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目的观察砷对大鼠脑细胞能量代谢和超微结构影响,探讨砷的中枢毒性作用和机制。方法SD成年大鼠,随机分为对照、低砷、中砷、高砷组和繁殖仔代组,染砷组自由饮三氧化二砷(AS2O3)水。6和16周后,测定成鼠和仔鼠脑细胞线粒体三磷酸腺苷(ATP)合成量并观察脑细胞超微结构变化。结果成鼠砷暴露6和16周后,脑细胞线粒体ATP合成量〔低砷6周(222.90±3.85)nmol/(mg.pr);16周(166.12±4.40)nmol/mg.pr〕比对照组〔(238.57±1.31)nmol/(mg.pr)〕明显减少,并与暴露剂量和暴露时间呈正相关;高砷繁殖组孕产的仔鼠出生后继续高砷喂养16周,ATP合成量〔(28.66±2.32)nmol/(mg.pr)〕比成鼠16周高砷组〔(54.25±4.92)nmol/(mg.pr)〕降低更明显。电镜观察染砷6周组脑细胞粗面内质网扩张,线粒体肿胀数目减少;16周中、高砷组还出现核肿胀和细胞器减少;16周仔代组核内结构疏松,线粒体等细胞器数目明显减少,胞质部分区域有空泡现象。结论慢性砷暴露对大鼠脑细胞超微结构和能量代谢功能有明显损伤作用,仔鼠损伤程度比成鼠更严重。
Objective To observe the effects of arsenic on energy metabolism and ultrastructure of rat brain cells and to explore the central toxic effects and mechanism of arsenic. Methods SD adult rats were randomly divided into control, low arsenic, high arsenic, high arsenic, and high density arsenic groups. Arsenic-exposed rats received free arsenic trioxide (AS2O3) water. After 6 and 16 weeks, the mitochondrial ATP synthesis was determined and the ultrastructural changes of brain cells were observed. Results After 6 and 16 weeks of arsenic exposure, mitochondrial ATP synthesis in brain cells (222.90 ± 3.85 nmol / (mg.pr) for low arsenic and 166.12 ± 4.40 nmol / mg.pr for 16 weeks Group 〔(238.57 ± 1.31) nmol / (mg.pr)〕 decreased significantly, and with exposure dose and exposure time was positively correlated; offspring of high arsenic breeding group continued high arsenic fed 16 weeks after birth, ATP synthesis [ (28.66 ± 2.32) nmol / (mg.pr)] than the 16-week high arsenic group [(54.25 ± 4.92) nmol / (mg.pr)]. Electron microscopy showed that the number of organelles in nucleus pulposus of 16-week-old progenitor cells was dilated and the number of mitochondria swelled. Significantly reduced, part of the cytoplasm vacuole phenomenon. Conclusion Chronic arsenic exposure can significantly damage the ultrastructure and energy metabolism of rat brain cells.