Chia K S, Mutti A, Tan C, Ong H Y, Jeyaratnam J, Ong C N, Lee E
Department of Community, Occupational and Family Medicine, National University of Singapore.
Occup Environ Med. 1994 Feb;51(2):125-9. doi: 10.1136/oem.51.2.125.
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.
尿N - 乙酰 - β - D - 氨基葡萄糖苷酶（NAG）已被证明是肾损伤的一种有用的早期标志物。在接触铅的工人中，它似乎是唯一的早期标志物，但剂量反应和剂量效应关系较弱。此外，尿NAG活性增加的意义及潜在机制远未明确。通过研究尿NAG的同工酶谱，其意义和潜在机制可能会进一步阐明。分析了一家铅稳定剂工厂128名接触铅工人的热不稳定（NAG - A）和热稳定（NAG - B）同工酶谱。NAG活性以总NAG、NAG - A和NAG - B活性以及比率（NAG - B/总NAG和NAG - B/NAG - A）表示。接触指标包括近期血铅浓度（BPb）、累积血铅指数（TBPb）以及近期血铅浓度变化（CBPb）。NAG指标与CBPb的相关性最佳。近50%的NAG - B活性变化可由所有三个接触指标共同解释，但只有CBPb具有高度显著性。当将这些接触指标分别代入回归方程时，CBPb占NAG - B活性变化的36.3%，TBPb占5.7%，BPb占2.7%。NAG变量与BPb或TBPb组之间也不存在剂量效应或剂量反应关系。对于CBPb，存在剂量效应和剂量反应关系。对于CBPb，在过去六个月血铅增加超过25%的组中，NAG变量增加。本研究中NAG活性的增加可能是由于近期血铅浓度升高，因此推测可能是近期无机铅肾负担增加。这表明尿NAG活性增加是对铅肾负担急剧增加的一种急性反应形式，而非对累积剂量的反应。热稳定NAG是溶酶体膜的一部分，当溶酶体破裂时会出现在尿液中。因此，我们的数据与尿NAG活性增加是由于胞吐作用的观点相矛盾。
