环境和饲料中的镉对畜禽的毒性研究进展

大量研究表明,饲料中的镉超标会对畜禽机体的肾脏、骨骼等部位产生一系列的毒害作用。从环境、饲料和动物体中镉的来源入手,综述了镉在动物体内的代谢,镉对畜禽的毒性及机理,镉与其它元素的交互关系,畜禽镉中毒的防治对策,并对这一研究领域的发展趋势进行了讨论。     

镉对大鼠雌性性腺与肾脏毒性比较研究

目的 探讨镉对大鼠的雌性性腺毒性；比较镉对大鼠雌性性腺和肾脏毒性。方法 雌性大鼠腹腔注射CdCl2（含Cd^2 ，0．25，0．5，1．0mg/kg体重）亚慢性染毒，观察镉对大鼠雌性性腺与肾脏毒性。结果 同肾脏一样，卵巢镉含量显性增高，高、中剂量染毒组大鼠动情周期、动情间期均比对照组显延长，闭锁卵泡构成比也明显高于对照组；却未出现明显肾脏病理改变和尿β2－微球蛋白升高。结论 镉具有明显的雌性性腺毒性，同样条件下，肾脏并未出现镉毒性损害的特征性改变。     

镉肾脏毒作用的研究近况

本文对目前研究较多的镉肾脏毒作用的病理改变，致病机理，早期监测指标及剂量－反应关系四方面作一综述报道。镉肾脏毒性的主要病变部位是肾近曲小管，严重时可累及肾小球，镉肾脏毒作用机理是一综合过程，其中金属硫蛋白在镉肾脏毒作用机理中起着重要作用，尿β２－ＭＧ尿ＴＢＰ及尿ＮＡＧ是镉肾脏损害主要的早期监测指标；镉接触与肾脏损害间存在一定的剂量－反应关系，但还有待进一步探讨。     

镉诱导猪肾近曲小管上皮细胞LLC-PK1的凋亡

镉(Cd)是环境和食物链中主要的的重金属污染物之一。动物实验和人群流行病学研究均表明镉可产生严重的毒性效应。大剂量、急性镉中毒可致肝、肺和睾九的损伤。而长期低剂量接触镉主要引起以近曲小管损害为主要特征的肾脏损害。体内动物实验研究表明，镉引起肾细胞凋亡是镉肾毒性的分子机制之一。近年来体外实验研究镉诱导肾细胞凋亡的分子毒理学机制已取得一定的进展。但尚未完全清楚。本研究选用猪肾近曲小管上皮细胞(LLC-PK1)为实验对象，观察了氯化镉对该细胞的毒性效应，以及诱导LLCPK1细胞凋亡的作用与细胞周期变化的影响，为进一步阐明镉诱导肾细胞凋亡及其分子机制提供依据。     

苯乙烯亚慢性肾脏毒性实验研究

苯乙烯亚慢性肾脏毒性实验研究李汇华，乔赐彬，林瑞存，张秀玲，乔建伟，姚庆强苯乙烯是一种神经毒剂，主要损害神经系统，其次为血液系统和肝脏［１］。有关苯乙烯肾脏毒性的研究报道甚少。近年来，药代动力学研究表明，苯乙烯吸入或灌胃染毒后肾脏中含量最高，肾脏可能...     

镉引起细胞凋亡

镉是重要的工业和环境污染物，主要来源于冶炼厂、电镀、蓄电池、采矿等工业中。人类对镉的研究已有一百多年的历史，早期主要对镉的急性毒作用的研究，而后慢性毒作用的研究较为深入。长期低剂量接触镉主要引起以近曲小管损害为主要特征的肾脏损害［１］。镉接触与生殖损害［２］、肿瘤和衰老等有一定的关系［３，４］。由于镉在工业上应用广泛，在土壤、植物中有蓄积作用，在人体的半衰期达１０－３０年，因此镉显然存在着对人类潜在的危害。再加上镉慢性毒作用如致癌、致衰老等机制尚未清楚。所以，人类持续对镉的毒性进行研究。进入分子…     

吸烟接触镉对糖尿病患者肾功能的影响

糖尿病肾病是糖尿病的主要并发症之一，严重威胁糖尿病患者的健康。肾脏也是镉（Cd）毒性作用的主要靶器官。近年来有研究发现，糖尿病可能对镉的肾脏毒性易感。吸烟是环境中接触镉的主要方式。烟草通常蓄积有镉，吸烟者每天通过呼吸道吸收约1～3μg／d。我们选择上海市某社区中的糖尿病患者作为研究对象，研究镉接触对糖尿病患者肾功能的影响。     

镉对小鼠睾丸的毒作用

为探讨镉对睾丸组织的毒性及其作用机制,研究了腹腔注射氯化镉对小鼠睾丸系数、睾丸脂质过氧化物（ＬＰＯ）值、血清乳酸脱氢酶（ＬＤＨ）活性、睾丸中镉、钙、铁等浓度及镉对雄性小鼠生殖能力的影响。结果提示染镉组小鼠上述各指标与对照组相比差异均有显著性,表明镉对小鼠睾丸有明显毒性,脂质过氧化作用及其所致的组织损伤和出血性炎症可能是镉对睾丸损害的重要病理过程。     

锌镉毒性研究进展

目的:总结近年来国内外对于锌镉毒性的研究进展。方法:搜集、分析国内外相关文献。结果:动物实验研究表明:镉对鼠类的生殖系统、骨骼发育以及听力系统均有毒作用,镉可引起鱼类卵壳破裂,锌能拮抗镉对动物的毒性作用。人体研究表明:锌不仅能提高人体免疫力而且能拮抗镉对人体的毒性作用,镉对人体的健康效应主要表现在对人体呼吸、泌尿、消化、运动、生殖系统等方面的毒性作用。结论:锌镉相互拮抗,锌可预防和减轻镉中毒的危害。     

镉——危及人体健康的有毒元素（综述）

镉是人体不需要的一种有毒的重金属元素，它对人体的肝、肾、骨骼、脑均可产生毒性，并可致癌，但人们对它的毒性机制并不十分了解，本文通过查阅一些文献上公开发表的关于镉的毒性文章，按镉的急性毒性作用，镉的骨毒作用、肾毒性、神经毒作用、致癌性给予综述，供同行参考。     

镉对钙代谢的影响及相关机制研究进展

镉作用于机体的肾脏、骨骼等部位可产生一系列毒性作用。钙代谢紊乱是镉毒性的一个重要方面,主要表现为肠钙吸收减少,尿钙排泄增加,机体处于负钙平衡,骨软化和骨质疏松。镉影响钙代谢有两种可能机制：一是直接机制,即镉通过与钙竞争直接抑制细胞对钙的主动转运;二是问接机制,镉通过损伤肾脏功能导致1,25(OH)2D3合成下降而间接影响钙代谢。进一步揭示镉如何直接抑制钙离子进入细胞和钙结合蛋白对钙的转运,明确低水平镉暴露人群肾脏1,25(OH)2D3的合成是否受影响。从分子生物学水平阐明镉影响钙代谢的机制,应是今后的研究方向。     

镉肾脏毒性生物标志物的研究进展

镉暴露会导致人体肾脏、肝脏、肺脏和心血管等多种器官毒性,其中,肾脏是镉毒性的主要靶器官。随着镉暴露人群的增加,镉毒性的早期监测愈显重要。镉效应生物标志物是一类可供客观测定的生理、生化指标。在镉暴露过程中,镉效应生物标志物的改变能敏感地反映出镉对机体损伤的程度及部位。该文就镉肾脏毒性监测中常用的效应生物标志物的优缺点作一...     

光化学搪瓷消毒产品的毒性试验研究

结果表明：光化学消毒产品中有害金属元毒锑、镉分别为０．０１ｍｇ／Ｌ和０．０２ｍｇ／Ｌ,铅未检出。ＬＰＯ体内试验,使用组和对照组体内脂质过氧化物含量无显著差异,ｔ＝０．３４８１,Ｐ＞０．０５。Ａｍｅｓ试验结果是光化学消毒的饮用水无菌株基因突变作用,Ａｍｅｓ试验结果阴性。在小鼠骨髓ＰＣＥ微核试验中,光化学消毒水对小鼠无致骨髓ＰＣＥ微核发生率升高的作用。小鼠精子畸变试验,光化学消毒水无致精子畸形作用。提示光化学消毒产品对人无毒无害,其安全性较好,其应用前景十分广阔     

Effect of cadmium administration on intestinal calcium absorption and vitamin D-dependent calcium-binding protein

The effects of cadmium on intestinal calcium absorption and calcium-binding protein (CaBP) were investigated in chicks by means of the in situ ligated duodenal loop technique. Dietary cadmium, administered in the feed or by gastric intubation, resulted in significant declines in intestinal calcium absorption and mucosal calcium-binding protein concentrations. Cadmium chloride injected directly into the ligated loop of naive chicks also diminished calcium absorption and CaBP concentrations in an apparently dose-response related fashion. No adverse effects of cadmium administration on either the 25- or 1α-hydroxylation reactions of vitamin D were observed. While the general effect of cadmium administration was a reduction in intestinal calcium absorption, plasma calcium levels were consistently elevated in Cd-treated chicks, with the exception of those also maintained on diets low in Ca. The results indicate that cadmium toxicity exerts at least two effects on Ca metabolism, one at the intestinal level and another at the level of the bone, kidney, or both.     

The effects of low environmental cadmium exposure on bone density

Recent epidemiological data indicate that low environmental exposure to cadmium, as shown by cadmium body burden (Cd-U), is associated with renal dysfunction as well as an increased risk of cadmium-induced bone disorders. The present study was designed to assess the effects of low environmental cadmium exposure, at the level sufficient to induce kidney damage, on bone metabolism and mineral density (BMD). The project was conducted in the area contaminated with cadmium, nearby a zinc smelter located in the region of Poland where heavy industry prevails. The study population comprised 170 women (mean age=39.7; 18-70 years) and 100 men (mean age=31.9; 18-76 years). Urinary and blood cadmium and the markers of renal tubular dysfunction (β₂M-U RBP, NAG), glomerular dysfunction (Alb-U and β₂M-S) and bone metabolism markers (BAP-S, CTX-S) as well as forearm BMD, were measured. The results of this study based on simple dose-effect analysis showed the relationship between increasing cadmium concentrations and an increased excretion of renal dysfunction markers and decreasing bone density. However, the results of the multivariate analysis did not indicate the association between exposure to cadmium and decrease in bone density. They showed that the most important factors that have impact on bone density are body weight and age in the female subjects and body weight and calcium excretion in males. Our investigation revealed that the excretion of low molecular weight proteins occurred at a lower level of cadmium exposure than the possible loss of bone mass. It seems that renal tubular markers are the most sensitive and significant indicators of early health effects of cadmium intoxication in the general population. The correlation of urinary cadmium concentration with markers of kidney dysfunction was observed in the absence of significant correlations with bone effects. Our findings did not indicate any effects of environmental cadmium exposure on bone density.     

Cadmium-induced effects on bone in a population-based study of women

High cadmium exposure is known to cause bone damage, but the association between low-level cadmium exposure and osteoporosis remains to be clarified. Using a population-based women's health survey in southern Sweden [Women's Health in the Lund Area (WHILA) ] with no known historical cadmium contamination, we investigated cadmium-related effects on bone in 820 women (53-64 years of age) . We measured cadmium in blood and urine and lead in blood, an array of markers of bone metabolism, and forearm bone mineral density (BMD) . Associations were evaluated in multiple linear regression analysis including information on the possible confounders or effect modifiers: weight, menopausal status, use of hormone replacement therapy, age at menarche, alcohol consumption, smoking history, and physical activity. Median urinary cadmium was 0.52 microg/L adjusted to density (0.67 microg/g creatinine) . After multivariate adjustment, BMD, parathyroid hormone, and urinary deoxypyridinoline (U-DPD) were adversely associated with concentrations of urinary cadmium (p < 0.05) in all subjects. These associations persisted in the group of never-smokers, which had the lowest cadmium exposure (mainly dietary) . For U-DPD, there was a significant interaction between cadmium and menopause (p = 0.022) . Our results suggest negative effects of low-level cadmium exposure on bone, possibly exerted via increased bone resorption, which seemed to be intensified after menopause. Based on the prevalence of osteoporosis and the low level of exposure, the observed effects, although slight, should be considered as early signals of potentially more adverse health effects. Key words: biochemical bone markers, bone mineral density, cadmium, lead, osteoporosis, women.     

Assessing the risk of metal mixtures in contaminated sediments on Chironomus riparius based on cytosolic accumulation

Sediments usually contain mixtures of trace metals introduced via natural geochemical processes and anthropogenic activities. Kinetics and effects of these metals are strongly dependent both on the composition of the mixture and on the physico-chemical characteristics of the sediment. Relating effects to metal concentration may consequently be advised. However, total accumulation may be a poor predictor of metal toxicity for Chironomus riparius exposed to contaminated field sediments. As an alternative, we proposed to relate effects on Chironomus growth with cytosolic metal accumulation, measured in larvae after a short exposure period. Dose–response relationships were derived for zinc, copper, and cadmium through single-metal exposure data analysed with toxicokinetics and toxicodynamics models. They permitted, on the basis of cytosolic accumulation measures, to predict successfully the effects of mixtures of cadmium, zinc, and copper on the growth of larvae exposed to spiked sediments, as well as to field sediments in which zinc and copper were assumed to be predominant.     

Airborne cadmium and carcinogenesis of the respiratory tract

Exposure to airborne cadmium occurs mainly at the workplace. Significant exposure also occurs through smoking. Results of a recent epidemiologic study suggest that occupational inhalation of cadmium is connected with an increased lung cancer risk. This finding corroborates the high lung cancer incidence found among rats after chronic low-level exposure to cadmium chloride aerosols. Differences in the tumor sites, exposure conditions, and the pulmonary metabolism of cadmium between rodents and man make it difficult to extrapolate quantitatively from rats to humans. In contrast to the workplace, concentrations of cadmium in ambient air are very low, and the risk of lung cancer is probably very low, even for people living close to cadmium-emitting industries. The chemical form of inhaled cadmium appears to be important. While cadmium oxide and cadmium chloride seem to be equally toxic, cadmium sulfide exhibits a lower acute pulmonary toxicity. However, whether this is also true for carcinogenic effects is not known. Additional long-term inhalation studies with animals and further evaluation of epidemiologic studies are necessary to answer questions about the carcinogenic potency of cadmium compounds of different chemical form. As long as such results are not available, it is prudent to regard all cadmium compounds as having a carcinogenic potential.