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Fluoride-induced histopathology and synthesis of stress protein in liver and kidney of mice.

机译:氟化物诱导的小鼠肝脏和肾脏的组织病理学和应激蛋白的合成。

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摘要

Selective low (15 mg sodium fluoride (NaF)/L) and relatively high (150 mg NaF/L) doses of in vivo fluoride (F) treatment to Swiss albino mice through drinking water elicited organ-specific toxicological response. All the F-exposed groups showed severe alterations in both liver and kidney architectures, but there was no significant change in the rate of water consumption and body weight. Vacuolar degeneration, micronecrotic foci in the hepatocytes, and hepatocellular hypertrophy were evident in the mice exposed to low dose (15 mg NaF/L for 30 days) while sinusoidal dilation with enlarged central vein surrounded by deep-blue erythrocytes were preponderant when treated with the same dose for a period of 90 days. Blood filled spaces, disintegration of tubular epithelium, and atrophy of glomeruli were also recorded in the kidney of the same treatment group. Change in reduced glutathione level (GSH), glutathione-s-transferase (GST) activity, malondialdehyde (MDA) production in both liver and kidney, disturbances in liver function, induction of heat shock protein 70 (Hsp 70) expression in kidney and its down regulation in liver were positively correlated with histopathological lesion.
机译:通过饮用水对瑞士白化病小鼠的体内低剂量(15 mg氟化钠(NaF)/ L)和相对高剂量(150 mg NaF / L)体内氟化物的选择性治疗引起器官特异性毒理学反应。所有暴露于F的组在肝脏和肾脏结构上均表现出严重的改变,但饮水率和体重没有明显变化。低剂量(15 mg NaF / L持续30天)的小鼠明显出现液泡变性,肝细胞中的微坏死灶和肝细胞肥大,而当使用低剂量小鼠治疗时,其正弦窦扩张,中心静脉扩大并被深蓝色红细胞包围是明显的现象。相同剂量的90天。在同一治疗组的肾脏中还记录了充满血液的空间,肾小管上皮的崩解和肾小球萎缩。肝脏和肾脏中谷胱甘肽水平降低(GSH),谷胱甘肽S-转移酶(GST)活性,丙二醛(MDA)产生,肝功能紊乱,肾脏中热休克蛋白70(Hsp 70)表达的诱导及其变化肝脏中的下调与组织病理学病变呈正相关。

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