CAJ | 학술논문

目的研究从胚胎期至生长期连续砷暴露对仔代鼠脑神经细胞线粒体呼吸功能和ATP合成量的影响,探讨砷对胎幼鼠中枢神经的毒性损伤机制。方法清洁级SD大鼠随机分成3组（对照组、低砷组、高砷组）,染砷组自由饮用含砷（As2O3）水（高砷组10 mg/（kg.d）,低砷组0.4 mg/（kg.d））,6周后,各组分别雄雌2∶1合笼产仔,仔鼠继续本组剂量染砷到断奶后6和16周,测定仔鼠脑神经细胞线粒体的呼吸活性和ATP合成量,同时观察线粒体的超微结构变化。结果断奶后继续染砷6和16周的高、低砷组的仔鼠,脑细胞线粒体Ⅲ态呼吸（R3）比对照组明显降低,以高砷组仔鼠最为显著（P〈0.01）;呼吸控制率（RCR）在各染砷组都有所降低,但以16周高砷组仔鼠降低更显著（P〈0.05）。染砷组的ATP合成量比对照组明显减少,高砷组仔鼠组减少更显著（P〈0.01）;电镜下线粒体有基质肿胀,部分脊减少甚至断裂,在高砷组仔鼠还见线粒体外膜断裂,部分线粒体呈空泡样改变,有的甚至溶解。结论从妊娠到生长发育期持续砷暴露可引起仔鼠脑神经细胞线粒体呼吸功能和能量代谢功能明显损伤,损伤程度有剂量和时间-效应关系。
목적연구종배태기지생장기련속신폭로대자대서뇌신경세포선립체호흡공능화ATP합성량적영향,탐토신대태유서중추신경적독성손상궤제。방법청길급SD대서수궤분성3조（대조조、저신조、고신조）,염신조자유음용함신（As2O3）수（고신조10 mg/（kg.d）,저신조0.4 mg/（kg.d））,6주후,각조분별웅자2∶1합롱산자,자서계속본조제량염신도단내후6화16주,측정자서뇌신경세포선립체적호흡활성화ATP합성량,동시관찰선립체적초미결구변화。결과단내후계속염신6화16주적고、저신조적자서,뇌세포선립체Ⅲ태호흡（R3）비대조조명현강저,이고신조자서최위현저（P〈0.01）;호흡공제솔（RCR）재각염신조도유소강저,단이16주고신조자서강저경현저（P〈0.05）。염신조적ATP합성량비대조조명현감소,고신조자서조감소경현저（P〈0.01）;전경하선립체유기질종창,부분척감소심지단렬,재고신조자서환견선립체외막단렬,부분선립체정공포양개변,유적심지용해。결론종임신도생장발육기지속신폭로가인기자서뇌신경세포선립체호흡공능화능량대사공능명현손상,손상정도유제량화시간-효응관계。
Objective To study on the toxic effects of arsenic on brain nerve cellular mitochondrial function and ultrastructure of F1 pups rats of gestated and growed in arsenic1 exposed surroundings.Methods Sprague-Dawley（SD） rats of cleanliness grade were randomly divided into three group which were lower dose and high-dose arsenic groups and control group.Each group rats of exposed arsenic were administered drinking water containing As2O3（high-dose 10 mg/（kg·d）,low-dose 0.4 mg/（kg·d）,control group drinked distilled water for 6 weeks.Rats of female and male were combined to give a birth young,F1 pups rats were milk feeded by parent of exposed arsenic until weaning,F1 pups rats continued exposed arsenic1 6 and 16 weeks after weaning.,respectively.Respiratory activity and ATP amounts of brain cellular mitochondria were determinined in all groups and mitochondria ultrastructure changes were observed.Results F1 pups rats of low-and high-arsenic1 continued exposed arsenic1 6 and 16 weeks after weaning,the III condition respiration rates（R3） of brain cellular mitochondria were obviously lower than control group,and the high-dose F1 pups rats group were more lower than that of low-dose F1 pups（P〈0.01）.F1 pups rat＇s respiratory control ratio（RCR）in high-dose arsenic1 exposed for 16 weeks were more degraded than that of arsenic1 exposed F1 pups（P0.05）.ATP amounts of brain cellular mitochondria of arsenic1 exposed group decreased as compared to that in the control group（P〈0.01）,and high-dose group more striking decreased.The ultrastructures of brain cells mitochondrion were investigated under electron microscope,mitochondria showed ground substance tumescence,lophos decrease and breakage,even adventitia breakage,vacuolus changed and dissolve in high-dose group were observed.Conclusion Arsenic may induce brain nerve cellular mitochondrial respiratory and energy metabolism function damaged of F1 pups rats consecutively exposed arsenic from gestation to growth period,degree of injury had positively relative to exposure dose and time.