汞作业工人尿N-乙酰-β-D-氨基葡萄糖苷酶活性测定

目的 探讨汞接触工人尿N－乙酰－β－D氨基葡萄糖苷酶（NAG）活性。方法 对某灯泡厂接触不同浓度汞的77名工人进行尿NAG活性测定。并对车间空气汞浓度，尿汞含量，汞作业工龄的关系进行相关分析。结果 接汞组尿NAG活性明显高于对照组（P＜0．005）。尿NAG活性随环境空气汞浓度的增高而逐渐升高，并具有明显的剂量反应关系。但汞作业工龄与NAG之间无显著性（P＞0．05）。结论 在低浓度汞接触时，NAG活性增高较尿汞异常出现得早。建议将尿NAG活性作为汞接触人群健康监护指标之一，在职业健康监护体检中与尿汞同时进行检测。     

职业性铅接触尿N-乙酰-β-D-氨基葡萄糖苷酶活性的变化

目的研究铅接触者尿N-乙酰-β-D.氨基葡萄糖苷酶(NAG)活性变化。方法对某蓄电池厂135名铅作业工人及52名非接触者进行了尿铅含量及尿NAG活性测定。结果接触组工人尿NAG[(13.91±1.62)U/gCr]活性明显高于对照组[(7.82±1.55)U/gCr]。随着尿铅水平升高,尿NAG活性有升高趋势。接铅1～3年组尿NAG活性开始上升,7年以上明显增加。结论尿NAG活性似可作为铅致肾损害的早期生物标志物。     

镉接触工人尿N—乙酰—β—D氨基葡萄苷酶结果分析

对某锌品厂接触不同水平镉的两组工人进行镉摄入量、尿镉、尿Ｎ－乙酰－β－Ｄ氨基葡萄糖苷酶（ＮＡＧ）的调查分析。结果显示：接触组工人镉摄入量、尿镉、尿ＮＡＧ水平显著高于对照组。尿ＮＡＧ的水平随着镉摄入量、尿镉排泄的增高而升高,并存在着明显的剂量－反应关系。当镉摄入量大于５０ｍｇ或尿镉的水平为ｕｇ／ｇＧｒ时,尿中ＮＡＧ就显著增加。说明尿ＮＡＧ活性可作为镉接触肾损害的早期监测指标,如这项指标经实践验证,稳     

尿中NAG、γ－GT酶对镉作业工人肾损害的诊断意义

本文调查了我省某矿务局６８名镉作业工人尿中ＮＡＧ、γ－ＧＴ酶的变化。结果发现，按尿蛋白和尿β＿２－ＭＧ水平对肾损害程度分级确定为无肾损害的镉作业工人体内尿中ＮＡＧ、γ－ＧＴ酶活性明显出现异常。提示，尿中ＮＡＧ和γ－ＧＴ酶活性的变化，是反映镉作业工人肾损害的早期灵敏指标。     

尿镉与肾功能异常指标尿β2—M和NAG关系研究

目的：探讨尿镉与肾功能异常指标尿β2－M及NAG酶之间的关系。方法：以1995－1997年调查某镉污染区93名及对照区83名25岁－55岁妇女的尿镉,尿NAG酶及尿β2－M分析结果为材料,以环境镉污染健康危害区判定标准（GB／T17221－1998）为指标值异常判定依据。应用SPSS for Windows软件包对该资料作方差,多元线性以及Logistic回归分析。结果：年龄对尿β2－M含量和异常率影响的标准偏回归系数和比值比分别咪0．250和1．79（P＜0．01）,尿镉对尿β2－M和NAG酶的含量和异常率影响的标准偏回归系数分别为0．188（P＝0．01）和0．182（P＜0．05）,比值比分别为．199和1．69。结论：受检年龄仅对β2－M的含量和异常率有正向效应,尿镉对尿β2－M和NAG酶的含量和异常率均有明显的正向效应。     

N-乙酰-β-D氨基葡萄糖苷酶在汞作业工人健康监护中的意义

将汞接触组（Hg组）以工龄4年为标准分为Hg-1组和Hg-2组,不接触汞的机关工作人员组成对照组（C组）,分别检测血清、尿NAG,以及尿β2－微球蛋白（β2－MG）、血肌酐水平。结果 Hg-1组和Hg-2组血清NAG总活性均高于C组（P＜0．05）;尿NAG总活性Hg-1组同C组比较差异无显著性,Hg-2组明显高于C组（P＜0．05）;Hg组的尿β2-MG、血肌酐水平与对照组比较差异均无显著性。     

环境镉污染区人群尿N—乙酰—β—D—氨基葡萄糖苷酶的活性变化

观察了７４名居住在含镉废水灌溉区２５年以上的居民尿中ＮＡＧ活性变化，通过与同期测定的尿镉、血镉和尿β２－微球蛋白等指标的比较分析发现，长期低剂量镉暴露可引起人群尿ＮＡＧ活性的增加，尿ＮＡＧ活性测定在监测镉对人群的早期毒性危害中是一个较为理想的生物监测指标。     

镉接触工人尿NAG活性的研究

近年来,重金属中毒性肾损害与尿Ｎ－乙酰－β－Ｄ－氨基葡萄糖苷酶（Ｎ－ａｃｅｔｙｌ－β－Ｄ－ｇｌｕｃｏｓａｍｉｎｉｄａｓｅ,ＮＡＧ）活性之间的关系受到关注。Ｋａｗａｄａ等人报道在镉污染区居民尿活性显著升高〔１〕,但未报道与剂量间的关系。本文在对５１名镉...     

铅镉联合作用对大鼠肾小管上皮细胞N-乙酰-β-D-氨基葡萄糖苷酶的影响

目的 探讨铅镉联合作用对大鼠肾小管上皮细胞N-乙酰-β-D-氨基葡萄糖苷酶（NAG）的影响。方法 对原代大鼠肾小管上皮细胞提取、纯化、鉴定、培养后,以醋酸铅0、0.02、0.1、0.5 mmol/L,氯化镉0、0.001、0.004、0.02 mmol/L进行染毒,以及铅、镉2X2联合染毒,测定NAG变化。结果 单独染铅0.02、0.1 mmol/L,NAG活力与对照组之间差异无显著性,染铅0.5mmol/L时,差异有显著性;单独染镉0.001、0.004mmol/L,NAG活力与对照组之间差异无显著性,染镉0.02 mmol/L时,差异有显著性。当铅+镉以（0.02+0.001）、（0.02+0.004）、（0.1+0.001）、（0.1+0.004）mmol/L的剂量联合染毒时,4组NAG活力明显高于对照组和单独染铅组;除（0.1+0.001）mmol/L组外,其余3组NAG活力明显高于单独染镉组。结论 铅镉联合作用使大鼠肾小管上皮细胞NAG释放增加。     

铅作业工人尿中N—乙酰—β—D—葡萄糖苷酶活性研究

对某铅冶炼厂262名男性和87名女性作业工人进行了铅对肾功能影响的研究。实验结果表明铅作业工人组尿蛋白显著增高。个别组尿溶菌酶增高;铅作业工人尿NAG显著高于对照组(7.37±2.04U/g.Cr),并与铅中毒指标及肾功能指标(尿LZM和尿Prot)显著相关,提示长期职业性铅接触可造成肾功能的损害。在铅作业工人分组中,NAG并非完全随铅性损害增加而持续上升。从而,提示NAG作为铅性肾损害敏感指标之一,在早期运用较为合适。     

铅作业工人血铅、尿铅和锌原卟啉测定结果分析

目的比较铅作业工人和非铅作业工人血铅、尿铅浓度、红细胞锌原卟啉和血常规的差异,探讨铅作业工人红细胞锌原卟啉和血铅、尿铅浓度的相关性。方法以蓄电池企业的252名铅作业工人作为接铅组,电子厂205名非铅作业工人作为对照组,测定血铅、尿铅浓度、红细胞锌原卟啉和血常规,并对结果进行统计学处理。结果接铅组血红蛋白含量低于对照组(P0.05),白细胞和红细胞、血小板则无差异(P0.05),接铅组红细胞锌原卟啉、血铅、尿铅浓度均显著高于对照组(P0.01),尿铅与红细胞锌原卟啉的相关系数(r)=0.166,血铅与红细胞锌原卟啉的相关系数r=0.406。结论长期接触铅可导致血铅、尿铅浓度和红细胞锌原卟啉升高,血红蛋白降低,对白细胞、红细胞、血小板无明显影响,血铅与红细胞锌原卟啉的相关性较尿铅与红细胞锌原卟啉的相关性好。     

铅作业工人尿N-乙酰-β-D-氨基葡糖苷酶同工酶活性的研究

本文对227名铅作业工人的肾功能和卟啉代谢状况进行了研究。结果表明卟啉代谢紊乱先于铅中毒性肾损害,铅接触组的尿NAG-A活性显著低于对照组,而尿NAG-B无明显变化;尿NAG-A活性下降是反映铅中毒性肾损害较敏感的指标,其检测价值比尿总NAG测定大。尿NAG-A活性检测可作为铝中毒性肾损害的监测指标。     

Urinary kallikrein activity of workers exposed to lead.

Two groups of men of different age ranges and with the same period of lead exposure were selected for study in a recently opened car-battery factory. Two other groups of age-matched men, not exposed to heavy metals in their work, were used as controls. Morning urines were collected from control and exposed groups for determination of urinary kallikrein activity, urinary delta-amino-levulinic acid (ALA) and lead levels. The environmental lead levels and the urinary ALA and lead values indicated that exposure in the factory was not heavy. The older group of lead-exposed workers showed greatly reduced urinary kallikrein activity compared with that of the age-matched controls. In contrast, the younger group did not show any significant alteration in urinary kallikrein excretion.     

Determination of catechol and quinol in the urine of workers exposed to benzene

Time weighted average concentrations of benzene in breathing zone air (measured by diffusive sampling coupled with FID gas chromatography) and concentrations of catechol and quinol in the urine (collected at about 1500 in the second half of a working week and analysed by high performance liquid chromatography) were compared in 152 workers who were exposed to benzene (64 men, 88 women). The concentration of urinary metabolites was also determined in 131 non-exposed subjects (43 men, 88 women). There was a linear relation between the benzene concentrations in the breathing zone and the urinary concentrations of catechol and quinol (with or without correction for urine density) in both sexes. Neither catechol nor quinol concentration was able to separate those exposed to benzene at 10 ppm from those without exposure. The data indicated that when workers were exposed to benzene at 100 ppm about 25% of benzene absorbed was excreted into the urine as phenolic metabolites, of which 13.2%, 1.6%, and 10.2% are phenol, catechol, and quinol, respectively.     

职业接触铟工人血和尿中铟的检测

目的 建立血和尿中铟(In)的检测方法, 评估职业接触工人In的接触水平。
方法 血样和尿样用体积分数0.1%的硝酸+体积分数0.02%的曲拉通溶液将原体积稀释至10倍后, 采用工作曲线法定量, 利用电感耦合等离子体质谱(ICP-MS)法测定血和尿样中In的质量浓度, 并用该法对某液晶屏生产企业的82名接触In工人血和尿样中In进行检测。
结果 血和尿中In在选定范围内均具有良好的线性关系, 相关系数大于0.999, 血和尿中In检出限分别为0.014 5 μg/L和0.005 1 μg/L, 最低检出的质量浓度分别为0.145 μg/L和0.051μg/L, 血和尿中In的加标回收率分别为98.3%~103.2%和95.2%~100.5%, 检测的批内精密度分别为1.11%~2.05%和1.02%~1.99%, 批间精密度分别为2.08%~3.99%和1.14%~1.82%。82名工人尿中In的质量浓度均低于最低检出浓度, 血中In的质量浓度为 < 0.145~1.730 μg/L。
结论 建立的方法有检出限低、灵敏度高、精密度好等优点, 可用于In接触工人血和尿中In的检测。
     

Urinary N-acetyl-beta-D-glucosaminidase activity in workers exposed to inorganic lead.

Urinary N-acetyl-beta-D-glucosaminidase (NAG) had been shown to be a useful early marker of renal injury. In workers exposed to lead it seems to be the only early marker but the dose response and dose effect relations are weak. Furthermore, the significance and underlying mechanism of increased urinary NAG activity is far from clear. By studying the isoenzyme profiles of urinary NAG, the significance and underlying mechanism may be further clarified. The heat labile (NAG-A) and heat stable (NAG-B) isoenzyme profiles of 128 workers exposed to lead from a lead stabiliser factory were analysed. NAG activity was expressed as total NAG, NAG-A, and NAG-B activity as well as ratios (NAG-B/total NAG and NAG-B/NAG-A). Exposure indices included the recent concentration of blood lead (BPb), a cumulative blood lead index (TBPb), and the recent change in concentration of blood lead (CBPb). The NAG indices correlated best with CBPb. Nearly 50% of the variation in NAG-B activity could be explained by the combination of all three exposure indices but only the CBPb was highly significant. When these exposure indices were entered separately into the regression equation, CBPb accounted for 36.3% of the variation in NAG-B activity, 5.7% was accounted for by TBPb and 2.7% by BPb. There was also no dose-effect or dose-response relation between the NAG variables and BPb or TBPb groups. With CBPb, there were dose-effect and dose-response relations. With CBPb, there was an increase in NAG variables in the group with more than 25% increase in blood lead over the past six months. The increase in NAG activity in this study is likely to be due to a recent increase in concentration of blood lead and hence presumably a recent rise in renal burden of inorganic lead. This suggests that the increase in urinary NAG activity is a form of acute response to a sharp increase in renal burden of lead, rather than to a cumulative dose. Heat stable NAG is part of the lysosomal membrane and is present in the urine when there is breakdown of lysosomes. Our data therefore contradict suggestions that the increase in urinary NAG activity is due to exocytosis.