Kost'ová D, Michnová E, Legáth J, Krupicer I
University of Veterinary Medicine, Kosice, Slovak Republic.
Vet Med (Praha). 1995 Dec;40(12):371-5.
Peroxidative lesions of cells and production of free radicals from endo- and exogenous reasons, eg. due to air pollution, can result in severe lesions of cells and subsequent pathological processes (Rieger, 1992; Robbins and Cotran, 1988). A pentose cycle plays an important role in the system of antioxidative protection: glucose-6-phosphate dehydrogenase (G-6-PD; EC 1.1.1.49) is its first enzyme. G-6-PD activity was evaluated in the erythrocytes of sheep kept in the region contaminated by heavy metals with mercury dominating among them, and in the same animals after administration of a feed mixture containing Hg, Pb Cd, Zn Cr, Cu, Fe and As (Fig. 1). Boehringer Mannheim test was used to determine the G-6-PD activity. There was no significant differences in the enzyme activity in the sheep from a contaminated region and in the animals outside the air-pollution region (control animals) before the applications of heavy metals started. The average value of G-6-PD activity was 13.96 +/- 0.94 mU.10 (-9) Ec in control animals and 14.39 +/- 1.49 mU.10 (-9) Ec in the animals from a contaminated region. After eight-day applications of heavy metals the G-6-PD activity increased statistically significantly to 18.71 +/- 2.45 mU.10 (-9) Ec; P < 0.01, and to 23.55 +/- 1.87 mU 10 (-9) Ec after 16 days of application; P < 0.001 (Fig. 2). An increase in G-6-PD activity after heavy metal applications is probably a compensation mechanism in the system of erythrocyte antioxidative protection due to higher peroxidation. The long term increased intake of heavy metals from polluted air did not lead to any rise of G-6-PD activity probably due to the lower dose of heavy metals and/or to adaptation of animal organisms to long run emission exposure. The results demonstrate that G-6-PD can be one of the biochemical indicators at organism load by heavy metals with mercury dominating among them.
内源性和外源性因素（如空气污染）导致的细胞过氧化损伤及自由基产生，可造成细胞的严重损伤及后续病理过程（里格，1992；罗宾斯和科特兰，1988）。戊糖循环在抗氧化保护系统中起重要作用：葡萄糖-6-磷酸脱氢酶（G-6-PD；EC 1.1.1.49）是其首个酶。对生活在重金属污染地区（其中汞占主导）的绵羊红细胞，以及给这些绵羊投喂含汞、铅、镉、锌、铬、铜、铁和砷的混合饲料后的红细胞，评估了G-6-PD活性（图1）。采用勃林格殷格翰检测法测定G-6-PD活性。在开始施用重金属之前，来自污染地区的绵羊与空气污染地区以外的动物（对照动物）的酶活性无显著差异。对照动物的G-6-PD活性平均值为13.96±0.94 mU·10⁻⁹ Ec，来自污染地区的动物为14.39±1.49 mU·10⁻⁹ Ec。施用重金属八天后，G-6-PD活性在统计学上显著增加至18.71±2.45 mU·10⁻⁹ Ec；P<0.01，施用16天后增加至23.55±1.87 mU·10⁻⁹ Ec；P<0.001（图2）。施用重金属后G-6-PD活性增加可能是红细胞抗氧化保护系统中因过氧化程度较高而产生的一种补偿机制。长期从污染空气中摄入重金属未导致G-6-PD活性升高，可能是由于重金属剂量较低和/或动物机体对长期排放暴露产生了适应性。结果表明，G-6-PD可能是生物体受以汞为主的重金属负荷影响的生化指标之一。
