑素受体反应性的保护作用。

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