硒和镉联合作用对大鼠肝脏TERT mRNA表达的影响

目的研究亚硒酸钠、氯化镉及其联合作用对大鼠肝脏端粒酶逆转录酶(TERT)mRNA表达的影响。方法健康雄性SD大鼠随机分组,每组动物5只。对照组,硒组(2.5、5和10μmol/kg Na2SeO3)、镉组(5、10和20μmol/kgCdCl2)以及硒镉联合作用组。染毒48h后取出肝脏,用RT-PCR方法检测TERT基因的表达。结果与对照组比较,3个剂量硒组的TERT mRNA虽有增高,但P>0.05,而3个剂量的镉组TERT mRNA表达均增多(P<0.01);在硒镉联合作用组中,虽然3个剂量的硒均可分别使3个剂量的镉诱导的大鼠肝脏TERT mRNA表达下降,但仅在2.5μmol/kg Na2SeO3 5μmol/kg CdCl2组、2.5μmol/kg Na2SeO3 10μmol/kg CdCl2组和5μmol/kg Na2SeO3 10μmol/kg CdCl2组,与相应剂量的镉组比较,TERT mRNA水平降低,差异具有显著性。10μmol/kg Na2SeO3 5、10和20μmol/kg CdCl2联合作用组与对照组相比,TERT mRNA水平均升高,与对应镉组相比,差异无显著性。结论镉在5~20μmol/kg的剂量条件下可以诱导大鼠肝脏高表达TERT mRNA,而一定剂量的硒对一定剂量镉引起的TERT mRNA的表达具有一定的拮抗作用。     

JNK基因RNAi对镉致293细胞凋亡的影响

目的利用RNAi技术探讨JNK基因在镉致293细胞凋亡过程中的作用。方法细胞转染siRNA-JNK后染镉,用rt-PCR、Western blotting法测JNK基因表达,流式细胞术测细胞凋亡,四甲基偶氮唑盐(MTT)法测细胞活力。结果30μmol/L氯化镉可使293细胞JNK基因mRNA和蛋白表达明显增高,细胞凋亡增加。siRNA-JNK可抑制这些效应,而错义siRNA-JNK和单纯转染试剂无效。结论JNK基因在镉致293细胞凋亡过程中起到关键作用。     

甘草酸二铵对镉致肝脂质过氧化损伤的保护作用

目的研究甘草酸二铵(DG)对染镉小鼠肝脂质过氧化损伤的保护作用。方法以昆明种小鼠为研究对象,经口灌胃给予不同剂量(20、40、60mg/kg)DG(10mL/kg)连续5d,末次给药后1h给予氯化镉(7·2mg/kg),24h后处死动物,测定肝匀浆中脂质过氧化代谢产物———丙二醛(MDA)、还原型谷胱甘肽(GSH)的含量,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)的活力。结果DG可明显降低肝组织MDA水平,使GSH含量升高,使肝组织中SOD、GSH-PX、CAT活性有一定程度恢复,均有剂量—效应关系。结论DG可对染镉小鼠肝组织脂质过氧化损伤起到一定的保护作用。     

石墨炉原子吸收光谱法测定禽、畜肝组织中镉

目的建立禽、畜肝组织中镉（cd）的石墨炉原子吸收光谱分析的方法。方法采用混合酸体系消解样品，以NHM2PO。＋Mg（N03）：作基体改进剂，石墨炉原子吸收光谱法定量。结果本方法在0-5.0μg/L浓度范围内，相关系数r=0．9994，方法的相对标准偏差（RSD％）为2．9—6．8，对国家标准物质：猪肝（GBW08551）、大米粉（GBW10010），杨树叶（GBW08513）中cd的测定值均在标准值范围。结论本方法具有方法简便、灵敏度高、稳定性好的特点，适用于禽、畜肝组织中Cd含量的测定。     

烟台市常见海产品镉含量水平与污染评价

目的了解烟台市常见海产品镉污染的状况。方法采用重金属单因子污染指数法对不同海产品中镉的污染程度进行评价。结果10种海产品镉的单项污染指数值大小顺序依次为:爬虾(1.34)>黄花鱼(0.77)>笔管蛸(0.75)>巴蛸(0.73)>螃蟹(0.64)>鲳鱼(0.52)>海虾(0.50)>扇贝(0.41)>鲅鱼(0.38)>带鱼(0.25)。结论大部分海产品未受到镉污染,个别品种受到轻度污染。     

Possible effects of environmental cadmium exposure on kidney function in the Japanese general population

Objectives: To examine whether the current level of environmental exposure to cadmium (Cd) is associated with kidney dysfunction among general populations in Japan. Methods: A nationwide survey was conducted in Japan from 1991 to 1997 at 30 survey sites (with no known environmental heavy metal pollution), by the collection of 24-h food-duplicate samples, peripheral blood specimens and morning spot urine samples. In practice, 607 non-smoking adult women provided these samples. After being wet-ashed, the samples were analyzed for Cd in food duplicates (Cd-F), in blood (Cd-B) and urine (Cd-U) by inductively-coupled plasma mass spectrometry (ICP-MS). Urine samples were also analyzed for α₁-microglobulin (α₁-MG), β₂-microglobulin (β₂-MG) and retinol-binding protein (RBP), creatinine (cr) and specific gravity. Possible tubular dysfunction in association with Cd exposure was examined by simple, multiple and logistic regression analyses, and comparison among three different Cd-dose groups. To minimize the confounding effects of aging, 367 women from 41 to 60 years old were selected and subjected to the same statistical analyses. Results: The analysis of a whole population of 607 women showed that α₁-MG and possibly β₂-MG increased as a function of Cd-F, Cd-B and Cd-U. When the analysis was repeated with the selected population of 367 women aged 41–60, the Cd dose-dependent changes in α₁-MG and β₂-MG became less evident. The distribution of the selected population with α₁-MG above two low cut-off values of >4.9 and >8.4 mg/g cr or with β₂-MG above the lowest cut-off value of >400 μg/g cr, was biased toward the group with higher Cd-Ucr, but such bias was not significant for both α₁-MG and β₂-MG when higher cut-off values were employed. No bias was detected with RBP. Logistic regression analysis with α₁-MG, β₂-MG and RBP (with cut-off values given above) in combination with age, Cd-F, Cd-B and Cd-Ucr gave essentially the same results. Conclusions: The evidence for kidney dysfunction was of borderline significance in the present study population for which geometric mean Cd-F, Cd-B and Cd-U were 24.7 μg/day, 1.76 μg/l, and 3.94 μg/g cr, respectively. The findings might suggest at the same time that the safety margin is small for the Japanese general population regarding environmental Cd exposure. Received: 26 February 1999 / Accepted: 24 July 1999     

环境镉污染与人体镉负荷关系的研究

本文报告了湖北省某冶炼厂周围镉污染区环境介质空气、土壤、水和食物中的镉含量。估算出该污染区居民每日镉摄入量为１４２．８４μｇ／日／人，通过对照区５１％。土壤镉与米镉的相关系数是０．９１（Ｐ〈０．０５），米镉与发镉、尿镉无相关。对该镉污染区和对照区３５９人（男女两性，１５￣６０岁）的调查结果表明，污染区人群尿镉１０μｇ／ｇ肌酐的超常率为３．３６％。该地区少数人已有镉吸收。     

镉致肾小管上皮细胞损伤时胞内肌动蛋白与ATP的改变及意义

从细胞功能与结构入手，着重观察镉染毒后细胞内能量代谢变化及其与细胞骨架、细胞形态学改变之间的关系。方法：采用离体肾灌注镉染毒模型，以免疫荧光及超微病理技术对肾小管细胞内肌动蛋白结构行时效分析。结果：染毒早期，肌动蛋白结构可迅速改变，且随着镉染毒时间的延长而愈趋明显；肌动蛋白结构的改变先于形态学变化；在肌动蛋白改变的同时伴有细胞内ＡＴＰ水平的降低，随着染毒时间延长而逐渐加重。当镉被洗脱后，细胞内ＡＴＰ水平开始上升，而肌动蛋白分布并未出现明显回复现象。结论：镉染毒可导致细胞内能量代谢抑制，肌动蛋白结构改变，从而导致细胞结构及功能异常。肌动蛋白结构改变在重金属镉所致的细胞形态、极性及功能损伤中起着重要的作用     

The inhibitory effect of cadmium on neuromuscular transmission in the rat.

Cadmium (0.125-1 mM) was found to inhibit the isometric response of the isolated rat hemidiaphragm during indirect stimulation, but not during direct stimulation. This effect of cadmium (1 mM) was completely reversed by ethyleneglycol bis-(aminoethyl)-N,N,N',N'-tetra-acetic acid (2 mM) or by L-cysteine (2 mM) but only partially by increased calcium. Cadmium (10 micronM) significantly reduced the quantal release of transmitter in the isolated phrenic diaphragm and a concentration of 0.1 mM frequently caused a complete failure of the endplate response after 30 min. The effect of cadmium on neuromuscular transmission could not be readily reversed by washing with cadmium-free solution. Miniature endplate potential frequency and amplitude were not significantly affected by cadmium (0.1 or 0.5 mM). The results suggest that the effect of cadmium on the isolated phrenic nerve-diaphragm is due largely to inhibition of calcium function at presynaptic nerve terminals.