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六氯-1:3-丁二烯诱导的小鼠肾小管坏死

Hexachloro-1:3-butadiene-induced renal tubular necrosis in the mouse.

作者信息

Ishmael J, Pratt I, Lock E A

出版信息

J Pathol. 1984 Mar;142(3):195-203. doi: 10.1002/path.1711420307.

Abstract

Administration of hexachloro-1:3-butadiene (HCBD) intraperitoneally at a dose of 50 mg/kg body weight caused necrosis of the proximal tubule of the mouse kidney. The earliest morphological changes detectable by light microscopy were observed after 4 h, and by 16 extensive proximal tubular necrosis was seen throughout the cortex. Active tubular regeneration was apparent by day 5 and by day 14 substantial recovery of morphology had occurred. In the electron microscope mitochondrial swelling was seen 1 and 2 h after dosing in the S1 and S2 segments of the proximal tubule, whereas by 4 and 8 h the major pathological changes were confined to the lower S2 and S3 segments and consisted of mitochondrial swelling and cellular necrosis. The extent of renal injury and regeneration correlated well with measurement of renal function. In conclusion, HCBD produces necrosis of the S2 and S3 segments of the proximal tubule in the mouse, this pattern of injury is different from that seen in the rat where HCBD produces selective necrosis of the S3 segment.

摘要

以50毫克/千克体重的剂量腹腔注射六氯-1:3-丁二烯(HCBD)会导致小鼠肾脏近端小管坏死。给药4小时后通过光学显微镜可观察到最早的形态学变化,到16小时时整个皮质可见广泛的近端小管坏死。到第5天可见活跃的肾小管再生,到第14天形态学有明显恢复。在电子显微镜下,给药1小时和2小时后,近端小管的S1和S2段可见线粒体肿胀,而到4小时和8小时,主要病理变化局限于S2段下部和S3段,表现为线粒体肿胀和细胞坏死。肾损伤和再生程度与肾功能测量结果密切相关。总之,HCBD可导致小鼠近端小管S2和S3段坏死,这种损伤模式与大鼠不同,在大鼠中HCBD可导致S3段选择性坏死。

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