中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2008年
11期
654-658
,共5页
溴氰菊酯%活性氧组分%巯基试剂%PC12细胞
溴氰菊酯%活性氧組分%巰基試劑%PC12細胞
추청국지%활성양조분%구기시제%PC12세포
Deltamethrin%Reactive oxygen species%Sulihydryl reagents%PC12 cell
目的 研究溴氰菊酯(DM)对大鼠肾上腺嗜铬细胞瘤(PC12)细胞活性氧(ROS)生成的影响.方法 对培养的PC12细胞分别进行处理:(1)终浓度为0、10和100 μmol/L的DM分别处理PC12细胞1、6和12 h(两因素析凶设计);(2)终浓度为0、10和100;μmol/L的DM分别处理PC12细胞1、6、24h或24、48 h;(3)PC12细胞分别在终浓度为10mmol/L乙酰半胱氨酸(NAC)预处理2 h、终浓度为500 μmol/L的DL-甲硫氨酸磺酰亚胺(BSO)及终浓度为40 μmol/L的叔丁基对苯二酚(tBHQ)预处理16 h,再给予10 μmol/LDM作用6ho所有处理结束时,用2',7'-二氯荧光黄双乙酸酯(DCFH-DA)探针法测定细胞ROS含量.结果 DM诱导ROS生成呈剂量和时间效应关系.10 μmol/L DM处理组PC12细胞增加ROS的DCF荧光强度,是溶剂对照组的2.24倍,差异有统计学意义(P<0.01).而分别用NAC、BSO及tBHQ预先处理PC12细胞均能明显降低DM所增加的ROS,分别是DM组的22%、62%、38%.差异均有统计学意义(P<0.05).结论 DM能诱导PC12细胞ROS生成增高,胞内巯基水平和抗氧化功能降低可能是ROS生成增高的影响因素.
目的 研究溴氰菊酯(DM)對大鼠腎上腺嗜鉻細胞瘤(PC12)細胞活性氧(ROS)生成的影響.方法 對培養的PC12細胞分彆進行處理:(1)終濃度為0、10和100 μmol/L的DM分彆處理PC12細胞1、6和12 h(兩因素析兇設計);(2)終濃度為0、10和100;μmol/L的DM分彆處理PC12細胞1、6、24h或24、48 h;(3)PC12細胞分彆在終濃度為10mmol/L乙酰半胱氨痠(NAC)預處理2 h、終濃度為500 μmol/L的DL-甲硫氨痠磺酰亞胺(BSO)及終濃度為40 μmol/L的叔丁基對苯二酚(tBHQ)預處理16 h,再給予10 μmol/LDM作用6ho所有處理結束時,用2',7'-二氯熒光黃雙乙痠酯(DCFH-DA)探針法測定細胞ROS含量.結果 DM誘導ROS生成呈劑量和時間效應關繫.10 μmol/L DM處理組PC12細胞增加ROS的DCF熒光彊度,是溶劑對照組的2.24倍,差異有統計學意義(P<0.01).而分彆用NAC、BSO及tBHQ預先處理PC12細胞均能明顯降低DM所增加的ROS,分彆是DM組的22%、62%、38%.差異均有統計學意義(P<0.05).結論 DM能誘導PC12細胞ROS生成增高,胞內巰基水平和抗氧化功能降低可能是ROS生成增高的影響因素.
목적 연구추청국지(DM)대대서신상선기락세포류(PC12)세포활성양(ROS)생성적영향.방법 대배양적PC12세포분별진행처리:(1)종농도위0、10화100 μmol/L적DM분별처리PC12세포1、6화12 h(량인소석흉설계);(2)종농도위0、10화100;μmol/L적DM분별처리PC12세포1、6、24h혹24、48 h;(3)PC12세포분별재종농도위10mmol/L을선반광안산(NAC)예처리2 h、종농도위500 μmol/L적DL-갑류안산광선아알(BSO)급종농도위40 μmol/L적숙정기대분이분(tBHQ)예처리16 h,재급여10 μmol/LDM작용6ho소유처리결속시,용2',7'-이록형광황쌍을산지(DCFH-DA)탐침법측정세포ROS함량.결과 DM유도ROS생성정제량화시간효응관계.10 μmol/L DM처리조PC12세포증가ROS적DCF형광강도,시용제대조조적2.24배,차이유통계학의의(P<0.01).이분별용NAC、BSO급tBHQ예선처리PC12세포균능명현강저DM소증가적ROS,분별시DM조적22%、62%、38%.차이균유통계학의의(P<0.05).결론 DM능유도PC12세포ROS생성증고,포내구기수평화항양화공능강저가능시ROS생성증고적영향인소.
Objective To investigate the effect of deltamethrin(DM )on production of reactive oxygen species (ROS) of rat pheochromocytoma(PC12 ) cells and its mechanism. Methods PC12 cells were treated with various dose of DM (0, 10 or 100 μmol/L) for 1,6 or 12 h respectively. Furthermore, PC l2 cells were treated with various dose of DM (0,10 or 100 μmol/L) for 24 or 48 h, respectively. PC 12 cells were pre-incubated with 10 mmol/L N-acetyl-L-cysteine (NAC) for 2 h,or with 500 μmol/L DL-Buthionine-[S,R]-Sulfoximine ( BSO ) for 16 h, or with 40 μmol/L tertiary butylhydroquinone(tBHQ ) for 16 h, prior to exposure to DM and then with 10 μmol/L DM for 6 h. After treatment,ROS production in PC12 cells were measured by a molecular probe, 2',7'-dichlorofluorescein diacetate (DCFH-DA). Results DM induced a dose- time dependent increase in ROS production (indicated by DCF fluorescence intensity ). 10 μmol/L DM treatment for 6 h enhanced DCF fluorescence intensity that reached approximately 2.24 times of values of control group. Furthermore,a pretreatment with NAC, BSO or tBHQ significantly reduced the DM-enhanced DCF fluorescence intensity that reached approximately 22%, 62% or 38% of values of DM treatment, respectively( P<0.05 ), indicating that all these pretreatments atteruate ROS production. Conclusion The in vitro studies demonstrate that DM could enhance ROS production, and may be the influential factor for the decreased mercapto level and antioxidative function.
