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首页> 外文期刊>Comparative biochemistry and physiology, Part C. Pharmacology, toxicology and endocrinology: An international journal >Dietary cadmium induces histopathological changes despite a sufficient metallothionein level in the liver and kidneys of the bank vole (Clethrionomys glareolus)
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Dietary cadmium induces histopathological changes despite a sufficient metallothionein level in the liver and kidneys of the bank vole (Clethrionomys glareolus)

机译：尽管田鼠肝脏和肾脏中的金属硫蛋白水平足够高，但饮食中的镉仍能引起组织病理学改变（Clethrionomys glareolus）

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The objective of this study was to correlate hepatic and renal cadmium (Cd) accumulation: Cd-binding capacity of metallothionein (MT) and lipid peroxidation with the tissue injury in the male bank voles raised under short (8 h light/16 h dark) and long (16 h light/8 h dark) photoperiods that affect differently Cd accumulation and MT induction in these rodents. The animals were exposed to dietary Cd (0, 40 and 80 mu g/g) for 6 weeks. The accumulation of Cd in the liver and kidneys appeared to be dose-dependent in bank voles from the two photoperiod groups. however, the short-photoperiod animals exhibited significantly higher concentrations of Cd in both organs than the long-photoperiod bank voles. Cd-Binding capacity of MT in the liver and kidneys of bank voles From the long photoperiod was sufficiently high to bind and detoxify all Cd ions, while in the animals fed 80 mu g Cd/g under the short photoperiod, the concentrations of Cd in both organs exceeded (by about 10 mu g/g) the MT capacity. However, similar histopathological changes in the liver (a focal hepatocyte swelling and granuloma) and kidneys (a focal degeneration of proximal tubules) occurred in Cd-80 bank voles from the two photoperiods. Likewise, in either photoperiod group, dietary Cd brought about a similar, dose-dependent decrease in the hepatic and renal lipid peroxidation, which paralleled closely that of the iron (Fe) concentrations. These data indicate that: (1) MT does not protect the liver and kidneys against Cd-induced injury in the bank vole exposed to the higher level of dietary Cd; and (2) lipid peroxidation cannot be responsible for the tissue damage. It is hypothesized that dietary Cd produces histopathological changes indirectly, through depressing the tissue Fe and Fe-dependent oxidative processes. (C) 2000 Elsevier Science Inc. All rights reserved. [References: 33]
机译：这项研究的目的是将肝和肾镉（Cd）的积累与金属硫蛋白（MT）和脂质过氧化的Cd结合能力与短时（8 h光照/ 16 h黑暗）饲养的雄性田鼠田鼠的组织损伤相关联。和长时间（16小时光照/ 8小时黑暗）的光周期会影响这些啮齿动物中的Cd积累和MT诱导。使动物暴露于饮食中的镉（0、40和80μg / g）6周。在两个光周期组的田鼠中，Cd在肝脏和肾脏中的积累似乎与剂量有关。然而，短光周期动物在两个器官中的镉含量都比长光周期银行的田鼠高。长期田鼠在肝脏和肾脏中MT的Cd结合能力足够长，足以结合和解毒所有Cd离子，而在短光周期下饲喂80μgCd / g的动物中，Cd的浓度很高。两个器官都超过了MT能力（约10μg / g）。但是，在两种光周期的Cd-80田鼠中，肝脏（局灶性肝细胞肿胀和肉芽肿）和肾脏（近端肾小管的局灶性变性）和肾脏发生了相似的组织病理学变化。同样，在任何一个光周期组中，饮食中的镉都会使肝和肾脂质过氧化发生类似的，剂量依赖性的下降，这与铁（Fe）浓度的下降非常相似。这些数据表明：（1）MT不能保护肝脏和肾脏免受Cd引起的高饮食Cd暴露的田鼠的伤害; （2）脂质过氧化不能造成组织损伤。假设饮食中的Cd通过抑制组织中的Fe和依赖于Fe的氧化过程间接产生组织病理学改变。 （C）2000 Elsevier Science Inc.保留所有权利。 [参考：33]

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