四氯化碳诱发大鼠肝损伤对镉肾脏毒性的影响

目的探讨肝损伤对镉肾毒性的影响。方法大鼠腹腔注射ＣｄＣｌ２（含镉０．５ｍｇ／ｋｇ）染毒，第４周末通过灌胃给予ＣＣｌ４９００ｍｇ／ｋｇ，观察大鼠肝、肾功能的变化。结果肝损伤使尿蛋白含量增高和肾小管坏死等肾脏病变提前出现。ＣＣｌ４仅引起一过性的肝损害而未见任何肾功能指标的异常。ＣｄＣｌ２＋ＣＣｌ４联合处理组肾镉临界浓度（７１．５０μｇ／ｇ）明显低于ＣｄＣｌ２组（１００．５５μｇ／ｇ）或ＣＣｌ４＋ＣｄＣｌ２联合处理组（１０３．８０μｇ／ｇ，Ｐ＜０．０５），表明镉染毒大鼠的肝损害能促进镉性肾病的发生和发展，并提高肾脏对镉毒作用的敏感性。结论肝脏功能状态在慢性镉中毒性肾病中起重要的作用。     

镉急性染毒各器官含量及致死机制研究

目的研究镉急性染毒时，机体重要器官镉分布及致死机制。方法通过静脉分别注射1．0．1．5mg氯化镉后，同步测定重要器官镉含量和功能。结果心、肝、肾、脑、血有一稳定的镉浓度，但镉对肝、肾功能的损害作用低于心功能的损害。结论镉急性染毒镉主要分布在肝和肾，但动物死亡原因不是肝、肾损害引起。而是由于心功能衰竭。     

三氧化二锑中毒性肝损害的实验研究

每天给小鼠腹腔注射４０ｍｇ／ｋｇ体重三氧化二锑后可引起明显的肝损害。进入体内的锑主要蓄积于肝脏；染毒２８天时，染毒组肝匀浆及肝线粒体中丙二醛（ＭＤＡ）分别为３０．２７±１．８９μｍｏｌ／Ｌ和４７．２７±１．２１μｍｏｌ／Ｌ，显著高于对照组（Ｐ＜０．０１）；肝线粒体Ｎａ＋Ｋ＋－ＡＴＰ酶及Ｃａ２＋－ＡＴＰ酶活性下降至４．８３５６±０．２６５和２．８０７２±０．１４９活力单位，明显低于对照组（Ｐ＜０．０１）。结果提示：肝脏是锑的主要蓄积器官之一，锑中毒性肝损害发病机理可能与肝脏脂质过氧化及肝线粒体ＡＴＰ酶活性受到抑制有关。     

金属硫蛋白与镉中毒性肝肾损害的关系

目的观察亚慢性镉中毒性肝肾损害,并初步探讨金属硫蛋白（ＭＴ）与肝肾损害的关系。方法用Ｗｉｓｔａｒ大鼠腹腔注射０．５ｍｇ／ｋｇＣｄ２＋的ＣｄＣｌ２３次／周,共１０周,染毒后不同时期处死大鼠,观察肝肾功能变化。结果染毒６周后,大鼠出现了明显的肝肾损害,相应组织中Ｃｄ∶ＭＴ的摩尔数之比均超过７,且随染毒总剂量的增加,Ｃｄ∶ＭＴ值明显增加,病变程度加重。结论肝肾是亚慢性镉中毒的靶器官,非ＭＴ结合的镉可能是损害肝、肾的主要成分。     

北京市成人血、发及脏器的铅、镉背景值

以中学教师和北京市瘁死居民为对象，在严格的质量保证措施下，对北京市居民血、发和脏器铅、镉背景值进行了研究。结果表明，北京市男性吸烟者、不吸烟者及女性不吸烟者的血铅均值分别为８５．０、７４．６和５６．７μｇ／Ｌ，血镉为２．２３、０．７８和０．８３μｇ／Ｌ，其９５％上限值血铅分别为１６０．２、１３１．４和１０７μｇ／Ｌ，血镉分别为６．５、１．９８和１．９５μｇ／Ｌ。各脏器（鲜重，以下同）铅、镉背景值分别为：肝，０．２２和０．８４ｍｇ／ｋｇ；肺，０．１１和０．１７ｍｇ／ｋｇ；心，０．０１４和０．０１２ｍｇ／ｋｇ；脾，０．０３８和０．０７１ｍｇ／ｋｇ；肾，０．０７９和３．９３ｍｇ／ｋｇ；肌肉，０．０５８和０．０２７ｍｇ／ｋｇ，并讨论了血、发和各脏器铅镉含量间的相关性及其意义。     

锌对镉所致胚胎毒性的保护作用研究

实验用Ｗｉｓｔａｒ大鼠，分为正常组、低锌组、低锌染镉组、正常染镉组和染镉高锌保护组，分别饲养，其中三组在孕８和１０天注射镉（２．０ｍｇ／ｋｇ）。妊娠第２０天处死动物，取血，并剖腹检查孕鼠内脏和胎鼠畸形情况。研究发现：与正常对照组相比，单纯缺锌即可引起胎鼠的吸收率增高和畸形的发生；而染镉（２．０ｍｇ／ｋｇ）也可引起胎鼠的吸收胎和迟死胎显著增加，并可引起皮下水肿、卷尾等外观畸形。在孕期缺锌的同时，给予孕鼠２．０ｍｇ／ｋｇ体重的镉，孕鼠在整个孕期体重呈负增长，胚胎不能形成；如给予孕鼠高锌饲养（２２７ｍｇ／ｋｇ），胎鼠可得到较好的保护，其吸收胎、死胎率明显下降，存活率显著上升，且胎鼠体重、身长也与对照组相差无几。提示孕鼠缺锌可引发胎儿畸形，缺锌染镉加重胚胎毒作用，而高锌膳食能拮抗镉所造成的胚胎毒作用。     

卵巢切除后镉对大鼠诱导的骨软化和骨质硬化症

卵巢切除后镉对大鼠诱导的骨软化和骨质硬化症本文报道用去卵巢大鼠静脉注射氯化镉连续１３周，观察其肾脏病理改变和骨软化改变。对大鼠静脉注射氯化镉，分为１．０ｍｇ／ｋｇ和２．０ｍｇ／ｋｇ两个剂量组，１周注射５天，连续１３周。同时设对照组一个。在２．０ｍｇ／...     

氯化镉对小鼠精子的影响

４０只小鼠随机分为４组：对照组，氯化镉３．５ｍｇ／ｋｇ，氯化镉７．０ｍｇ／ｋｇ，氯化镉１４．０ｍｇ／ｋｇ。灌胃染毒，灌胃量为０．１ｍｌ／１０ｇ体重。３天后处死动物，检测精子活动率及精子密度。结果表明，氯化镉７．０ｍｇ／ｋｇ和氯化镉１４．０ｍｇ／ｋｇ组精子活动率比对照组降低（Ｐ〈０．０５），氯化镉７．０ｍｇ／ｋｇ和氯化镉１４．０ｍｇ／ｋｇ组精子密度比对照组降低有非常显著意义（Ｐ〈０．０１）。     

氧自由基在急性镉中毒性肾损伤中的作用

目的探讨氧自由基在急性镉中毒性肾损伤中的作用。方法给大鼠腹腔注射ＣｄＣｌ２（１５μｍｏｌ／ｋｇ）与巯基乙醇（３００μｍｏｌ／ｋｇ）混合液制备急性镉中毒性肾损伤模型，观察染镉后不同时间肾细胞线粒体、胞浆中一系列脂质过氧化指标的变化，同时测定肾皮质镉含量，检测肾功能和肾脏超微结构的改变。结果染镉后２小时肾皮质镉含量已达峰值；超微结构出现改变；氧自由基生成及丙二醛（ＭＤＡ）含量亦显著高于对照组（Ｐ＜０．０１），超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活力下降。至染镉后１２小时，氧自由基产生及脂质过氧化反应达到高峰；肾功能损害亦十分明显；线粒体、溶酶体等细胞器严重受损。结论氧自由基大量生成及由此引起的脂质过氧化反应可能在镉对肾组织的损害中起重要作用。     

甘草甜素和齐墩果酸对大鼠镉中毒性肝损伤的防护作用与机理

为探讨甘草甜素（ＧＬ）和齐墩果酸（ＯＡ）对大鼠镉中毒性肝损伤的防护作用及其作用机理,给大鼠腹腔注射ＣｄＣｌ２溶液（０．８ｍｇＣｄ＾２＋／ｋｇ体重）,两组染镉大鼠分别同时皮下注射ＧＬ的生理盐水溶液（２０ｍｇ／ｋｇ,每周３次）和ＯＡ的吐温－生理盐水混悬液（６０ｍｇ／ｋｇ,每周５次）,测定血清转氨酶、肝镉（Ｃｄ）、金属硫蛋白（ＭＴ）含量,检查肝组织病理形态学。结果显示：ＧＬ和ＯＡ延缓、降低了镉引起的血清     

Organ and subcellular distribution of selenium in rats exposed to cadmium,mercury, and selenium

Three groups of rats were given sodium selenite (Se), sodium selenite and cadmium chloride (Se + Cd), or sodium selenite, cadmium chloride, and mercuric chloride (Se + Cd + Hg), respectively. All animals received subcutaneous doses of ¹¹⁵CdCl₂ (0.3 mg Cd/kg) every other day for a fortnight. Mercuric chloride was administered intravenously at doses of 0.5 mg Hg/kg every other day and Na₂⁷⁵SeO₃ intragastrically at doses of 0.1 mg Se/kg every other day for 2 weeks. The whole-body retention of selenium was slightly elevated by cadmium and increased threefold by cadmium with mercury (mainly blood, liver, and kidneys). Cadmium did not affect subcellular levels of selenium in the kidneys and slightly increased the selenium content in the soluble fraction of the liver. On the other hand, combined administration of mercury and cadmium induced a significant elevation of the selenium content in all subcellular fraction of the kidneys and in the nuclear and mitochondrial fractions of the liver. In all animal groups selenium was bound in the soluble fractions of both the liver and kidneys by high-molecular-weight proteins.     

氯化镉对小鼠脏器系数及睾丸生殖细胞线粒体D-Loop基因突变的影响

[目的]研究氯化镉对发育中的小鼠睾丸、肾、肝等脏器系数及对睾丸生殖细胞线粒体DNA控制区（D-Loop）基因突变的影响,探索氯化镉对睾丸影响的机制。[方法]取7周龄雄性ICR小鼠40只[体重（19.5±2.5）g],随机分为低（1μmol/kg）、中（5μmol/kg）、高（10μmol/kg）剂量氯化镉腹腔注射染毒组和阴性对照组共4组,每组10只,隔天染毒,共10次,对照组腹腔注射等体积的生理盐水。第21天取小鼠双侧睾丸、肾和肝,测定脏器系数;提取睾丸生殖细胞基因组DNA,聚合酶链反应（PCR）扩增线粒体D-Loop基因,纯化后测序分析基因突变。[结果]高剂量组睾丸脏器系数明显低于对照组（P〈0.001）,但肝脏器系数明显高于对照组（P〈0.05）;低剂量组肾脏脏器系数明显高于对照组（P〈0.001）。测序结果显示各组小鼠睾丸生殖细胞线粒体D-Loop基因未检测到突变。[结论]高剂量的氯化镉对小鼠睾丸和肝脏脏器系数产生影响,低剂量的氯化镉对小鼠肾脏脏器系数产生影响。氯化镉处理小鼠21d,未检测到睾丸生殖细胞线粒体D-Loop基因突变。     

Organ and subcellular distribution of cadmium in rats exposed to cadmium, mercury, and selenium

Four groups of rats were given: cadmium chloride (Cd), cadmium chloride and mercuric chloride (Cd + Hg), cadmium chloride and sodium selenite (Cd + Se), or cadmium chloride, mercuric chloride, and sodium selenite (Cd + Hg + Se). All animals received subcutaneous doses of 115mCdCl2 (0.3 mg Cd/kg) every other day for 2 weeks. Mercuric chloride was administered intravenously at doses of 0.5 mg Hg/kg every other day, and Na2 75SeO3 intragastrically at doses of 0.1 mg Se/kg every day for a fortnight. The whole-body and organ retention of cadmium changed slightly with the type of exposure. A significant interaction effect of the examined elements was noted in the nuclear and soluble fractions of the liver and kidneys. Mercury decreased the cadmium concentration in both the nuclear and soluble fractions of the kidneys and diminished the effect of selenium on the cadmium level in the soluble fraction of the kidneys. In the liver the presence of mercury contrary to selenium, lowered the cadmium level in the nuclear fraction. The pattern of cadmium binding to proteins of the soluble fraction of the kidneys and liver remained the same in all groups of animals.     

Tissue distribution of cadmium and metallothionein as a function of time of day and dosage

Cadmium-109 chloride (1 mg or 48 ng Cd²⁺/kg body wt) was administered intraperitoneally to rats at one of eight selected times of day. Exactly 48 hr later each animal was sacrificed, and the cadmium content of the blood, brain, heart, kidney, liver, and testes was determined. Metallothionein levels in the liver and kidney were also measured. Distribution and retention of cadmium was very different at the different dose levels. Approximately 60% of the higher dose of cadmium was retained in the six tissues examined, while only 11.5% of the lower dose could be accounted for in these six tissues. The liver retained the largest percentage of the administered cadmium at both dose levels, but the magnitude of the retention differed by a factor of 6 (57.3% of the higher dose and 9.6% of the lower dose). The pattern of cadmium distribution among the other tissues was also different. At the 1-mg Cd²⁺/kg body wt level, the kidneys accumulated the second largest fraction of cadmium, followed by the blood, heart, testes, and brain. In the 48-ng Cd²⁺/kg body wt groups the order was kidney, testes, blood, heart, and brain. Only in the testes of animals receiving the low dose of cadmium was there an effect of time of day, and here the effect was marked. When cadmium was administered during the dark phase of the daily cycle, the testes contained an average of six times more cadmium than when cadmium was given during the light phase. Similarly, levels of metallothionein in the kidney were significantly higher when cadmium was administered during the dark phase. A trend toward higher metallothionein levels in the liver during the dark phase was also observed, but this trend was not statistically significant.     

亚硒酸钠对镉和汞肝肾氧化损伤影响的实验研究

目的:观察一次染镉和汞对大鼠肝、肾组织氧化损伤作用,探讨亚硒酸钠预处理对镉和汞氧化损伤的影响。方法:Wister大鼠48只,随机分成6组,每组8只,第1组为染镉实验对照组,第2组为单纯染镉组,第3组为亚硒酸钠预处理组,第4组为染汞实验对照组,第5组为单纯染汞组,第6组为亚硒酸钠预处理干预组。第1、4组大鼠先腹腔注射生理盐水,2 h后皮下注射生理盐水。第2组大鼠先腹腔注射生理盐水,2 h后皮下注射35μmol/kg氯化镉溶液。第3组大鼠先腹腔注射10μmol/kg亚硒酸钠溶液,2 h后皮下注射35μmol/kg氯化镉溶液。第5组大鼠先腹腔注射生理盐水,2 h后皮下注射2.5 mg/kg HgCl2溶液,第6组大鼠先腹腔注射20μmol/kg亚硒酸钠溶液,2 h后皮下注射2.5 mg/kg HgCl2溶液。染毒24 h后测定肝、肾皮质镉或汞、谷胱甘肽、丙二醛含量和谷胱甘肽过氧化物酶活性。结果:与对照组比较,单纯染镉组大鼠肝GSH、MDA含量显著升高,GSH—Px活性显著下降。Na2SeO3预处理组肝、肾皮质GSH和镉含量显著降低,肝脏GSH—Px活性及肾皮质MDA含量显著升高。单纯染汞组大鼠肝、肾皮质及尿汞含量均显著高于对照组。单纯染汞组肝MDA含量显著高于对照组,GSH含量和GSH—Px活性显著低于对照组。Na2SeO3预处理组的肝脏GSH含量和GSH—Px活性均较单纯染汞组升高,有显著性差异。单纯染汞组肾皮质MDA含量显著高于对照组,GSH含量和GSH—Px活性显著降低。Na2SeO3预处理组中肾皮质MDA含量低于单纯染汞组,GSH—Px含量高于单纯染汞组。结论:给大鼠一次染镉和汞,可以对肝和肾脏产生明显的氧化损伤作用。亚硒酸钠对急性染镉和汞所致肝肾损伤具有一定的拮抗作用,其机制可能与增加内源性GSH、使GSH—Px活性增强以及清除自由基能力提高有关。     

镉急性染毒对兔心功能影响研究

目的：研究镉急性染毒对心功能的影响。方法：用一细导管从颈总动脉插入左心室内，观察心功能的改变，并取动物血液和器官标本进行镉含量测定。结果：静注氯化镉７．５ｍｇ／ｋｇ体重，所观察的指标均有明显改变，左室收缩期最高压（ｐｅａｋ）降低。左室舒张期最低压（ＥＤＰ）增大，左室内压上升最大变化率（＋ｄｐ／ｄｔｍａｘ）降低，左室内压下降最大变化率（－ｄｔ／ｄｐｍａｘ）升高，心室内压在５．３２ｋＰａ时心肌纤维缩短的速度（Ｖｃｅ５．３２）下降。静脉注射氯化镉１０ｍｇ／ｋｇ后，动物死亡。镉测定结果：血液１７０μｍｏｌ／Ｌ，肝，肾，心，脑分别为２５０，２５０，１１０，３０μｇ／ｇ干重。结论：急性镉染毒明显抑制心功能。     

经口摄入高硒镉对大鼠肝,肾组织中镉,锌,铜含量影响的研究

选用4周龄SD大鼠,经口染毒高硒(5.68mg/kg)、富硒(0.73mg/kg)和(或)高镉(33.3mg/kg)12周,并分别在实验的第3、6、9、12周末各处死一批大鼠,研究经口摄入高硒高镉对大鼠肝、肾组织中镉、锌、铜含量的影响。结果表明:同时摄入高硒高镉组大鼠体内镉蓄积明显低于单纯摄入高镉组;对单独摄入高硒、高镉所诱导的大鼠肝脏锌含量增加表现为拮抗作用;对单独摄入高硒所致大鼠肾脏锌含量降低的影响表现为拮抗作用;对单独摄入高硒、高镉所致大鼠肾脏铜含量增加的影响表现为协同作用。