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Oxidative stress induced by chromium (VI) in bone of suckling rats.

机译:铬(VI)诱导的乳鼠骨骼中的氧化应激。

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Exposure to hexavalent chromium Cr(VI) compounds is of concern in many Cr-related industries and their surrounding environments. K(2)Cr(2)O(7) is widely recognized as an animal and human carcinogen, mutagen, and teratogen. The present study investigated the bone maturity of suckling rats whose mothers were treated with K(2)Cr(2)O(7). Experiments were carried out on female Wistar rats given 700 ppm of K(2)Cr(2)O(7) in their drinking water from the 14th day of pregnancy until day 14 after delivery. Exposing dams to K(2)Cr(2)O(7) caused disorders in the bone of their progeny. As corollary to this, malondialdehyde levels increased, while glutathione, a non-protein thiol and vitamin C decreased. Alteration of the antioxidant system in the treated group was also confirmed by the significant decline of superoxide dismutase, catalase, and glutathione peroxidase activities. Furthermore, K(2)Cr(2)O(7) induced changes in bone mineralization, especially calcium and phosphorus levels, which decreased. Whereas, in plasma and urine, they increased and decreased inversely. These results suggest that K(2)Cr(2)O(7) accelerated bone resorption activity. In fact, in treated pups, total tartrate-resistant acid phosphatase, which reflected bone resorption, was enhanced while total alkaline phosphatase, which reflected bone formation, was reduced. The impairment of bone function was corresponded histologically.
机译:在许多与铬有关的行业及其周围环境中,六价铬Cr(VI)化合物的暴露是令人关注的问题。 K(2)Cr(2)O(7)被广泛认为是动物和人类致癌物,诱变剂和致畸剂。本研究调查了其母鼠用K(2)Cr(2)O(7)处理的乳鼠的骨骼成熟度。实验从雌性Wistar大鼠开始,从怀孕的第14天到分娩后第14天,在饮用水中给予700 ppm的K(2)Cr(2)O(7)。将水坝暴露于K(2)Cr(2)O(7)会导致后代骨骼中的疾病。结果,丙二醛水平增加,而谷胱甘肽,非蛋白质硫醇和维生素C减少。超氧化物歧化酶,过氧化氢酶和谷胱甘肽过氧化物酶活性的显着下降也证实了治疗组抗氧化系统的改变。此外,K(2)Cr(2)O(7)引起骨矿化的变化,尤其是钙和磷的水平下降。而在血浆和尿液中,它们反比增加和减少。这些结果表明K(2)Cr(2)O(7)加速骨吸收活动。实际上,在经过处理的幼犬中,反映骨骼吸收的总抗酒石酸酸性磷酸酶增加,而反映骨骼形成的总碱性磷酸酶减少。骨功能损害在组织学上是对应的。

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