癌变·畸变·突变
癌變·畸變·突變
암변·기변·돌변
CARCINOGENSES,TERATOGENSIS AND MUTAGENESIS
2015年
3期
221-224,229
,共5页
薄存香%张振玲%赛林霖%张放%杨治峰%谢琳%贾强
薄存香%張振玲%賽林霖%張放%楊治峰%謝琳%賈彊
박존향%장진령%새림림%장방%양치봉%사림%가강
2,4-二氯苯氧乙酸%神经行为%丙二醛%还原型谷胱甘肽%谷胱甘肽过氧化物酶
2,4-二氯苯氧乙痠%神經行為%丙二醛%還原型穀胱甘肽%穀胱甘肽過氧化物酶
2,4-이록분양을산%신경행위%병이철%환원형곡광감태%곡광감태과양화물매
2,4-dichlorophenoxyacetic acid%neurobehavior%malondialdehyde%glutathione%glutathion peroxidase
目的:研究大鼠孕期和哺乳期暴露2,4-二氯苯氧乙酸(2,4-D)对子代发育及脑组织脂质过氧化的损伤作用。方法:Wistar大鼠于受孕后第2天开始经口灌胃染毒2,4-D(0、25、50和100 mg/kg)直至仔鼠出生后第21天,每天1次,连续42 d。期间检测仔鼠生理及早期神经行为发育指标。断乳1周后处死仔鼠检测脑组织丙二醛(MDA)、还原型谷胱甘肽(GSH)的含量及谷胱甘肽过氧化物酶(GSH-Px)的活力。结果:与对照组相比,100 mg/kg剂量组仔鼠体质量从出生后14 d开始降低,50 mg/kg剂量组仔鼠体质量从出生后21 d开始降低,差异均有统计学意义( P<0.05),而其他各生理发育指标差异均无统计学意义( P>0.05)。神经行为测试中100 mg/kg剂量组仔鼠断崖回避、空中翻正及听觉惊愕的阳性发生率均明显低于对照组(P<0.05),出现神经行为发育迟缓。50和100 mg/kg剂量组仔鼠脑组织中MDA含量升高,100 mg/kg剂量组仔鼠脑组织GSH含量及GSH-Px的活性下降,与对照组相比差异均有统计学意义(P均<0.05)。结论:大鼠孕期和哺乳期暴露2,4-D致子代神经发育迟缓可能与2,4-D引起脑组织脂质过氧化损伤有关。
目的:研究大鼠孕期和哺乳期暴露2,4-二氯苯氧乙痠(2,4-D)對子代髮育及腦組織脂質過氧化的損傷作用。方法:Wistar大鼠于受孕後第2天開始經口灌胃染毒2,4-D(0、25、50和100 mg/kg)直至仔鼠齣生後第21天,每天1次,連續42 d。期間檢測仔鼠生理及早期神經行為髮育指標。斷乳1週後處死仔鼠檢測腦組織丙二醛(MDA)、還原型穀胱甘肽(GSH)的含量及穀胱甘肽過氧化物酶(GSH-Px)的活力。結果:與對照組相比,100 mg/kg劑量組仔鼠體質量從齣生後14 d開始降低,50 mg/kg劑量組仔鼠體質量從齣生後21 d開始降低,差異均有統計學意義( P<0.05),而其他各生理髮育指標差異均無統計學意義( P>0.05)。神經行為測試中100 mg/kg劑量組仔鼠斷崖迴避、空中翻正及聽覺驚愕的暘性髮生率均明顯低于對照組(P<0.05),齣現神經行為髮育遲緩。50和100 mg/kg劑量組仔鼠腦組織中MDA含量升高,100 mg/kg劑量組仔鼠腦組織GSH含量及GSH-Px的活性下降,與對照組相比差異均有統計學意義(P均<0.05)。結論:大鼠孕期和哺乳期暴露2,4-D緻子代神經髮育遲緩可能與2,4-D引起腦組織脂質過氧化損傷有關。
목적:연구대서잉기화포유기폭로2,4-이록분양을산(2,4-D)대자대발육급뇌조직지질과양화적손상작용。방법:Wistar대서우수잉후제2천개시경구관위염독2,4-D(0、25、50화100 mg/kg)직지자서출생후제21천,매천1차,련속42 d。기간검측자서생리급조기신경행위발육지표。단유1주후처사자서검측뇌조직병이철(MDA)、환원형곡광감태(GSH)적함량급곡광감태과양화물매(GSH-Px)적활력。결과:여대조조상비,100 mg/kg제량조자서체질량종출생후14 d개시강저,50 mg/kg제량조자서체질량종출생후21 d개시강저,차이균유통계학의의( P<0.05),이기타각생리발육지표차이균무통계학의의( P>0.05)。신경행위측시중100 mg/kg제량조자서단애회피、공중번정급은각량악적양성발생솔균명현저우대조조(P<0.05),출현신경행위발육지완。50화100 mg/kg제량조자서뇌조직중MDA함량승고,100 mg/kg제량조자서뇌조직GSH함량급GSH-Px적활성하강,여대조조상비차이균유통계학의의(P균<0.05)。결론:대서잉기화포유기폭로2,4-D치자대신경발육지완가능여2,4-D인기뇌조직지질과양화손상유관。
OBJECTIVE:To study the effects of 2,4-dichlorophenoxyacetic acid (2,4-D) on early neuro-behavior development and oxidative stress in offsprings.METHODS:Pregnant Wistar rats were treated with 2,4-D by gavage,in doses of 0,25,50,100 mg/kg once a day from gestation day 2 until postnatal day 21. Then the early physiological and neurobehavioral indexes in the offsprings were measured. The levels of MDA,GSH and the GSH-Px activities in brain tissues of newborn rat were determined.RESULTS:The weights of offspring in the 100mg/kg 2,4-D groupwere lower than in control after postnatal day 14(P<0.05) and the weights of offspring inthe 50 mg/kg 2,4-D were lower than in control after postnatal day 21(P<0.05). The physiologic markers including eye opening,pinna detachment,hair growth,tooth growth etc in all treated groups were not affected in contrast to the control group,cliff avoidance,mid-air righting and acoustic startle in the 100 mg/kg 2,4-D group were delayed(P<0.05). The level of GSH and GSH-Px activities decreased in the 100 mg/kg 2,4-D group,while the level of MDA was elevated in the 50 and 100 mg/kg 2,4-D groups. CONCLUSION:Early neurobehavioral development of offspring rats could be impaired by 2,4-D due to its disturbance to the homeostasis of oxidation and anti-oxidation system.