Urinary kallikrein activity in workers exposed to cadmium, lead, or mercury vapour.
Urinary kallikrein activity in workers exposed to cadmium, lead, or mercury vapour.
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接触镉、铅或汞蒸气的工人的尿液激肽释放酶活性。
DOI：
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发表时间：
1990
期刊：
影响因子：
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通讯作者：
G. V. Houte
中科院分区：
文献类型：
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作者：
H. Roels;R. Lauwerys;J. Buchet;A. Bernard;P. Lijnen;G. V. Houte
在64名平均接触镉11年、尿镉浓度为2.2 ~ 33.1 μ g/g肌酐的血压正常的工人中发现尿激肽释放酶活性显著降低（由其酰胺分解活性测定）。平均（几何）尿激肽释放酶活性（单位：U/g肌酐）为0.52（范围0.11-1.90），对照组（n = 193）为0.39（范围0.10-1.03）在镉组中，以及异常低活动水平的普遍性（小于或等于0.20 U/g肌酐）在镉组为17.2%，对照组为5.2%。还观察到与尿钠排泄增加相关的醛固酮释放（尿中醛固酮）减少。这可能是一种代偿机制，维持血压在正常范围内。镉的这些生物学效应在从接触中去除后是不可逆的。本研究提示镉对远端肾单位有不可逆的毒性作用。它还表明，过量的镉体内负荷本身可能不足以诱发高血压，但在血压调节可能受到其他因素损害的个体中，镉可能会刺激高血压的发展。这项研究也支持防止高血压受试者接触镉的建议。没有迹象表明中度接触汞蒸气（n = 53;尿中汞，范围为11-224微克/克肌酐;平均接触时间：6年）或无机铅（n = 23;血中铅，范围为40-67微克/100毫升;平均接触时间：8年）与肾脏产生的激肽释放酶减少有关。
A significant reduction of kallikrein activity in urine (assayed by its amidolytic activity) was found in 64 normotensive workers who had been exposed to cadmium for 11 years on average and whose cadmium concentrations in urine ranged from 2.2 to 33.1 micrograms/g creatinine. The mean (geometric) urinary kallikrein activity (in U/g creatinine) amounted to 0.52 (range 0.11-1.90) in the control group (n = 193) against 0.39 (range 0.10-1.03) in the cadmium group, and the prevalence of abnormally low activity levels (less than or equal to 0.20 U/g creatinine) amounted to 17.2% in the cadmium group against 5.2% in the control group. A reduction of aldosterone release (aldosterone in urine) associated with an increased natriuresis was also observed. This might constitute a compensatory mechanism maintaining blood pressure in the normal range. These biological effects of cadmium were not reversible after removal from exposure. This study indicates that cadmium can induce an irreversible toxic effect in the distal nephron. It also suggests that an excessive cadmium body burden alone may not be sufficient to induce hypertension, but in individuals whose blood pressure regulation may be impaired by other factors cadmium could stimulate the development of hypertension. This study also supports the recommendation to prevent hypertensive subjects from being exposed to cadmium. There was no indication that moderate exposure to mercury vapour (n = 53; mercury in urine, range 11-224 micrograms/g creatinine; average duration of exposure: six years) or to inorganic lead (n = 23; lead in blood, range 40-67 micrograms/100 ml; average duration of exposure: eight years) was associated with a reduction of kallikrein production by the kidney.