论文部分内容阅读
取大鼠分为:(1)低硒组,喂以含0.017 ppm Se的克山病病区混合饲料及重蒸馏水;(2)低硒加硒组,喂以低硒组饲料,从饮水中加Na_2SeO_3使之达到摄入量0.30 ppm Se;(3)对照组,饲以常备饲料,含0.06 ppm Se。在30、60、90d时测得各组大鼠血谷胱甘肽过氧化物酶(GSH-px)的活力,低硒组比低硒加硒组、对照组显著降低(p<0.001、p<0.025)。形态学所见:低硒组大鼠发生严重肝坏死肝出血(10/16),心肌灶性坏死(3/16)及骨胳肌坏死(5/16)。低硒加硒组大鼠,肝坏死及骨胳肌坏死各2只。对照组大鼠各脏器未发现明显改变。电镜显示低硒组:大鼠肝细胞、心肌细胞线粒体发生明显的嵴溶解、肝细胞粗面内浆网空泡化及骨胳肌细胞含多量残质体。
The rats were divided into: (1) low-selenium group fed with mixed feed and redistilled water in Keshan disease area containing 0.017 ppm Se; (2) low selenium plus selenium group fed with low-selenium group feed from drinking water Na 2 SeO 3 was added to achieve an intake of 0.30 ppm Se; (3) The control group was fed a standing feed containing 0.06 ppm Se. The activity of blood glutathione peroxidase (GSH-px) was measured at 30, 60, and 90 days in each group. The low selenium group was significantly lower than the low selenium plus selenium group and the control group (p<0.001, p <0.025). Morphological findings: Severe hepatic necrosis hepatic hemorrhage (10/16), myocardial focal necrosis (3/16), and skeletal muscle necrosis (5/16) in rats with low selenium status. In selenium plus selenium rats, there were 2 hepatic necrosis and skeletal muscle necrosis. No significant changes were found in the organs of the control group. Electron microscopy showed that in the low-selenium group, the mitochondria of rat hepatocytes and cardiomyocytes were significantly lysed, the vacuolization of hepatic cells in the rough surface, and the amount of residual bodies in the skeletal muscle cells.