镉致大鼠慢性肾损伤模型的探讨

目的 探讨复制镉致大鼠慢性肾损伤模型的最佳染毒方案.方法 按正交设计表L9(34),对雄性SD大鼠腹腔注射镉(CdCl2)和巯基乙醇(ME)复合物,Cd剂量分别为3、6、12 μmol/kg及ME剂量分别为60、120、240 μmol/kg,染毒1～5 d,分别于染毒后第7、21、35天处死动物.以肾镉、尿β2-微球蛋白(β2-MG)、血镉及肾脏病理改变为指标,优选出模型复制方案.结果 尿β2-MG水平:实验组3第28天为(70.684±18.622)μg/g Cr,实验组8第35天为(70.304±9.776)μg/g Cr,均显著高于对照组水平(P＜0.05);尿白蛋白水平:实验组6第14天为(2.787±0.855)μmol/mol Cr,显著高于对照组水平(P＜0.05);尿镉水平:实验组3、4、8与对照组比较均显著性升高(P＜0.05或P＜0.01);肾镉水平:实验组6、8、9分别为(9.930±6.482)、(16.179±2.256)、(29.003±7.050)μg/g,均显著高于对照组水平(P＜0.01);血镉水平:实验组6、8分别为(1. 319±0.458)、(1.254±0.089)μg/L,均显著高于对照组水平(P＜0.01或P＜0.05);病理检查:实验组6、8、9动物出现肾小管空泡变性.结论 Cd 3.0 μmol/kg+ME 60.0μmol/kg混合液,腹腔注射,连续5 d,是复制大鼠肾功能性损伤未出现病理性损伤模型的最佳方案.     

镉致作业工人肾功能损害可逆性研究初探

[目的 ]观察接受依地酸二钠 (EDTA)治疗慢性镉接触工人尿镉和肾功能改变 ,以探讨镉接触致肾损害的可逆性。 [方法 ]收集 1986年以来某冶炼厂接受EDTA治疗的 17名镉接触工人 (其中男 14名 ,女 3名 )每年治疗前后尿镉和尿 β2 微球蛋白 (β2 MG)的记录 ,分析其变化的情况。 [结果 ]尿 β2 MG一直异常 (≥ 0 8mg/g·Cr)或由正常转为异常的工人 ,尿镉平均水平基本高于 10 μg/g·Cr ,治疗期间尿 β2 MG一直正常或出现异常又转为正常的工人 ,尿镉平均水平在 10μg/g·Cr以下 ;整个治疗过程中 ,不论尿镉升高或降低 ,尿 β2 MG异常率均有所上升 ;随着镉接触终止时间的延长 ,尿 β2 MG没有下降 ;尿镉水平低于 10 μg/gCr ,肾损害可以恢复 ,反之 ,则不可逆。[结论 ]尿镉的水平是影响镉接触工人肾功能变化的主要因素 ,EDTA对镉接触工人肾功能损害没有明显疗效。     

含镉粉尘治理前后工人尿镉与血镉水平分析

目的 分析某锌粉加工厂含镉粉尘治理前后作业工人尿镉、血镉和尿β2-微球蛋白的变化.方法 对锌粉加工厂粉尘进行治理,对粉尘治理前后84名镉作业工人尿镉、血镉、β2-微球蛋白水平进行自身对照分析.结果 治理后,作业场所锌尘几何均数由3.38mg/m3降至2.22mg/m3,差异有统计学意义(P＜0.01).治理前调查对象的血镉、尿镉几何均数浓度[血镉(2.19±1.19)μg/L,尿镉(1.96±0.74)μg/gCr]明显高于治理后1年[(1.63±0.83)μg/L,(1.25±0.83)μg/g Cr]和治理后2年[(1.36±0.95)μg/L,(0.94±0.72)μg/g Cr],差异有统计学意义(P＜0.01).治理前及治理后1年、2年接触工人尿镉与血镉浓度作相关分析,r=0.466,差异有统计学意义(P＜0.01).结论 粉尘治理能降低低浓度镉作业工人的血镉、尿镉水平,对防止镉中毒效果明显.     

镉致人体健康损害的环境流行病学研究

[目的 ]通过对环境镉接触人群的流行病学调查 ,探讨和评价环境镉接触和所致人体健康不良效应间的剂量 效应关系。 [方法 ]选择居住在污染区 3 5年以上并以当地自产米为主食的居民为调查对象 ,通过问卷和体检收集其既往接触史及健康状况 ,同时采集血、尿等样本 ,以尿镉、血镉和估计镉摄入量作为镉接触生物标志物 ;以尿 β2 微球蛋白、视黄醇结合蛋白、NAG酶和白蛋白 (肾损害 )、骨密度 (骨损害 )和性激素及前列腺特异抗原 (男性生殖系统损害 )为损害效应生物标志物。 [结果 ]不同污染地区调查对象的体内镉负荷与环境镉污染程度呈正相关 ,且各地区间调查对象尿镉水平差异具有显著性 (P <0 0 1)。值得注意的是 ,不同性别之间的尿镉水平存在明显的差别 ,女性高于男性。对照组尿镉均低于 5 μg/L ,低接触组大多小于 5 μg/L ,但高接触组大多大于 5 μg/L ,而且大多数尿镉异常增高者也在该组中。高污染区居民尿中 β2 微球蛋白、视黄醇结合蛋白、NAG酶和白蛋白水平均显著高于对照区 ,且与镉接触 (尿镉 )有着明显的剂量 效应关系。研究同时提示镉引起肾脏损害的广泛程度与镉接触的水平有关 :低剂量时仅累及 1～ 2个肾小管效应生物标志物变化 ,而高剂量时则引起 2个以上肾小管效应生物标志物的变化。同时也     

职业性镉接触女性尿镉含量调查

为了解职业性镉接触女性的尿镉含量,选取2012年9月至2013年6月进行体检的某镉-镍电池生产厂的镉作业女工353人为暴露组,未接触有害因素且体检未见异常的女工286人为对照组,对两组女工进行尿镉含量检测。结果显示,暴露组女工尿镉含量[(9.8±6.1)μg/g Cr]高于对照组[(3.1±1.5)μg/g Cr],差异有统计学意义(P0.01);暴露组尿镉含量随着工龄的增加而升高,工龄大于5年的女工尿镉含量随年龄增加而升高。提示镉接触可引起体内尿镉含量升高,且随着工龄的增加有升高趋势。     

稳定同位素镉-112对大鼠子代发育的影响

目的 探讨雌性SD大鼠给予低浓度富集稳定同位素镉-112(112Cd)后对子代生长发育的影响.方法 40只健康雌性SD大鼠按体重随机分为对照组和染镉组,每组20只.分别皮下注射去离子水(对照组)以及112Cd40μg/(kg·d)(染镉组),每天1次.第24天上午采集血、尿标本,采用原子吸收光谱法检测镉水平.当天下午与健康雄性SD大鼠同笼交配,交配期及孕期雌鼠继续染毒.妊娠第20天再次采集血、尿标本后剖杀雌鼠.取脐血检测血镉水平;取子宫及胎鼠检测母鼠生殖力及胎鼠生长发育指标;取母鼠及胎鼠部分脏器和胎盘采用电感耦合等离子体质谱法检测脏器镉水平;剩余部分脏器和胎盘包埋固定后观察病理学改变;去除内脏的胎鼠经固定染色后检测骨骼改变.结果 染镉组第24天和孕第20天雌鼠血镉含量明显升高,分别为(64.51±17.07)和(80.65±9.72) μg/L,与对照组[(0.94±0.71)和(0.86±0.64) μg/L]较,差异均有统计学意义(P＜0.01).孕第20天雌鼠尿镉[(2.72±2.50) μg/g Cr]明显升高,与对照组[(1.09±0.74)μg/gCr]比较,差异有统计学意义(P＜0.05).染镉组脐血镉[(1.45±1.08) μg/L]明显高于对照组[(0.12±0.08) μg/L],差异有统计学意义(P＜0.01).染镉组雌鼠及胎鼠的脑、心脏、肝脏、肾脏等脏器和胎盘镉水平分别为(63.19±63.92)、(1.51±1.82)、(124.84±74.76)、(87.24±17.91)、(0.023±0.012)、(0.037±0.019)、(0.065±0.020)、(0.036±0.019)和(5.072±1.127) μg/g,明显高于对照组[(0.02±0.01)、(0.01±0.01)、(0.02±0.01)、(0.07±0.02)、(0.007±0.006)、(0.014±0.016)、(0.005±0.003)、(0.020±0.013)和(0.001±0.001) μg/g],差异均有统计学意义(P＜0.01).染镉组第24天和孕第20天雌鼠尿视黄醇结合蛋白含量分别为(13.70±8.13)和(15.04±9.58)g/mol Cr,与对照组[(7.29±6.18)和(6.71±4.53)g/molCr]相比明显升高,差异均有统计学意义(P＜0.05或P＜0.01).染镉组孕第20天雌鼠子宫连胎重量[(59.73±11.87) g]、胎鼠重量[(3.66±0.70)g]以及胎盘重量[(0.51±0.08)g]均降低,活胎率下降,吸收胎率升高,与对照组[(84.27±22.99)、(4.02±0.71)和(0.54±0.09)g]比较,差异均有统计学意义(P＜0.01).染镉组雌鼠肝脏、肾脏的病理改变率明显高于对照组(P＜0.01).染镉组胎鼠较对照组骨骼发育迟缓,主要表现为胸骨骨化不全、胸骨及掌骨的未骨化等(P＜0.01)..结论 低浓度持续镉暴露可以通过胎盘屏障影响胎鼠生长发育.     

镉接触工人尿镉血镉与尿β_2MG RPB含量的跟踪研究

目的:跟踪调查镉接触工人停止接触镉后尿镉、血镉的变化及肾功能损害情况,寻找镉接触指标与肾功能损害指标的关系,初步探讨职业性镉引起的肾功能特点及规律。方法:选择深圳某镍镉电池厂29名镉中毒观察对象(尿镉连续2次超过5μmol/mol肌酐)为研究对象,分析尿镉、血镉含量与尿β2-微球蛋白(β2MG)、尿视黄醇结合蛋白(RPB)排出量的关系;并通过跟踪研究他们在停止接触镉1年后,接触指标(尿镉、血镉)及肾功能损害指标的变化的规律。结果:镉中毒观察对象在停止接触1年后,尿镉由(7.16±2.81)μmol/mol肌酐下降至(7.03±2.84)μmol/mol肌酐,尿镉含量下降没有显著性差异(P>0.05);血镉明显下降,由(5.8±1.81)μg/L下降至(3.5±1.24)μg/L,有显著性差异(P<0.01);尿β2-微球蛋白含量(中位数)由1.19μmol/mol肌酐上升至1.21μmol/mol肌酐,尿视黄醇结合蛋白含量(中位数)由0.39μmol/mol肌酐上升至0.42μmol/mol肌酐,统计学秩和检验结果显示均没有显著性差异(P>0.05)。尿镉与血镉存在明显的线性正相关,相关系数(r)为0.721,(P<0.01),回归分析得出的方程为:y=1.132x+3.656,(y代表尿镉,x代表血镉)。尿镉、血镉与尿β2-微球蛋白含量的相关系数分别为0.321,0.346,统计学上均没有显著性相关(P>0.05)。结论:职业性镉中毒观察对象停止接触镉1年后,血镉明显下降,尿镉含量下降不明显,尿镉与血镉存在线性正相关,尿β2-微球蛋白、尿视黄醇结合蛋白含量总体水平变化不显著,但有个别仍可以出现肾功能异常,镉对肾功能损害存在明显个体差异性。     

环境镉污染暴露人群尿NAG和尿Cd-MT的变化

为探讨环境镉暴露人群尿镉与肾脏损害之间的关系,观察90名居住在含镉污水灌溉区30年以上的居民尿镉、尿NAG、尿Cd-MT和尿肌酐的变化.结果显示,尿镉、尿NAG和尿Cd-MT分别为5.17±2.40μg/g.cre、12.74±2.14U/g.cre和6.42±2.35μg/g.cre;尿镉、尿NAG、尿Cd-MT之间密切相关;尿镉升高1.96倍和5.49倍时,尿NAG分别升高0.58和0.66倍,而尿Cd-MT升高1.12倍和2.24倍.提示尿Cd-MT可作为慢性镉接触造成肾损害的一个敏感而特异的早期监测指标.     

镉接触工人尿镉含量水平影响因素分析

目的分析镉接触工人尿镉含量的影响因素。方法选取深圳市3家镍-镉电池厂镉接触工人375名为接触组,另选取153名未接触镉的上岗前工人作为对照组,分析两组人群的尿镉含量水平,同时对3间镍-镉电池厂工作场所进行职业卫生学调查。结果工作场所空气中氧化镉短时间接触浓度平均为0.027 mg/m3,超标率为37.0%;接触组尿镉含量为(3.36±2.43)μmol/molCr,明显高于对照组[(2.09±1.74)μmol/molCr](P<0.01),接触组女性尿镉含量为(3.68±2.92)μmol/molCr,明显高于男性接触组[(2.76±2.21)μmol/molCr](P<0.01);高浓度组尿镉含量[(3.79±3.41)μmol/molCr]明显高于低浓度组[(2.82±2.12)μmol/molCr](P<0.01),高浓度接触组尿镉异常率(21.9%)也高于低浓度接触组(7.7%)(P<0.01);多元线性回归分析结果显示,工龄、工种(接触浓度)、年龄、性别与尿镉含量的相关系数依次为0.559、0.266、0.233和0.092(均P<0.05)。结论工龄增加、工作场所氧化镉浓度超标是尿镉增高的主要危险因素,降低氧化镉浓度至职业接触限值以下和减少接触时间是预防慢性镉中毒的关键。     

金属硫蛋白和职业性镉接触

为了解金属硫蛋白(MT)是否可作为预防镉中毒性肾病的生物学监测指标,本文研究了(1)镉的累计时间加权接触量(cumulative time weighted exposure)(μg/m~3年)与血清或尿MT的关系,(2)肾功能与血清及尿MT的关系,(3)血、尿镉与血清及尿MT的关系。     

Reduction in cadmium teratogenesis by prior cadmium exposure

The administration of cadmium 24–48 hr prior to an optimal teratogenic dose reduces both the number and severity of congenital malformations in hamster embryos. Intraperitoneal administration is more effective in inducing this protective effect than is the subcutaneous route. Oral administration of cadmium at the same pretreatment intervals does not seem to afford any protection. It is suggested that this protection is due to the induction of maternal synthesis of a metal-binding protein, possibly metallothionein. The significance of this protective induction as it relates to the possible role of cadmium in human malformations as well as teratogenic testing is discussed.     

Carcinogenicity of cadmium

Cadmium has been thought to be carcinogenic for these ten years. The present author reviewed 98 papers on its carcinogenicity. Ten papers describing epidemiological studies on cadmium workers, re-evaluated by the present author, do not derive a solid conclusion that cadmium is carcinogenic. However, there still exists a certain probability that cadmium is a weak carcinogenic substance in the human, because of some data on chromosomal aberrations in cadmium workers, tumorigenesis at the site of cadmium injection in animals, and Leydig cell tumor formation in animals given subcutaneous injections of cadmium.     

Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan

Long-term exposure to cadmium (Cd) causes renal damage in the general population. The maximum allowable urinary Cd concentration, which was calculated from our previous study performed in a Cd-polluted area, was almost the same as the mean urinary Cd concentration of people living in nonpolluted areas. We assessed whether environmental Cd exposure is related to renal dysfunction of people in nonpolluted areas in Japan. Blood and urine samples were collected from 2753 subjects (1105 men and 1648 women) ages over 50 years old in three nonpolluted areas. Blood was analyzed for Cd and urine was analyzed for Cd, total protein, beta(2)-microglobulin (beta(2)-mg), and N-acetyl-beta-D-glucosaminidase (NAG). Cd in blood or urine was employed as indicators of internal dose; and urinary total protein, beta(2)-mg, and NAG were used as an indicator of renal dysfunction. Multiple regression analysis and logistic regression analysis were performed to clarify the dose-effect and dose-response relationship between blood or urinary Cd concentration and indicators of renal dysfunction. Multiple regression analysis demonstrated a significant dose-effect relationship between Cd in blood and urine and indicators of renal dysfunction. Logistic regression analysis also showed that the probability that individual subjects would have abnormal values of the renal variables was significantly related to Cd in blood and urine.     

Effect of Chlorella vulgaris intake on cadmium detoxification in rats fed cadmium

The aim of this study was to investigate if dietary Chlorella vulgaris (chlorella) intake would be effective on cadmium (Cd) detoxification in rats fed dietary Cd. Fourteen-week old male Sprague-Dawley (SD) rats weighing 415.0 ± 1.6 g were randomly divided into two groups and fed slightly modified American Institute of Nutrition-93 Growing (AIN-93G) diet without (n=10) or with (n=40) dietary Cd (200 ppm) for 8 weeks. To confirm alteration by dietary Cd intake, twenty rats fed AIN-93G diet without (n=10) and with (n=10) dietary Cd were sacrificed and compared. Other thirty rats were randomly blocked into three groups and fed slightly modified AIN-93G diets replacing 0 (n=10), 5 (n=10) or 10% (n=10) chlorella of total kg diet for 4 weeks. Daily food intake, body weight change, body weight gain/calorie intake, organ weight (liver, spleen, and kidney), perirenal fat pad and epididymal fat pad weights were measured. To examine Cd detoxification, urinary Cd excretion and metallothonein (MT) concentrations in kidney and intestine were measured. Food intake, calorie intake, body weight change, body weight gain/calorie intake, organ weight and fat pad weights were decreased by dietary Cd intake. Urinary Cd excretion and MT concentrations in kidney and small intestine were increased by dietary Cd. After given Cd containing diet, food intake, calorie intake, body weight change, body weight gain/calorie intake, organ weights and fat pad weights were not influenced by dietary chlorella intake. Renal MT synthesis tended to be higher in a dose-dependent manner, but not significantly. And chlorella intake did not significantly facilitate renal and intestinal MT synthesis and urinary Cd excretion. These findings suggest that, after stopping cadmium supply, chlorella supplementation, regardless of its percentage, might not improve cadmium detoxification from the body in growing rats.