毒死蜱对雄性小鼠生殖毒性的影响

为研究毒死蜱对雄性小鼠生殖毒性的影响,利用不同浓度毒死蜱染毒小鼠.以昆明小鼠为受试动物,毒死蜱按3、6和12mg·kg-13个剂量水平,灌胃染毒小鼠7d.以睾丸组织匀浆测定活性氧(reactive oxygen species,ROS)和还原型谷胱甘肽(glutathione,GSH)的含量;以睾丸细胞测定DNA-蛋白...     

邻苯二甲酸二乙基己酯与双酚A联合染毒对小鼠学习记忆障碍及淀粉样前体蛋白酶解通路的影响

研究邻苯二甲酸二乙基己酯(diethylhexyl phthalate, DEHP)与双酚A(bisphenol A, BPA)联合染毒对小鼠学习记忆障碍及淀粉样前体蛋白(APP)酶解通路的影响。选用昆明种小鼠80只,随机分为空白对照(CT)组、BPA染毒组(1 mg·L^(-1))、不同浓度的DEHP染毒组(100、250和500 mg·kg(-1))、不同浓度的DEHP染毒组(100、250和500 mg·kg^(-1))与联合染毒组。经口灌胃染毒,以0.01 mL·g(-1))与联合染毒组。经口灌胃染毒,以0.01 mL·g^(-1)的剂量灌胃,7次/周,持续6周。使用Morris水迷宫、避暗、跳台的行为学实验方法检测2种污染物单独及联合染毒对小鼠学习记忆的影响;检测小鼠大脑组织中丙二醛(MDA)的含量和单胺氧化酶(MAO)、过氧化氢酶(CAT)、乙酰胆碱酯酶(AChE)的活性;采用酶联免疫分析(ELISA)法检测脑组织中的β、γ-分泌酶活性和Aβ_(1-42)的含量;Western Blot法检测APP、PS1、BACE1和Tau的蛋白表达水平;免疫组化法观察小鼠脑组织海马区HE染色情况。行为学测试结果表明,与CT组比较,单独染毒处理组小鼠学习记忆能力出现障碍,空间探索能力较弱;联合染毒组与单独染毒组相比,小鼠于目标象限停留时间短,穿台次数少,差异具有统计学意义(P<0.05);生化学指标结果显示,随着毒物浓度增加,脑组织中MAD含量、MAO和AChE活性逐渐增加,CAT活性逐渐降低,联合染毒组的变化更为明显,染毒处理组β、γ-分泌酶活性和Aβ_(1-42)含量增加,联合染毒组比单独染毒组酶活性增加更明显;各组差异均具有统计学意义(P<0.05)。DEHP与BPA单独染毒,对小鼠脑组织均显示有神经毒性作用,会造成小鼠学习记忆功能障碍;随着联合染毒组DEHP浓度的增加,联合染毒组与对应剂量的单独染毒组相比,小鼠行为学测试结果与生化指标变化更加明显,采用效应相加模型对其联合毒性作用进行评价,表现为协同作用;染毒组小鼠脑组织神经递质明显减少,具体机制可能与氧化应激及APP酶解通路的作用有关。     

毒死蜱(CPF)对克氏原螯虾的急性毒性及组织病理观察

采用静水生物测试法研究毒死蜱(CPF)对克氏原螯虾(Procambarus clarkii)的急性毒性效应及克氏原螯虾的组织病变情况并进行安全评价。设定0、2、10、20、40和80μg·L-1 6个CPF浓度梯度进行急性暴露试验,结果表明,CPF浓度升高对克氏原螯虾产生较大毒性,24、48和96 h半致死浓度〔ρ(LC50)〕分别为(28.24±2.81)、(19.50±2.03)和(13.13±1.70)μg·L-1,ρ(LC50)随着暴露时间延长呈显著下降趋势,符合双曲线衰减模型(r=0.999 9,P<0.000 1),安全浓度为(2.79±0.31)μg·L-1。组织病理观察发现,染毒虾心脏上皮细胞增生,心肌肌束间充满血淋巴细胞;神经细胞肿大,尼氏体溶解消失,细胞由多极形状变为圆形,神经纤维坏死并解体;肝胰腺小管收缩并充血,空泡增加;鳃组织空泡化,表面出现黑色素沉积,被多量血淋巴细胞浸润;肌肉纤维萎缩并溶解。     

丙烯腈暴露对大鼠脑组织损伤及iNOS/p38 MAPK信号通路关键蛋白表达的影响

通过探究iNOS/p38 MAPK信号通路在丙烯腈(acrylonitrile,ACN)诱导脑组织损伤中的作用,为进一步研究ACN的神经毒性作用提供依据。选取50只SPF级健康成年雄性SD大鼠,随机分为5组,每组10只。适应性饲养一周后,以12.5、25.0、50.0 mg·kg~(-1)ACN对大鼠进行灌胃染毒,对照组给予玉米油,另设NAC组(300.0 mg·kg~(-1)NAC+50.0 mg·kg~(-1)ACN),1次·天~(-1),6天·周~(-1),共染毒13周。次日称重并处死大鼠,测定大鼠脑组织NO含量、总NOS水平及iNOS、p-p38和p38蛋白表达水平。结果显示,ACN各剂量组大鼠脑组织脏器系数与对照组比较均显著降低(P0.05),高剂量组大鼠脑脏器系数与NAC组比较降低(P0.05)。高剂量组NO含量和总NOS水平显著高于对照组,与NAC组比较,高剂量组NO含量降低(P0.05),总NOS水平升高(P0.05)。Western blot结果显示,ACN高剂量组大鼠脑组织iNOS、p-p38蛋白表达水平和p-p38/p38比值显著高于对照组和NAC组(P0.05)。ACN可激活iNOS/p38MAPK信号通路,这可能是ACN致大鼠脑组织损伤的机制之一。     

有机磷及氨基甲酸酯类农药单独和联合作用对PC_(12)细胞DNA损伤的影响

研究有机磷类农药毒死蜱和对硫磷、氨基甲酸酯类农药克百威和残杀威单独及联合染毒大鼠嗜铬细胞瘤株(PC12细胞)所致的DNA损伤情况及联合作用模式。分别以0μmol·L~(-1)、50μmol·L~(-1)、100μmol·L~(-1)、200μmol·L~(-1)、400μmol·L~(-1)的有机磷农药毒死蜱、对硫磷与0μmol·L~(-1)、25μmol·L~(-1)、50μmol·L~(-1)、100μmol·L~(-1)、200μmol·L~(-1)的氨基甲酸酯类农药克百威、残杀威单独及两两联合染毒PC12细胞12 h后进行彗星实验,采用彗尾长度、尾部DNA百分含量、尾矩3个指标来衡量DNA损伤程度。结果表明:毒死蜱、克百威、对硫磷、残杀威染毒PC12细胞12 h后,细胞出现拖尾,呈现典型的彗星图像。染毒后PC12细胞彗尾长度、尾部DNA百分含量、尾矩较对照组显著增加,差异有统计学意义(P0.01)。析因分析表明,无论低剂量联合还是高剂量联合,毒死蜱与克百威、对硫磷与残杀威均有交互作用(P0.01),作用模式为协同作用。以上结果提示,有机磷及氨基甲酸酯类农药单独及联合作用均可引起PC12细胞DNA损伤,联合作用后损伤程度要高于单独作用,且低剂量和高剂量联合时均存在交互作用,作用模式为协同作用。     

二氧化硫体内衍生物对雄性小鼠精子的毒性效应

为了探讨二氧化硫(SO2)的雄性生殖毒理效应,研究了SO2体内代谢衍生物———亚硫酸钠(Na2SO3)和亚硫酸氢钠(NaHSO3)混合液(物质的量比为3:1)对雄性昆明小鼠精子的毒性作用.采用腹腔注射(i.p.)染毒方法,每天注射一次,连续5 d,于染毒后d 35处死动物,观察和分析小鼠的精子活动度、数量和畸形率.结果表明:(1)SO2衍生物可引起小鼠精子数量尤其是正常活动度精子数量减少,引起不活动精子数量增加,且呈剂量-效应关系;(2)SO2衍生物可引起多种类型的精子畸形增加,尤其可引起不定形畸变精子的频率显著增加,总精子畸变率随染毒剂量的增加而呈剂量依赖性增高.由此推论,SO2污染有一定的雄性生殖毒性.图1表2参14     

挥发性有机物混合暴露对小鼠脑组织的氧化损伤及学习记忆能力的影响

为探讨挥发性有机物混合急性暴露对小鼠脑组织氧化损伤及学习记忆能力的影响,选用雄性昆明种小鼠50只,随机分为对照组和4个染毒组。1到4号染毒组中甲醛、苯、甲苯和二甲苯浓度依次为:(1.0+1.1+2.0+2.0)、(3.0+3.3+6.0+6.0)、(5.0+5.5+10.0+10.0)、(10.0+11.0+20.0+20.0)mg·m~(-3)。各染毒组混合气体组分的浓度分别是我国室内空气质量标准(GB/T18883—2002)的10、30、50和100倍。结果显示,在Morris水迷宫实验第4天,2、3和4号染毒组小鼠的逃避潜伏期分别为(68.9±10.3)、(72.2±4.0)和(71.5±5.1)s,比对照组(48.5±10.1)s显著延长(P<0.05或P<0.01),但小鼠的脑体比和抓力在染毒期间没有明显变化。同时,随着染毒剂量的增加,小鼠脑组织中GSH含量显著降低,ROS和MDA含量显著升高。研究表明,挥发性有机物混合暴露可导致小鼠学习记忆能力降低,而脑组织氧化损伤可能是引起神经毒性,导致学习记忆能力降低的原因之一。     

围生期毒死蜱暴露致子代8周雄鼠睾丸组织的氧化损伤

毒死蜱是目前全世界使用和销售量最大的有机磷杀虫剂之一。为探讨围生期毒死蜱暴露致8周雄性子鼠睾丸组织的氧化损伤,选择健康Wistar妊娠母鼠于妊娠期(gestation days,GD)第6天至子鼠出生后(postnatal days,PND)21天通过灌胃染毒0、0.75、1.35和2.70 mg·kg~(-1)剂量的毒死蜱,待雄性子鼠8周龄取左侧睾丸实施组织病理学检查,右侧睾丸用以检测丙二醛(maleic dialdehyde,MDA)的含量和谷胱甘肽S转移酶(glutathione S transferases,GST)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)、总超氧化物歧化酶(total superoxide dismutase,T-SOD)的活力。结果表明,与对照组比较,随着染毒剂量的增加子鼠体重和睾丸、附睾脏器系数有下降的趋势(P0.05);而MDA呈升高趋势(P0.05)。各组T-SOD和1.35、2.70 mg·kg~(-1)剂量组GSH-Px活力的下降及2.70 mg·kg~(-1)剂量组GST活力的升高均有统计学意义(P0.05)。睾丸组织病理学检查结果可见2.70mg·kg~(-1)剂量组睾丸组织有明显的损伤,管腔中精液量减少,生精细胞脱落增多。上述研究结果提示母鼠于围生期暴露于毒死蜱,可通过氧化损伤诱导子代雄性大鼠睾丸的毒性作用。     

全氟辛烷磺酸（PFOS）对小鼠T、B淋巴细胞增殖功能和NK细胞活性的干扰效应研究（Disturbance of Mice Lymphocyte Proliferation Function and NK-cell Activity by Perfluorooctane Sulfonate（PFOS）Exposure）

为初步探讨全氟辛烷磺酸(Perfluorooctane sulfonate,PFOS)的细胞免疫毒性,采用每天1次经口灌胃染毒的方法,研究了PFOS经口重复剂量染毒对C57BL/6小鼠淋巴细胞增殖功能和NK细胞活性的影响.选择雄性C57BL/6小鼠40只,随机分为4组.实验组PFOS染毒剂量分别为5、10、20mg·kg-1(bw),对照组给予2%Tween-80.每天1次经口灌胃染毒7d后,制备脾脏T淋巴细胞悬液,以刀豆蛋白A(ConA)和大肠杆菌脂多糖(LPS)作为刺激源,采用MTT法检测T、B淋巴细胞增殖功能,乳酸脱氢酶释放法检测NK细胞活性.结果表明,10mg·kg-1和20mg·kg-1PFOS染毒组小鼠体重呈明显的下降趋势,且小鼠胸腺和脾脏指数显著低于对照组(p<0.05),而各PFOS染毒组小鼠肝脏指数均显著高于对照组(p<0.05).PFOS各染毒组T淋巴细胞的增殖功能均显著低于对照组(p<0.05);10mg·kg-1和20mg·kg-1PFOS染毒组小鼠NK细胞的活性显著降低(p<0.05).研究结果显示,PFOS暴露可降低小鼠淋巴细胞增殖功能和NK细胞活性,表明PFOS具有免疫抑制效应.     

全氟辛烷磺酸对雌鹌鹑的生殖毒性研究

为了探讨全氟辛烷磺酸(PFOS)对雌性禽类的生殖毒性,以雌鹌鹑为禽类指示动物进行了PFOS经口染毒实验.染毒组PFOS染毒剂量分别为12.5、25.0、50.0mg·kg-1(以饲料中的PFOS计),同时设对照组,连续染毒71天,检测体重、产卵率、受精率、孵化率及雏鹌鹑死亡率、畸形率等指标.结果表明,染毒第33天起50.0mg·kg-1剂量组雌鹌鹑体重显著低于对照组(p<0.01),并出现死亡;各染毒组开始产卵时间均滞后于对照组,产卵率均低于对照组;各染毒组雌鹌鹑受精率、孵化率、孵化12h后雏鹌鹑体重均低于对照组,雏鹌鹑畸形率、孵化后12h内雏鹌鹑死亡率均高于对照组;随着染毒剂量的增加,雌鹌鹑血清及卵黄中PFOS含量也相应升高,均呈显著正相关(p<0.01);各染毒组雌鹌鹑开始产卵5天内所产卵中PFOS含量均显著高于实验结束前3天所产卵(p<0.01).以上研究结果提示,PFOS可推迟雌鹌鹑产卵时间,降低产卵率,对受精率、孵化率及孵化后雏鹌鹑的生存和发育均有不利影响.     

Subacute chlorpyrifos-induced alterations in serum lipids and some oxidative stress biomarkers in male Wistar rats: beneficial effect of acetyl-L-carnitine

The present study evaluated the beneficial effect of acetyl-L-carnitine (ALC) on subacute chlorpyrifos (CPF)-induced alterations in serum lipid profiles and some biomarkers of oxidative stress in Wistar rats. Twenty-eight adult male rats divided into four groups of seven animals each (group I–IV) were used: I (S/oil) received soya oil (2 ml kg^?1), II (ALC) received ALC (300 mg kg^?1); III (CPF) received CPF (8.5 mg kg^?1 ～ 1/10th LD₅₀); IV (ALC+CPF) was pretreated with ALC (300 mg kg^?1) and then exposed to CPF (8.5 mg kg^?1), 30 min later. The treatment was orally for 28 days duration. Sera obtained from blood samples were evaluated for the levels of triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-c), malondialdehyde (MDA), and the activities of superoxide dismutase (SOD) and catalase (CAT). The levels of low density lipoprotein-cholesterol (LDL-c), very low density lipoprotein-cholesterol (VLDL-c), and atherogenic index (AI) were calculated. The result showed that elevated levels of TG, TC, LDL-c, VLDL-c, AI, and MDA, and the decreased levels of HDL-c, CAT, and SOD induced by CPF were modulated by ALC. It was concluded that ALC ameliorated the alterations in serum lipid and oxidative stress induced by CPF exposure in the rats, partly through its antioxidant properties.     

Impact of chlorpyrifos on cerebrum and cerebellum maturity in suckling rats

The purpose of our study is to assess the effect of chlorpyrifos (CPF) on rat cerebral and cerebellar maturity during the suckling period. Female Wistar rats were given 0.2?g?L^?1 of CPF in drinking water, equivalent to 40?mg?kg^?1 of body weight?day^?1, from day zero until day ten after delivery. In treated pups, plasma butyrylcholinesterase (BuChE) activity was inhibited by 70%. Cerebrum and cerebellum acetyl-cholinesterase (AchE) activities were reduced by 71 and 75%, respectively. The results suggest that CPF was distributed in pup tissues through the milk of lactating mothers, resulting in inhibition of AchE activities. At age 10 days, the CPF-treated pups showed a 28% decrease in body weight, a 23 and 41% decrease in plasma free T₃ and T₄ levels and reduction in cerebral and cerebellar protein content by 36 and 38%, respectively. Consistent histological changes were found in the cerebellum of CPF treated pups, with the external granular layer being markedly developed, the Purkinje cell bodies being poorly differentiated and abnormally distributed into the internal granular layer.     

Propetamphos enhances chlorpyrifos-induced organophosphate-induced delayed neurotoxicity (OPIDN) in Hens: a role for plasma butyrylcholinesterase

This study examined dose-response effects of chlorpyrifos (CPF) and propetamphos (PRO) on producing organophosphorus-induced delayed neurotoxicity (OPIDN) in hens. A single oral dose of 1, 3, 30, or 100 mg/kg of each compound was administered individually, or in combination to groups of 10 hens. Plasma butyrylcholinesterase (BChE) activity was inhibited by all doses of each individual compound. Chlorpyrifos alone or in combination with PRO resulted in decreased acetylcholinesterase (AChE) activity. No dose of CPF or PRO alone resulted in the inhibition of neuropathy target esterase (NTE) or produced OPIDN. In contrast, combined exposure to high doses of CPF and PRO produced diminished NTE activity and produced OPIDN. Brain NTE activity was decreased by 67% and 71% by combined treatment of 100 mg/kg CPF with 30 mg/kg and 100 mg/kg PRO, respectively, consistent with the development of ataxia and paralysis, characteristic of OPIDN. Only the highest dose of CPF 100 mg/kg interacted with the two highest doses of PRO to block NTE and induce OPIDN, whereas no marked interaction occurred at lower doses. Data indicate that PRO enhances the ability of high doses of CPF to produce OPIDN by binding to plasma BChE that appears to act as a buffering system to modulate the toxicity of CPF. In effect, the ability of BChE to bind to CPF is diminished by PRO, resulting in more CPF delivery to the brain, and subsequent development of OPIDN at a dose that does not initiate this effect by itself.     

气管滴注大气细颗粒物对大鼠心脏的急性毒性及其机制研究

为探讨大气细颗粒物(PM2.5)对大鼠心脏的急性毒性及其机制,将28只健康雄性Wistar大鼠随机分为空白膜对照组、7.5mg·kg-1、15mg·kg-1和30mg·kg-1剂量组.细颗粒物采用一次性咽喉部气管滴注染毒,24h后处死动物.分别于染毒30min、1h和24h后测定大鼠心电图,采用间接免疫荧光化学方法测定大鼠心脏缝隙连接蛋白Cx43的分布,采用免疫印迹法(Western blot)测定连接蛋白Cx43的表达;光镜下观察心脏的组织病理学改变.结果发现,染毒30min后,各组大鼠心律失常发生率均高于基础测量时,染毒1h后对照组恢复正常心律,而颗粒物染毒组仍显示异常心律,与对照组相比,15mg·kg-1和30mg·kg-1剂量组大鼠心律失常发生频率显著增加(p<0.05),染毒24h后各组均恢复正常心律.Cx43免疫荧光结果显示,染毒24h后,15mg·kg-1和30mg·kg-1剂量组大鼠心肌Cx43荧光强度显著降低(p<0.01);Western blot测定结果显示,随着PM2.5染毒剂量的增加,心肌组织Cx43表达逐渐减少,15mg·kg-1和30mg·kg-1剂量组Cx43蛋白水平分别为对照的57%和51%,与对照组相比,差异具有显著性(p<0.01);病理切片结果发现,对照组和各剂量均可见到心肌横纹,心肌排列正常,横纹清晰,未见明显心肌细胞萎缩、变性,亦未见炎细胞浸润.本次研究结果表明,大气PM2.5可引起健康Wistar大鼠心律异常的发生,心肌组织Cx43分布和表达的异常可能是其机制之一.     

赤霉酸暴露对SD大鼠青春期发育的影响

赤霉酸是目前国内外使用极其广泛的一种植物生长调节剂,但是针对其发育毒性的数据依然较少。本文探讨了赤霉酸暴露对SD大鼠青春期发育的影响。参考国内外环境内分泌干扰物危害的评价方法,将144只初断乳SD大鼠按体重随机分为4组,分别为对照组和1、10、100 mg·kg-1bw剂量组,采用经口灌胃方式对雄鼠连续染毒28 d,雌鼠连续染毒21 d。暴露结束后检测大鼠的体重、食物利用率、雄鼠包皮分离时间/雌鼠阴道开口时间、血清生化指标、脏器系数及组织病理学的变化。研究结果表明,与对照组相比,仅10和100 mg·kg-1bw剂量组雄鼠的肌酐水平显著升高(P<0.01),100 mg·kg-1bw剂量组雌鼠谷丙转氨酶水平有显著升高(P<0.01)。而与对照组相比,所有剂量组均未观察到大鼠的体重、食物利用率、雄鼠包皮分离时间/雌鼠阴道开口时间、脏器系数等指标有显著性差异的改变(P>0.05),组织病理学结果亦显示大鼠重要器官无损害性改变。因此,在本试验给予的剂量范围内赤霉酸染毒不会对SD大鼠青春期发育产生显著影响。     

2,3,7,8-四氯二苯并对二噁英对大鼠卵巢颗粒细胞雌二醇和孕酮分泌的影响

为研究2,3,7,8-四氯二苯并对二噁英(TCDD)对体外原代培养大鼠卵巢颗粒细胞活力和雌二醇(Estradiol,E2)、孕酮(Progestone,P)分泌的影响,探索TCDD对卵巢颗粒细胞的毒性作用阈值和程度,对未成熟SD大鼠卵巢颗粒细胞进行了原代培养,并设2组体外染毒实验:终浓度分别为0.1、1、10、100nmol·L-1TCDD染毒24h和10nmol·L-1TCDD染毒1、3、6、18、24h.染毒结束后采用MTT法检测细胞活力,RIA法检测收集培养液中的E2和P含量.结果表明,1、10、100nmol·L-1TCDD可显著抑制大鼠卵巢颗粒细胞活力和E2、P的分泌,与阴性对照、0.1%DMSO组、0.1nmol·L-1TCDD组比较差异均有显著性(p<0.05);10nmol·L-1TCDD染毒6、18、24h可明显抑制细胞活力和E2、P的分泌,与对照组和短期染毒组(1h、3h)差异均有显著性(p<0.05).痕量的TCDD可显著降低大鼠卵巢颗粒细胞活力并抑制细胞E2和P分泌,对大鼠卵巢颗粒细胞的毒性作用阈值可能为1nmol·L-1或更低.TCDD的生殖毒性作用可能与直接对卵巢颗粒细胞的毒性作用和抑制甾体激素的生物合成以及分泌有关.     

Potential correlation between perfluorinated acids and liver morphology in East Greenland polar bears (Ursus maritimus)

In this study, residual concentrations of chlorpyrifos (CPF) were determined in feed (40) and fodder (25) samples collected from various locations of Tarai region of Uttarakhand. For extracting residues, liquid–liquid partition followed by alumina column clean up was used and the detection and quantification of residues was undertaken with the help of high-performance liquid chromatography using C18 column and diode array detector at 220?nm. Of the total 40 feed samples analyzed, 7 (17.5%) samples were found positive for CPF with the mean residual concentration of 0.058?µg?g^?1; while out of 25 fodder samples, CPF residues were detected in a single (4%) sample with residual concentration of 0.39?µg?g^?1. However, none of the feed or fodder samples contained CPF residues above the prescribed limit.     

胚胎期和哺乳期全氟辛烷磺酸(PFOS)暴露致大鼠学习记忆能力下降

为了探讨全氟辛烷磺酸(PFOS)的发育神经毒性,寻找PFOS发育神经毒性作用的敏感期,利用水迷宫和组织病理切片技术,研究了胚胎期和哺乳期暴露于PFOS后新生大鼠发育情况、学习记忆能力、抓力以及海马组织病理学改变。结果显示：PFOS导致仔鼠发育迟缓,睁眼期延迟。仔鼠出生后体重与对照组相比出现显著性降低。同一PFOS暴露浓度下,胚胎期暴露组体重低于哺乳期暴露组,抓力差异不显著。水迷宫实验结果显示,TT15(胚胎期和哺乳期均暴露于15 mg·L^-1 PFOS)和TC15(仅胚胎期暴露于15 mg·L^-1 PFOS)暴露组仔鼠逃避潜伏期显著高于对照组,且TC15暴露组仔鼠逃避潜伏期显著性高于CT15(仅哺乳期暴露于15 mg·L^-1 PFOS)暴露组。空间探索实验中,TT15暴露组仔鼠在目标象限的游泳时间显著性低于对照组,其他组无显著性差异。组织病理切片结果显示暴露组海马组织细胞数量减少,出现细胞凋亡现象。结果表明,PFOS造成仔鼠的发育延迟以及学习记忆能力下降的关键作用时期可能是胚胎期。     

胚胎期及哺乳期全氟辛烷磺酸盐(PFOS)暴露对大鼠长时程突触可塑性影响的miRNA组学研究

为探讨PFOS胚胎期及哺乳期暴露对动物子代学习记忆能力影响的分子机理,采用微小RNA(miRNA)芯片技术检测PFOS胚胎期及哺乳期暴露对出生第1和7天大鼠脑组织miRNA表达的影响,分析突触可塑性相关miRNA表达的差异变化。结果显示,经PFOS暴露后出生第1和7天的大鼠脑组织中分别有24和17个miRNA发生显著性差异表达(p<0.05),其中与突触传递和神经递质转运等相关的miRNA的差异表达最为显著,主要包括miR-466b、miR-672、miR-297、miR-674-3p和miR-207。差异表达miRNA的路径分析显示出生后1和7d的大鼠的长时程增强效应(LTP)均受PFOS显著影响(p<0.05),这说明PFOS胚胎期及哺乳期暴露可能通过影响LTP的形成、发展和维持过程对大鼠子代大脑学习记忆能力造成威胁,并且miR-466b、miR-672、miR-297、miR-674-3p和miR-207可能参与了其中的调控过程。     

Does colour matter? The importance of colour in avoidance learning, memorability and generalisation

Aposematic species exploit the ability of predators to associate, for example, conspicuous colouration with the unprofitability of prey. We tested the importance of colour for avoidance learning, memory and generalisation in wild-caught great tits (Parus major). First, we determined the birds’ initial colour preferences for red, yellow, orange and grey artificial prey items. The birds showed some preferences, as they were more willing to eat grey prey as their first choice, but these were not strong preferences. We then trained birds to discriminate red, yellow or variable (red and yellow) signals from grey where colours signalled palatable and unpalatable food. In general, the birds learned the discrimination task equally well, irrespective of which colours signalled unpalatability, and subsequently remembered the distinction between previously palatable and previously unpalatable colours in the memorability test. We did not find strong evidence that variability in the signal affected learning or memory. Our results suggest that, in a task where birds must discriminate between palatable and unpalatable prey, it does not matter which specific colour signals unpalatability, although this might be context-dependent. To study whether training also affects responses to unconditioned stimuli, we included orange prey items in the memorability test. Although orange had been palatable in the initial preference test, the birds ate fewer orange prey items after they had been trained to avoid red, yellow or both colours (variable signal) as unpalatable prey, but did not change their preference when trained that these colourful signals were palatable. This indicates that generalisation occurred more readily after a negative experience than a positive experience, a situation that would potentially allow imperfect mimicry to occur.