生态毒理学报
生態毒理學報
생태독이학보
ASIAN JOURNAL OF ECOTOXICOLOGY
2008年
4期
331-336
,共6页
娄小华%段丽菊%杨光涛%吴凯%王黎明%柯珂%朱燕%杨旭
婁小華%段麗菊%楊光濤%吳凱%王黎明%柯珂%硃燕%楊旭
루소화%단려국%양광도%오개%왕려명%가가%주연%양욱
甲醛%谷胱甘肽%遗传毒性%DNA-蛋白质交联%Hela细胞%昆明小鼠
甲醛%穀胱甘肽%遺傳毒性%DNA-蛋白質交聯%Hela細胞%昆明小鼠
갑철%곡광감태%유전독성%DNA-단백질교련%Hela세포%곤명소서
formaldehyde%glutathione%genotoxicity%DNA-protein crosslink%Hela cell%Kun Ming mouse
研究发现,在环境水平的甲醛染毒之后,动物体内的谷胱甘肽(GSH)含量会发生显著减少,并呈现剂量一效应关系.值得思索的是,GSH的减少对甲醛所致的遗传毒性指标DNA-蛋白质交联(DPC)没有明显的保护作用.为了深入探讨GSH与甲醛的联合作用,进行了体外和体内两项实验.体外实验以Hela细胞为实验材料,实验组分为4组:对照组、250μM GSH组、250μM甲醛组、250μM甲醛和250μM GSH联合作用组;体内实验以昆明小鼠为实验材料,采用腹腔注射方法连续染毒两周.实验组分为4组:对照组、1mM GSH组、1mM甲醛组、1mM甲醛和1mM GSH联合作用组.体外实验与体内实验结果表明,单独GSH染毒组所致DPC与试剂对照组之间没有统计学差异(p>0.05;p>0.05),甲醛染毒组所致DPC显著高于对照组(p<0.01;p<0.05),联合作用组所致DPC不但显著高于试剂对照组(p<0.01;p<0.01)而且还显著高于甲醛染毒组(p<0.05;p<0.01).结果提示,GSH单独作用不能诱导DPC形成,但是GSH对甲醛所致的DPC具有促进作用.同时论文对这种协同作用的发生机制进行了讨论,作者认为GSH与甲醛的协同作用,和GSH与一氧化氮的协同作用的分子机制类似.
研究髮現,在環境水平的甲醛染毒之後,動物體內的穀胱甘肽(GSH)含量會髮生顯著減少,併呈現劑量一效應關繫.值得思索的是,GSH的減少對甲醛所緻的遺傳毒性指標DNA-蛋白質交聯(DPC)沒有明顯的保護作用.為瞭深入探討GSH與甲醛的聯閤作用,進行瞭體外和體內兩項實驗.體外實驗以Hela細胞為實驗材料,實驗組分為4組:對照組、250μM GSH組、250μM甲醛組、250μM甲醛和250μM GSH聯閤作用組;體內實驗以昆明小鼠為實驗材料,採用腹腔註射方法連續染毒兩週.實驗組分為4組:對照組、1mM GSH組、1mM甲醛組、1mM甲醛和1mM GSH聯閤作用組.體外實驗與體內實驗結果錶明,單獨GSH染毒組所緻DPC與試劑對照組之間沒有統計學差異(p>0.05;p>0.05),甲醛染毒組所緻DPC顯著高于對照組(p<0.01;p<0.05),聯閤作用組所緻DPC不但顯著高于試劑對照組(p<0.01;p<0.01)而且還顯著高于甲醛染毒組(p<0.05;p<0.01).結果提示,GSH單獨作用不能誘導DPC形成,但是GSH對甲醛所緻的DPC具有促進作用.同時論文對這種協同作用的髮生機製進行瞭討論,作者認為GSH與甲醛的協同作用,和GSH與一氧化氮的協同作用的分子機製類似.
연구발현,재배경수평적갑철염독지후,동물체내적곡광감태(GSH)함량회발생현저감소,병정현제량일효응관계.치득사색적시,GSH적감소대갑철소치적유전독성지표DNA-단백질교련(DPC)몰유명현적보호작용.위료심입탐토GSH여갑철적연합작용,진행료체외화체내량항실험.체외실험이Hela세포위실험재료,실험조분위4조:대조조、250μM GSH조、250μM갑철조、250μM갑철화250μM GSH연합작용조;체내실험이곤명소서위실험재료,채용복강주사방법련속염독량주.실험조분위4조:대조조、1mM GSH조、1mM갑철조、1mM갑철화1mM GSH연합작용조.체외실험여체내실험결과표명,단독GSH염독조소치DPC여시제대조조지간몰유통계학차이(p>0.05;p>0.05),갑철염독조소치DPC현저고우대조조(p<0.01;p<0.05),연합작용조소치DPC불단현저고우시제대조조(p<0.01;p<0.01)이차환현저고우갑철염독조(p<0.05;p<0.01).결과제시,GSH단독작용불능유도DPC형성,단시GSH대갑철소치적DPC구유촉진작용.동시논문대저충협동작용적발생궤제진행료토론,작자인위GSH여갑철적협동작용,화GSH여일양화담적협동작용적분자궤제유사.
Our previous studies found that the glutathione(GSH) content in experimental animals reduced significantly with a dose-effect manner after the exposure of formaldehyde(FA)at the environmental levels. Moreover, the reduction of glutathione has no apparent protective effect for the genetic toxicity indicator DNA-protein crosslink (DPC) caused by formaldehyde. For an in-depth understanding on the combined effects of GSH and FA we undertook this study. Hela cells were used for experimental materials in vitro, the experimental group was divided into four groups: the control group, 250μM GSH Group,250μM formaldehyde group, 250μM formaldehyde and 250μM GSH combined group; Kun Ming mice were used for experimental materials in vivo, intraperitoneal injection was used for the exposure, which last for two weeks, the four experimental groups included control group, 1mM GSH group, 1mM formaldehyde group, and 1mM formaldehyde and 1mMGSH combined group. The in vitro and in vivo experimental results were similar, there were no significant differences between the control groups and GSH groups (p>0.05; p>0.05 ); the DPC induced by formaldehyde groups were significantly higher than that of control groups (p<0.01; p<0.05); the DPC induced by the combined groups were not only significantly higher than that of control groups (p<0.01; p<0.01) but also significantly higher than that of formaldehyde exposure group (p<0.05; p<0.01). The results suggest that GSH would not lead to the formation of DPC alone, but glutathione has a promotive effect on the DPC induced by formaldehyde. Meanwhile, the mechanism of the promotive effect was discussed in this paper; the authors suggest that the promotive effect of glutathione on formaldehyde molecules may be similar to the mechanism of glutathione on nitric molecules.