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Differential Susceptibility to Cadmium-Induced Liver and Kidney Injury in Wild and Laboratory-Bred Bank Voles Myodes glareolus

机译:野生和实验室繁殖的田鼠田鼠Myodes glareolus对镉诱发的肝肾损伤的敏感性差异

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摘要

The objective of the study was to compare the sensitivity of wild and laboratory-bred bank voles to cadmium (Cd)-induced histopathological changes in the liver and kidneys. For 4 weeks, the male bank voles—both wild and laboratory-bred—were provided with diet containing Cd in quantities <0.1 (control), 30, and 60 μg/g dry weight. At the end of exposure period, histopathology and analyses of Cd, metallothionein (MT), glutathione (GSH), zinc (Zn), copper (Cu), iron (Fe), and lipid peroxidation—all considered to be critical factors during the development of Cd toxicity in the liver and kidneys—were carried out. Histopathological changes (focal hepatocyte swelling, vacuolation and inflammation [leukocyte infiltration] in the liver, and focal proximal tubule degeneration [including epithelial cell swelling] in the kidneys) occurred only in the wild bank voles fed a diet containing 60 μg Cd/g. There were no differences in concentrations of Cd, MT, GSH, Zn, and Cu in liver and kidney between the respective groups of wild and laboratory-bred animals. However, a decrease of hepatic Fe and lipid peroxidation was observed in the wild voles exhibiting histopathological changes. These data indicate the following: (1) wild bank voles are more susceptible to Cd-induced liver and kidney injury than those bred and raised in the laboratory; (2) the difference in sensitivity may be associated with a distinct decrease of hepatic Fe in response to Cd exposure between the two groups of bank voles; and (3) dietary Cd may produce histopathological changes indirectly through decreasing the hepatic Fe and Fe-dependent oxidative processes. These results also suggest that histopathology in the liver and kidney of wild bank voles living in a contaminated environment may occur at relatively low levels of tissue Cd.
机译:这项研究的目的是比较野生和实验室繁殖的田鼠对镉(Cd)引起的肝脏和肾脏组织病理学变化的敏感性。在4周的时间内,向雄性河岸田鼠(无论是野生的还是实验室饲养的)提供日粮,其日粮中的Cd含量<0.1(对照),30和60μg/ g干重。在暴露期结束时,镉,金属硫蛋白(MT),谷胱甘肽(GSH),锌(Zn),铜(Cu),铁(Fe)和脂质过氧化的组织病理学和分析均被认为是关键因素。进行了在肝脏和肾脏中Cd毒性的发展。组织病理学改变(肝脏中局灶性肝细胞肿胀,空泡化和炎症[白细胞浸润],以及肾脏中局灶性近端小管变性[包括上皮细胞肿胀])仅在以60μgCd / g的饮食喂养的野生河岸田鼠中发生。在野生和实验室饲养的动物中,肝脏和肾脏中Cd,MT,GSH,Zn和Cu的浓度没有差异。然而,在表现出组织病理学变化的野生田鼠中观察到肝铁和脂质过氧化的减少。这些数据表明:(1)野生岸田鼠比在实验室繁殖和饲养的野鼠更容易受到Cd引起的肝肾损害; (2)敏感性的差异可能与两组岸田鼠对镉的暴露而引起的肝铁的明显减少有关; (3)饮食中的镉可能通过减少肝脏中铁和铁依赖性氧化过程而间接产生组织病理学改变。这些结果还表明,生活在受污染环境中的野生河岸田鼠的肝脏和肾脏的组织病理学可能在组织Cd含量较低的情况下发生。

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