四川省克山病地区儿童的抗氧化能力和氧化因素

Antioxidant ability and oxidant stress of children in Keshan disease endemic area in Sichuan Province

在四川克山病区和非病区考察了学龄儿童抗氧化能力,发现病区儿童红细胞中的抗氧,化酶系,谷胱甘肽过氧化物酶 (GSH-Px),超氧化物歧化酶 (SOD),触酶 (Cat) 的活力均显著低于非病区,补充硒预防克山病的地区的儿童红细胞中 GSH-Px 活力显著上升,但仍未达到适硒地区的水平,而 SOD 和 Cat 的活力仍未上升,克山病地区儿童血浆中维生素 E 水平虽然在正常值范围以上,但也低于非病区儿童。体外用活性氧氧化红细胞以检验其抗氧化能力也证明区儿童红细胞的抗氧化能力也低于非病区。表现在红细胞经超氧阴离子 (O_2^-) 或抗坏血酸氧化后血红蛋白被氧化的量,出现形态不正常的红细胞的人数,和红细胞膜骨架蛋白的成份和结构受损的程度均是病区高于非病区。测定亚急型克山病患儿血中自由基水平高于病区的健康儿童,与感染儿童相近,而亚急克患儿大多数夹杂有感染病患,因此推测感染等因素可能使抗氧化能力降低的克山病区儿童体内的氧化因素增强,从而使氧化与抗氧化失衡而诱发了克山病。

It was found that the activities of GSH-Px,SOD and Cat in erythrocyte ofchildren in Keshan disease (KD) endemic area were significantly lower thanthat of children in unendemic areas.GSH-Px activity in erythrocyte of childrensupplemented with sodium selenite for prevention of KD in endemic area formany years increased significantly.However,supplementation of sodium seleni-te did not effect on activities of SOD and Cat.Plasma vitamin E levels of chil-dren in these two KD endemic areas were little lower than that of Children inunendemic arae either,though all plasma vitamin E levels were above normalvalue (5μg/ml).The evidences of testing oxidative ability of erythrocyte in vitro also showedthat oxidative ability of children in KD endemic areas was lower than that ofchildren in unendemic areas,indicated by higher percentage of hemoglobin oxi-dized,more abnormal erythrocytes appeared and more serious damage to mem-brane in erythrocytes of children in KD areas,after exposure to superoxideanion or ascorbic acid.In addition,it was observed that free radicals levels detected by ESR in free-zing dried whole blood of subacute KD patients were very significantly higher th-an that of normal children,but similar to that of children with infectious disea-ses in KD endemic areas,Most KD patients were complicated by infection whichmight cause increasing oxidant stress in selenium deficient children,and resultedin loss of balance between oxidant stress and antioxidant ability,that may beresponsible for attack of subacute KD.