CAJ | 학술논문

目的观察贫铀(DU)诱发细胞氧化损伤和二甲基亚砜(DMSO)的保护作用.方法以人支气管上皮细胞(BEAS-2B)为靶细胞,分别用辣根过氧化物酶介导的酚红氧化法、细胞色素C还原法和番红花红褪色法测定细胞外过氧化氢(H2O2)、超氧阴离子(O2-·)和羟自由基(·OH)含量;细胞内H2O2和O2-·分别用2,7'-二氯荧光黄双乙酸盐(DCFH2DA)和氢化乙锭(HE)标记,荧光法测定荧光产物2,7'-二氯荧光黄(DCF)和溴乙锭(EB)荧光强度.化学发光法检测SOD活力,分光光度法检测谷胱甘肽活力.结果 BEAS-2B细胞经DU染毒后,细胞内和细胞外ROS含量显著增高;细胞SOD活力及GSH活力下降,DMSO对贫铀诱发的ROS增高及SOD、GSH活力的降低有明显的抑制作用.结论贫铀可造成细胞的氧化损伤,DMSO通过清除活性氧而达到保护作用,可为DU损伤的防护提供有效措施.
목적 관찰빈유(DU)유발세포양화손상화이갑기아풍(DMSO)적보호작용.방법 이인지기관상피세포(BEAS-2B)위파세포,분별용랄근과양화물매개도적분홍양화법、세포색소C환원법화번홍화홍퇴색법측정세포외과양화경(H2O2)、초양음리자(O2-·)화간자유기(·OH)함량;세포내H2O2화O2-·분별용2,7'-이록형광황쌍을산염(DCFH2DA)화경화을정(HE)표기,형광법측정형광산물2,7'-이록형광황(DCF)화추을정(EB)형광강도.화학발광법검측SOD활력,분광광도법검측곡광감태활력.결과 BEAS-2B세포경DU염독후,세포내화세포외ROS함량현저증고;세포SOD활력급GSH활력하강,DMSO대빈유유발적ROS증고급SOD、GSH활력적강저유명현적억제작용.결론 빈유가조성세포적양화손상,DMSO통과청제활성양이체도보호작용,가위DU손상적방호제공유효조시.
Objective To observe the oxidative damage in human bronchial epithelial cells(BEAS-2B) induced by depleted uranium(DU)and protection of DMSO.Methods The measurement of extracellular superoxide anions(O2-·)was based on the reduction of ferricytochrome C.Quantitative analysis of extracellular hydrogen peroxides(H2O2)was used by the horseradish peroxidase-dependent oxidation of phenol red.The determination of extracellular hydroxyl radicals(·OH)was based on discoloration of safranine T.Ethidium bromide and 2,7'-dichlorofluorescein,fluorescent products of the membrane-permeable dyes-hydroethineand 2,7'-dichloroflurescin diacetate were used to monitor the intracellular production of O2-·and H2O2 by fluorometric method.The enzyme activity of SOD and GSH were measured by chemiluminescence and spectrophotometric method,respectively.Results The ROS production,including H2O2,O2-·and·OH,increased remarkably which induced by DU in BEAs-2B cells.The enzyme activity of SOD and GSH was descended remarkedly.These changes could be effectively inhibited by 0.5% of DMSO.Conclusions DU causes oxidative damage to BEAS-2B cells.Through removing active oxygen,DMSO can inhibit oxidative damage of DU.