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将60只断乳小鼠分3组各20只。低硒组喂含硒0.0045mg/kg 半合成饲料;补硒组于低硒饲料内加 Na_2SeO_3,含硒0.496mg/kg;对照组喂常备饲料,含硒0.174mg/kg。结果:低硒组全血 GSH—Px 活力明显下降,胶体金免疫电镜图象分析:低硒组心肌 GSH—Px 含量,较补硒组(肌丝0.62±0.0846:1.13±0.1305,P<0.01;线粒体1.36±0.696:2.77±0.2118,P<0.001)及对照组(肌丝0.625±0.0846:1.48±0.2266,P<0.01;线粒体1.36±0.696:3.16±0.3428,P<0.001)均明显减少,差异有非常显著意义,补硒组与对照组间差异无显著意义(P 值均>0.05),电镜下低硒组心肌线粒体、肌原纤维、膜系统均有显著改变。喂养至56天,每组抽7只,腹腔注射速尿及 NaNO_2,低硒组心肌出现多发性灶性坏死。本文还讨论了低硒对心肌病变的发病学机制。
Sixty weanling mice were divided into 3 groups of 20 each. The low-selenium group was fed with semi-synthetic feed containing 0.0045mg / kg of selenium. In the selenium-enriched group, Na_2SeO_3 was added to the low-selenium diet and selenium was 0.496mg / kg. The control group was fed with feedstuff containing 0.174mg / kg selenium. Results: The activity of GSH-Px in the selenium group was significantly lower than that in the selenium-supplemented group (myofilament 0.62 ± 0.0846: 1.13 ± 0.1305, P <0.01; Mitochondria 1.36 ± 0.696: 2.77 ± 0.2118, P <0.001) and control group (0.625 ± 0.0846: 1.48 ± 0.2266, P <0.01; mitochondria 1.36 ± 0.696: 3.16 ± 0.3428, P <0.001) There was no significant difference between the selenium group and the control group (P> 0.05). The mitochondria, myofibrillar and membranous systems in the selenium-deficient group under electron microscope were all significantly changed. Feeding to 56 days, each group pumping 7, intraperitoneal injection of furosemide and NaNO_2, low selenium group myocardial focal necrosis. This article also discusses the pathogenesis of low selenium on myocardial lesions.