The impact of long-term past exposure to elemental mercury on antioxidative capacity and lipid peroxidation in mercury miners
The impact of long-term past exposure to elemental mercury on antioxidative capacity and lipid peroxidation in mercury miners
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DOI：
10.1016/s0946-672x(04)80028-2
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发表时间：
2004-01-01
影响因子：
3.5
通讯作者：
Osredkar, Josko
中科院分区：
文献类型：
--
作者：
Kobal, Alfred B.;Horvat, Milena;Osredkar, Josko
关于长期汞接触对心血管疾病风险的影响，现有信息有限。体外和体内研究表明，汞可通过促进自由基的产生、与抗氧化酶相互作用以及减少生物可利用的硒来促进脂质过氧化。本研究的目的是检验假设，长期过去的职业接触元素汞（Hg 0）可以改变抗氧化能力，促进脂质过氧化作用的矿工。研究人群包括54名汞矿工和58名工人作为对照组。在接触后阶段对矿工进行了检查。我们评估了他们以前接触过的Hg 0，某些非特异性症状和微量汞中毒体征的推定外观，以及CVD的主要行为和生物风险因素，并确定：1）血和尿中汞和硒水平，2）抗氧化酶，Cu/Zn超氧化物歧化酶红细胞中CuZn-SOD、CAT和硒酶谷胱甘肽过氧化物酶（GSH-Px）活性作为自由基活性的间接指标; 3）血液和尿液中松果体激素褪黑素（MEL）;脂质过氧化产物为脂质过氧化氢（LOOHs）和丙二醛（MDA）。汞矿工间歇性暴露于Hg 0的时间为7至31年。暴露期总数从13到119不等。累积的铀汞峰值水平从794- 11，365微克/升不等。目前的血液和尿液中的汞浓度几乎在同一水平的矿工和控制。矿工表现出一些神经毒性和肾毒性的后遗症微量汞中毒。矿工和对照组之间没有发现心血管疾病的行为和生物危险因素的显着差异。弱相关性矿工收缩压与平均既往接汞量呈显著正相关（r = 0.36，p < 0.01），矿工平均磷硒含量与平均既往接汞量呈显著负相关（r = 0.36，p < 0.01（71.4 mug/L）明显较低（p < 0.05）（77.3 mug/L），而矿工的平均尿硒（16.5 mug/g肌酐）比对照组（14.0 mug/g肌酐）更高（p < 0.05）。红细胞抗氧化酶活性中，只有CAT活性极显著高于对照组（P < 0.01）（3.14MU/gHb）。矿工的B-MEL平均浓度（44.3 ng/L）显著高于对照组（14.9 ng/L）（p < 0.01）。矿工的U-MEL硫酸盐平均值（31.8 mug/L）显著低于对照组（46.9 mug/L）（p < 0.01）。在所观察到的脂质过氧化产物中，矿工组的U-MDA平均浓度（0.21 mumol/mmoL肌酐）显著高于对照组（0.17 mumol/mmol肌酐）（p < 0.01）。
Limited information is available on the effects of chronic mercury exposure in relation to the risk of cardiovascular disease (CVD). It is known from in vitro and in vivo studies that Hg can promote lipid peroxidation through promotion of free radical generation, and interaction with antioxidative enzymes and reduction of bioavaitable selenium. The objective of the study was to test the hypothesis that tong-term past occupational exposure to elemental Hg (Hg0) can modify antioxidative capacity and promote lipid peroxidation in miners. The study population comprised 54 mercury miners and 58 workers as the control group. The miners were examined in the post-exposure period. We evaluated their previous exposure to Hg0, the putative appearance of certain nonspecific symptoms and signs of micromercurialism, as well as the main behavioural and biological risk factors for CVD, and determined: 1) Hg and Se Levels in blood and urine, 2) antioxidative enzymes, Cu/Zn superoxide dismutase (CuZn-SOD), catalase (CAT), and selenoenzyme glutathione peroxiclase (GSH-Px) activity in erythrocytes as indirect indices of free radical activity, 3) pineal hormone melatonin (MEL) in blood and urine, and 4) lipid hydroperoxides (LOOHs) and malondialdehyde (MDA) as lipid peroxidation products. The mercury miners were intermittently exposed to Hg0 for periods of 7 to 31 years. The total number of exposure periods varied from 13 to 119. The cumulative U-Hg peak Level varied from 794-11,365 mug/L. The current blood and urine Hg concentrations were practically on the same level in miners and controls. Miners showed some neurotoxic and nephrotoxic sequels of micromercurialism. No significant differences in behavioural and biological risk factors for CVD were found between miners and controls. A weak correlation (r = 0.36, p < 0.01) between systolic blood pressure and average past exposure U-Hg Level was found. The mean P-Se in miners (71.4 mug/L) was significantly Lower (p < 0.05) than in the controls (77.3 mug/L), while the mean U-Se tended to be higher (p < 0.05) in miners (16.5 mug/g creatinine) than in the controls (14.0 mug/g creatinine). Among antioxidative enzyme activities, only CAT in erythrocytes was significantly higher (p < 0.01) in miners (3.14 MU/g Hb) than in the controts (2.65 MU/g Hb). The mean concentration of B-MEL in miners (44.3 ng/L) was significantly higher (p < 0.01) than in the controls (14.9 ng/L). The mean value of U-MEL sulphate (31.8 mug/L) in miners was significantly Lower (p < 0.01) than in the control group (46.9 mug/L). Among the observed lipid peroxidative products, the mean concentration of U-MDA was statistically higher (p < 0.01) in miners (0.21 mumol/mmoL creatinine) than in the controts (0.17 mumol/mmol creatinine).