外源性核苷酸对孕期饮酒小鼠子代生长发育的影响

目的 探讨外源性核苷酸对孕期饮酒C57BL/6J小鼠子代生长发育的影响.方法 C57BL/6J孕鼠随机分为空白对照组、酒精对照组和低(0.01％)、中(0.04％)、高(0.16％)3个核苷酸干预组,对照组动物喂饲普通小鼠饲料,核苷酸干预组喂饲含有相应剂量核苷酸的饲料,并于孕6～15 d给予酒精对照组和各干预组孕鼠5 g/kg bw酒精灌胃,观察母鼠和仔鼠整个实验周期内体重、进食量、食物利用率的变化和子代小鼠生长发育、神经发育指标达标的时间.结果 0.04％核苷酸干预组孕鼠孕期的体重增长值明显高于酒精对照组(P＜0.05),3个核苷酸干预组孕鼠的食物利用率也显著高于酒精对照组(P＜0.01);断乳后4周内,酒精对照组子代小鼠的体重增长值和食物利用率均明显低于其他各组(P＜ 0.05和P＜0.01);酒精对照组子代小鼠出生后门齿萌出、睁眼的时间和平面翻正、悬崖回避、空中翻正等神经反射达标的时间也明显比其他各组迟缓(P＜0.05和P＜0.01).结论 孕期补充核苷酸可以干预宫内酒精暴露引起的生长发育迟缓.     

被动吸烟对子代小鼠学习记忆的影响及抗氧化物干预研究

目的:研究烟雾环境对孕鼠的子代智力发育的影响及抗氧化剂的神经系统保护作用。方法:雌性小鼠20只,随机均分为吸烟(TS),吸烟+槲皮素(TS+Q,quercetin80mg/kgdiet),吸烟+VE(TS+VE,100mg/kgdiet)和对照4组,前3组暴露于香烟的雾染毒柜中6h/d,5d/w,连续3个月,之后每组放1只雄鼠进行交配,雌鼠继续染毒至孕20d左右待产时,产仔后,选子代雄鼠每组15只,分别给予相应饲料至仔鼠体重20±2g时进行水迷宫试验,测定其仔鼠空间学习记忆能力、长时程增强(LTP)和脑组织中一氧化氮(NO)含量和一氧化氮合酶(NOS)、乙酰胆碱脂酶(AChE)活性、血清维生素E(VE)浓度和活性氧(ROS)的影响及VE的干预效果。结果:仔鼠水迷宫测试6d后,对照组和TS+VE、TS+Q干预组小鼠到达终点平台所需时间(潜伏期)和进入盲端的次数(错误次数)明显低于TS组(P<0.05)。10d后,TS组与对照组和TS+VE干预组潜伏期比差异显著(P<0.05)。TS组LTP增强受到抑制,与对照组比差异显著(P<0.05)。TS组子代小鼠脑组织NOS活性明显高于对照组(P<0.05),TS+VE干预组和TS组与其它组比,NO的含量差异显著(P<0.05)。血清VE浓度和ROS活性与子代小鼠学习记忆能力的测定结果相一致。结论:孕期被动吸烟可降低仔鼠大脑海马齿状回(DG)神经突触的可塑性及神经元的兴奋性,抑制LTP的形成,使学习记忆功能下降,VE干预可得到改善。     

低硒对F344纯系大鼠子代神经行为发育和学习记忆能力的影响

目的建立F344纯系大鼠低硒动物模型,观察低硒对子代仔鼠神经行为发育和空间学习记忆能力的影响。方法以纯系F344大鼠为实验对象,采用人工半合成饲料(低硒组饲料硒含量<0.01mgkg,补硒对照组饲料中硒含量为0.1～0.3mgkg)建立低硒大鼠模型,观测子一代仔鼠哺乳期的生长体重变化、生长发育生理学指标和神经反射指标,并采用开场实验、Morris水迷宫实验检测其行为活动和空间学习记忆能力。结果(1)低硒组大鼠尾血GSHPx活性极其显著地低于对照组(P<0.001)。(2)低硒组仔鼠的出生体重和哺乳期神经发育不同时间点体重明显低于对照组。(3)仔鼠出生后第4天平面翻正和悬崖回避、第10天听觉惊愕反射实验中,低硒组评分均低于对照组(P<0.05),但在第7天平面翻正、悬崖回避和第11天后的听觉惊愕反射实验以及第12、14天前肢悬挂、后肢行走能力实验中,两组仔鼠结果差异无统计学意义(P>0.05)。(4)开场实验中:低硒组雄仔鼠在中央格停留时间、穿行格数较对照组明显减少(P<0.05)。(5)Morris水迷宫实验:①低硒组仔鼠第4、5天的定位航行实验中,平均潜伏期比对照组明显延长(P<0.05);在第6、9时间段的直线式搜索方式也较对照组减少(P<0.05);②低硒组在空间探索实验中,原站台象限活动时间较对照组减少(P<0.05)。结论成功利用纯系F344大鼠建立了低硒动物模型,母代长期硒缺乏导致了子一代F344仔鼠出生体重减低、生后体格发育和神经行为发育的迟缓,雄性仔鼠对新异环境中的适应能力减弱,并且导致了子代仔鼠空间学习和记忆能力能力的减弱。     

加热或丙二醛氧化大豆蛋白对小鼠体内自由基水平及抗氧化能力的影响

目的探讨加热或脂质过氧化产物丙二醛(MDA)氧化修饰大豆蛋白对小鼠体内自由基水平及抗氧化能力的影响。方法将大豆蛋白加热或MDA氧化处理,饲喂6w龄雄性KM小鼠(40只),按体重随机分成4组:对照组(未处理蛋白)、MDA氧化组(MDA氧化蛋白)、加热氧化组(100℃加热蛋白)、硫辛酸(LA)组(100℃加热蛋白+0.08%LA)。4w后测定小鼠血液和组织的自由基水平、总抗氧化能力、抗氧化酶活性、MDA含量。结果饲喂氧化大豆蛋白提高小鼠全血、肝脏、胰腺、十二指肠、空肠自由基水平,MDA氧化组自由基水平最高(P<0.01);与对照组相比,加热与MDA氧化组的小鼠组织的总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活力显著下降(P<0.05),MDA含量显著增加(P<0.01);添加0.08%LA能加速自由基的清除,提高小鼠抗氧化能力。结论摄食加热或脂质氧化产物MDA氧化的大豆蛋白,导致小鼠血液及消化器官自由基显著增加,组织抗氧化能力降低。添加抗氧化剂LA可有效清除活性氧自由基,提高机体抗氧化能力,缓解营养性氧化应激。     

大鼠繁殖实验评价牛奶对生殖发育的影响

目的观察牛奶和高剂量大豆异黄酮(SI,1g/kg)对亲代大鼠生殖能力和F1代仔鼠发育状况的影响,以评价牛奶的安全性。方法选择交配前期、宫内暴露期、哺乳期和仔鼠性成熟期(受孕前11周至仔鼠35天性成熟)分别饲喂某品牌全脂牛奶及含高剂量SI的饲料,观察亲代体重、形态学、生殖能力、生殖器官、激素水平和F1子代发育状况的变化。使用SPSS13.0统计分析,均数比较采用方差分析的统计方法。结果牛奶和高剂量的SI对亲代的动情周期、交配指数、繁殖力指数、怀孕指数、孕周、每窝活产数、子代性别比、出生身长、4日生存率均没有影响。但是牛奶组仔鼠出生体重显著增加,亲代雄鼠血液中的促黄体生成素(LH)显著降低,雌鼠血液中孕酮显著低于空白组(P<0.05);植物雌激素SI组亲代雄鼠血液中卵泡刺激素(FSH)显著降低,雌鼠血液中孕酮和催乳素(PRL)显著低于空白组(P<0.05)。牛奶和高剂量SI对F1代仔鼠只数、性别比、肛门生殖孔间距体重比、阴道开口时间和包皮分离时间均没有显著影响。结论一代繁殖实验未发现牛奶对生殖能力和子代发育能力有显著影响,但亲代大鼠血液中激素水平有所改变,其是否影响子代大鼠二代繁殖能力,需进一步实验验证。     

邻苯二甲酸酯宫内暴露对子代小鼠致肥作用的研究

目的:研究围产期宫内暴露邻苯二甲酸酯(MEHP)对子代小鼠肥胖的程序化作用。方法:不同剂量MEHP(0.05、0.25、0.5mg/kg体重)灌胃处理孕鼠做为低中高剂量组,等体积橄榄油灌胃处理的孕鼠做为对照组。处理周期为孕鼠妊娠第12天直至新生鼠出生后第7天。每周监测仔鼠体重直至第8周,并检测8周龄仔鼠的肝重、脂肪垫质量、血脂和血糖水平。结果:3组剂量MEHP宫内暴露均引起新生仔鼠体重增加(P<0.001);成年后(8周龄)雌性仔鼠体重接近对照组,而低剂量组成年雄性仔鼠体重明显高于对照组(P<0.01),附睾和肾周脂肪垫质量明显增加(P<0.001和P<0.01),血清总胆固醇、甘油三酯和血糖水平明显上升(P<0.01、P<0.05、P<0.001)。中高剂量对成年雄性仔鼠的体重、体脂组成、血脂和血糖水平无明显影响。结论:MEHP可以增加子代雄鼠肥胖发生风险,它可能作为一种潜在的化学诱导因子诱发肥胖及相关疾病发生。     

枳实提取物对实验性糖尿病小鼠肝脏抗氧化防御功能的影响

目的研究枳实提取物对试验性糖尿病小鼠肝脏抗氧化能力的影响。方法用高、中、低剂量的枳实提取物治疗糖尿病小鼠5周后,观察其一般状况、肝脏的抗氧化能力及肝脏组织形态学变化。结果枳实提取物治疗组,与糖尿病模型组比较,血糖水平显著降低(P<0.05),谷胱甘肽含量(GSH)显著增加(P<0.05),谷胱甘肽过氧化物酶活性、丙二醛和NO含量显著降低(P<0.01),超过氧化物歧化酶活性有所增加。光镜下枳实提取物治疗组肝组织细胞损伤较糖尿病组降低。结论枳实提取物具有增强肝脏的抗氧化能力,降低肝细胞损伤作用。     

甲基汞对亲仔两代大鼠的神经行为毒性效应

目的探讨大鼠妊娠期甲基汞暴露的母体毒性及对仔代的神经行为毒性效应。方法Wistar孕鼠52只于妊娠第6～9天用甲基汞0.00、0.01、0.05、2.00mg/(kg·d)连续灌胃。分别观察母体毒性 ;常规致畸实验 ;记录205只仔鼠早期生理发育和神经行为发育指标 ;10周龄仔鼠32只进行程序控制行为测试 ;分娩后5周母鼠和10周龄仔鼠各24只进行脑组织形态学观察和单胺类神经递质的测定。实验遵循随机、双盲原则。结果未观察到母体毒性和仔代形态畸形 ;3个暴露组胎仔的体重、尾长低于对照组 (P<0.01) ;各暴露组仔鼠体重增长、早期生理及神经行为发育滞后于对照组 (P<0.05) ;程序控制行为学习成绩比对照组降低 (P<0.05) ,有剂量_效应关系 (rs= -0.7273 ,P<0.01) ;各暴露组母鼠和仔鼠脑组织无形态学改变 ,但单胺类神经递质含量均比对照组显著增高 (P<0.05) ,有剂量_效应关系 (rs=0.7124～0.9257 ,P<0.01)。结论本研究剂量的妊娠期甲基汞暴露未观察到对孕鼠的毒性效应 ,但有轻度胚胎毒性 ,影响仔鼠的神经系统发育 ,导致仔鼠学习记忆能力降低 ,亲仔两代大鼠脑组织中单胺类神经递质的含量增高     

孕期尼古丁暴露对高脂饮食子代大鼠糖代谢的影响

目的 探讨孕期尼古丁暴露(prenatal nicotine exposure,PNE)对高脂饮食诱导下成年子代大鼠糖代谢的影响.方法 尼古丁组5只Wistar孕鼠妊娠第11d给予尼古丁皮下注射(2 mg/kg,d,分二次给予)至自然分娩,对照组5只孕鼠等容量生理盐水相同处理.在俩组孕鼠中分别每窝挑选雄鼠和雌鼠各1只,最终获得对照组和尼古丁组雄、雌性仔鼠分别各10只.仔鼠断奶后给予高脂饮食,记录每周体重及体重增长率.仔鼠出生后第20周(postnatal week 20,PW20)行口服糖耐量实验(oralglucose tolerance test,OGTT).PW24经麻醉后处死,苏木精-伊红染色法(hematoxylin-eosin staining,HE)观察胰腺形态.结果 PNE雄性和雌性仔鼠在PW1体重较对照组明显下降(P＜0.01),PNE组雄性子代体重PW16显著高于对照组(P＜0.05);对应的体重增长率从PW4到PW24均显著升高(P＜0.05或P＜0.01).PNE组雌性子代体重与对照组无显著性差异(P＞0.05),对应的体重增长率PW8到PW24显著升高(P＜0.05或P＜0.01).OGTT结果表明,雌性对照组在30min出现血糖高峰值,而PNE雌性组在60min出现高峰值;糖负荷120min后PNE雄、雌性子代血胰岛素仍高于对照组.结论 PNE子代出现宫内发育迟缓(intrauterine growth retardation,IUGR),在断奶后给予高脂饮食出现明显追赶性生长,以雄性更为显著.PNE子代糖代谢相关指标发生改变,以雌性更明显.     

饮水中低浓度甲基汞对小鼠仔代生长发育及神经行为的影响

[目的]ICR小鼠通过饮水暴露于低浓度氯化甲基汞(MeHgCl),观察其子代生长发育和行为及可能产生的毒作用。[方法]ICR孕鼠随机分为对照组、低浓度组(0.01mg/L)和高浓度组(0.1mg/L),于怀孕第6天起分别自由饮用蒸馏水、氯化甲基汞含量为0.01mg/L、0.1mg/L的蒸馏水直至哺乳期结束,观察母鼠和仔鼠的一般状况、仔鼠的早期发育、行为反射和学习认知能力等指标。[结果]在低浓度甲基汞作用下(相当于饮用水汞卫生标准8倍和80倍水平),亲仔两代均未出现明显的毒性反应。染毒组仔鼠的各项神经发育指标与对照组相比差异无显著性(P>0.05),但是仔鼠的学习能力显著降低(P<0.05)。[结论]在饮水中低浓度甲基汞虽然对子代的生长和行为发育没有明显的损害,但是子代的学习能力已受影响。     

Prenatal exposure to alcohol in rat: effect on intestinal enzymes in offspring

Intestinal hydrolase activities were studied during postnatal development in the offspring of rats exposed to 20% ethanol during gestation; alcohol was withdrawn at birth. Controls received water during gestation. Sucrase, lactase, glucoamylase and aminopeptidase activities were determined 2 and 4 weeks after birth in the proximal jejunum. Offspring prenatally exposed to ethanol showed a deficit in body weight and lower aminopeptidase activity during the suckling period (2 weeks). These effects were reversible by 4 weeks when alcohol was withdrawn at birth. The prenatal exposure to ethanol did not change the pattern of sucrase maturation in the intestine of offsprings. The activities of lactase and glucoamylase were not modified following prenatal exposure to ethanol. In conclusion, exposure to ethanol during gestation caused decreased abilities for the intestine of the offspring to digest protein.     

Lithium and the neonate: developmental and metabolic aspects

The interrelationship between lithium salts, which has been used in clinical trials of alcoholism, and ethanol, which evoke fetal alcohol syndrome by chronic use, was studied. This was made by evaluating the effect of prenatal and postnatal exposure to LiCl on ethanol and acetaldehyde metabolizing enzymes in the newborn mouse. The three Li-treatment regimens made consisted of acute and short-term prenatal exposure to LiCl in addition to postnatal exposure until weaning of the neonates. The weaned mice were then kept on water for a subsequent two weeks prior to sacrifice. The effects of LiCl, given in drinking fluid, on body weight, selected organ weights, hepatic alcohol dehydrogenase, aldehyde dehydrogenase and heart lactate dehydrogenase of the offspring were determined. Prenatal and postnatal ingestion of LiCl by the nursing mother resulted in decreased brain weight of offspring from both sexes. Concomitantly, there was a reduction in female but not male kidney weight. A marked decrease in the testis weight also occurred. The Li-treatment induced both neonatal hepatic alcohol dehydrogenase and heart lactate dehydrogenase in both sexes. Conversely, an inhibition of hepatic mitochondrial aldehyde dehydrogenase, for the enzyme with the apparent high Km, was determined in the male offspring. Maternal postnatal ingestion of LiCl decreased brain and spleen weights from corresponding control of neonatal male and female, respectively. This Li-treatment also induced hepatic neonatal alcohol dehydrogenase in both sexes. The results suggest that maternal ingestion of LiCl may interfere in brain development.(ABSTRACT TRUNCATED AT 250 WORDS)     

酒精对小鼠胚胎脑线粒体发育的影响

目的探讨孕期酒精染毒对后代脑线粒体发育的影响。方法ICR孕鼠随机分成3个酒精染毒组和一个空白对照组,染毒期为孕6～15天,孕18天剖腹取胎,提取胎鼠脑线粒体,测定线粒体膜电位、呼吸酶活性、ATP合成酶活性和线粒体内ATP含量。结果随着酒精染毒剂量的增高,胎鼠头体重比逐渐降低,中、高剂量组出现小头畸形;流式细胞检测显示胚胎脑线粒体幼稚群的比例逐渐增多,由对照组的18%上升到34%;在中、高剂量组呼吸酶复合体Ⅰ和Ⅳ的活性均较对照显著降低,30g(kg·d)染毒组分别相当于对照的917%和879%,60g(kg·d)染毒组分别相当于对照的724%and697%,呈剂量反应关系;60g(kg·d)染毒组胎鼠脑线粒体ATP合成酶的活性较对照显著降低,相当于对照的803%;30g(kg·d)和60g(kg·d)染毒组胎鼠脑线粒体内ATP的含量均较对照组显著降低。结论孕期酒精染毒能够影响胚胎脑线粒体的发育和功能成熟,可能与酒精所致神经管畸形有关。     

Effects of prenatal alcohol exposure on the developmental pattern of temperature preference in a thermocline

Prenatal alcohol exposure is associated with a variety of impairments in neonatal state regulatory systems. Since prenatal alcohol exposure causes thermoregulatory deficits in response to both heat and cold stress in rats, body temperature set-point might be altered in alcohol-exposed offspring. The effect of prenatal alcohol exposure on behavior in a thermocline was investigated in 10-, 15-, and 125-day-old male and female rats from three prenatal treatment conditions: alcohol liquid diet, pair-fed liquid diet control, or standard control. Subjects were placed in the thermocline in the cold, hot, or middle start positions and observed for 60 min. Subjects exposed to alcohol prenatally had a wider “preference zone” than control subjects at 10 and 15 days of age, but did not as adults. This widening of the temperature set-point in young subjects prenatally exposed to alcohol may represent a developmental lag in the development of body temperature set-point or a central compensatory process allowing the animal to adapt to alternating experiences of heat and cold stress.     

母鼠铅染毒对仔鼠生理发育与行为能力的影响及其与锌的相互作用

目的 研究孕期铅染毒对仔鼠生理发育与行为能力的影响及其与锌的相互作用。方法 给孕期母鼠喂饲含有铅、锌及铅加锌的水，观察母鼠孕期体重变化及仔鼠成活率和体重变化；采用动物行为学观察方法测试并评价其子代鼠生理发育及行为学能力，并对仔鼠脑组织单胺类神经递质及脂质过氧化产物丙二醛（MDA）含量进行了检测。结果 在未对母鼠孕期体重增大产生不良影响的铅、锌剂量下，孕期铅染毒可降低仔鼠成活率，抑制仔鼠体重增长，延迟仔鼠生理发育及新生反射发育的同时，仔鼠脑组织单胺类神经递质合成与代谢紊乱，MDA含量明显增加，母鼠孕期给锌对仔鼠成活率、体重增长未见明显物保护作用。等摩尔锌对仔鼠新生反射发育有明显的干预效果，锌还可抑制铅所致仔鼠脑组织MDA含量增加的作用。铅染毒同时给半量的锌反而使其仔鼠生理发育时间有明显的延迟作用，并促进多巴胺和5-羧色胺分解。结论 孕期铅染毒对仔鼠生理发育与行为能力有不良的影响，锌的浓度不同所表现的联合作用类型也不同，锌与铅的相互作用是十分复杂的，利用锌拮抗铅的神经毒作用时，应持慎重态度。     

Thermoregulatory deficits following prenatal alcohol exposure: structural correlates

Prenatal exposure to alcohol delays the development of thermoregulation in newborn rats. This study examined two possible physiological correlates of this effect. In the first experiment, the effect of prenatal alcohol exposure on the availability of brown adipose tissue for nonshivering thermogenesis was investigated in rat pups from birth to weanling age. Male and female pups were chosen from independent litters with one of three prenatal treatment histories: 35% ethanol-derived calories (35% EDC), pair-fed control (0% EDC), or lab-chow control (LC). Prenatal alcohol exposure resulted in decreased body weight from postnatal (PN) day 1 to 20 compared to controls. Similarly, alcohol-exposed subjects had lighter interscapular brown adipose tissue pads than controls. However, the proportion of brown adipose tissue to body weight in alcohol-exposed pups was not different from controls. It appears that thermoregulatory deficits at birth due to prenatal alcohol exposure are not due to decreased substrate availability. In the second experiment, the relative growth rate of the tail compared to the growth rate of the body was measured in male and female pups from the three prenatal treatment groups. Five-day-old rat pups exposed to alcohol prenatally had relatively slower tail growth than control pups. Since tail growth rate has been associated with ambient temperature, these results suggest that alcohol-exposed rat pups may be experiencing transient periods of cold stress in the nest because of their thermoregulatory deficiencies, which, in turn, could have important implications for neural and body growth retardation seen in Alcohol Related Birth Defects.     

孕期暴露苯并[a]芘对子代大鼠神经发育毒性的影响

目的 研究孕期暴露苯并(a)芘(B[a]P)对子代大鼠生理发育、早期行为发育、对环境的适应能力及学习记忆能力的影响.方法 SD孕鼠随机分为未处理对照组(每日正常饲养)、溶剂对照组(橄榄油)、低剂量组(25mg/kgB[a]P)、中剂量组(50mg/kgB[a]P)、高剂量组(100mg/kg B[a]P),于妊娠第17天开始,每天1次腹腔注射染毒,连续3 d,待其自然分娩.仔鼠出生后第1、4、7、14、28天称量体重,检测仔鼠生理发育、运动反射及感觉功能等发育指标,用Morris水迷宫试验和旷场试验分别评价仔鼠的学习记忆能力和对新异环境的适应能力.结果 与未处理对照组[(3.3±0.5)d]和溶剂对照组[(3.4±0.6)d]比较,中、高剂量组仔鼠张耳时间[(4.1±0.4)、(5.0±0.4)d]延长,差异有统计学意义(P＜0.01).与未处理对照组(36、1%)相比,第4天高剂量组平面翻正试验达标率(6.5%)明显降低,与未处理对照组和溶剂对照组(81.3%、79.3%)相比,第7天时高剂量组仔鼠平面翻正试验达标率(50.0%)明显降低,差异有统计学意义(P＜0.05).与未处理对照组比较,第12、14天时各染毒组仔鼠前肢悬挂时间均减少;与溶剂对照组比较,第14天时高剂量组仔鼠前肢悬挂时间减少,差异有统计学意义(P＜0.01).与未处理对照组(94.3%)相比,第12天时高剂量组仔鼠嗅觉定向试验达标率(61.9%)明显降低,差异有统计学意义(P＜0.05).Morris水迷宫试验结果表明,与未处理对照组和溶剂对照组比较,各剂量组仔鼠逃避潜伏期明显增加,高剂量组在目标象限停留时间和穿越平台次数减少,差异均有统计学意义(P＜0.01).旷场实验结果表明,与未处理对照组[(2.40±0.89)、(82.2±15.9)、(17.4±3.9)s]比较,中、高剂量组仔鼠中央格停留时间[(9.67±1.53)、(12.80±3.77)s]明显延长,跨格次数(51.3±8.7、49.4±20.0)明显减少,高剂量组直立次数(8.0±2.6)明显减少,差异均有统计学意义(P＜0.05);与溶剂对照组相比,各剂量组跨格次数明显减少,差异均有统计学意义(P＜0.01,P＜0.05).结论 孕期暴露B[a]P对仔鼠的生理发育、早期行为发育产生一定的抑制作用,并对仔鼠大脑学习记忆能力及其对新异环境的适应能力有一定影响.

Abstract：

Objective To study the effects of prenatal exposure to benzo[a]pyrene (B[a]P) on the physical development, early behavioral development, the adaptability to new environment and the learning and memory ability of rat offspring. Methods Pregnant rats were randomly divided into five groups: control group,olive oil group, 3 exposure groups (25, 50 and 100 mg/kg B [a]P). The rats were exposed to B [a]P) by intraperitoneal injection on the 17th-19th days during gestation. The offspring were weighed on postnatal days (PND)1, PND 4, PND 7 and PND 28, the indices of physical development, reflective ability and sensory function were detected for offspring, the Morris water maze and Open-field tests were used to measure the ability of learning and memory and the adaptability to new environment of offspring. Results The time of ear opening in middle and high-dose groups[(4. 1 ±0.4),(5.0±0.4) d] was posterior to that in untreated and solvent groups[(3.3±0.5),(3.4±0.6) d](P＜0.01).The attainment rate (6.5%) of the surface righting reflex test in highdose group on the 4th day was significantly lower than that (36.1%) in untreated group, the attainment rate(50.0%) in high-dose group on PND7 was significantly lower than those (81.3% and 79.3%) in untreated group and solvent group (P＜0.05). Compared to the untreated group, the time of forelimb hanging test in all exposure groups on PND12 and PND14 significantly decreased; compared to the solvent group the time of forelimb hanging test decreased in high-dose group on the 14th day significantly decreased (P＜0.01). The attainment rate (61.9%) of olfactory discrimination in high-dose group on PND 12 was significantly lower than that (94.3%) in untreated group (P＜0.05). The results of morris water maze test showed that the escape latency of different dose groups significantly increased, and the time of spatial probe and the times of traversing flat in high-dose group decreased significantly, as compared to the untreated and solvent groups(P＜0.01). The results of open-field test indicated that the center retention time in middle and high-dose groups significantly prolonged, the times of crossing lattice obviously reduced, and the rearing times decreased in high-dose group,as compared to untreated(P＜0.05).Compared to the solvent group, the times of crossing lattice in all exposure groups reduced significantly(P＜0.01 or P＜0.05). Conclusion The prenatal exposure to B[a]P could inhibit the physical development and early behavioral development, and influence the adaptability to new environment and learning and memory ability for offspring.     

茶多酚对乙醇所致原代肝细胞损伤的保护作用研究

目的研究乙醇对原代肝细胞的氧化损伤作用,同时探讨茶多酚对乙醇所致的原代肝细胞损伤模型的保护作用。方法分离小鼠原代肝细胞,直接以不同浓度乙醇作用于肝细胞,或以茶多酚预处理后再用乙醇作用于肝细胞,测定各组细胞存活率、抗氧化酶及丙氨酸氨基转移酶(ALT)活性的变化。结果随着乙醇浓度的增加,小鼠原代肝细胞存活率逐渐下降,抗氧化酶活性降低,转氨酶升高;而茶多酚的预处理对于乙醇所致的小鼠原代肝细胞损伤具有明显的保护作用,表现为相同乙醇浓度作用下,随茶多酚浓度的升高,细胞存活率逐渐升高,抗氧化酶活性增加,转氨酶下降,且差异有统计学意义(P<0.05)。结论乙醇可以诱导小鼠原代肝细胞的氧化损伤,而茶多酚对其氧化损伤具有明显的保护作用。     

Prenatal alcohol exposure and the effects of environmental enrichment on hippocampal dendritic spine density

The effects of environmental enrichment on synaptic spine density in hippocampal area CAI were examined in rats exposed prenatally to alcohol. Pregnant dams were given ethanol via intragastric intubation (6 g/kg/day) from gestational days 8 through 19, or given isocaloric sucrose. An untreated control group was also used. After weaning, offspring from the three groups were then reared for 10 weeks in either isolated (caged alone, not handled) or enriched (group housed with “toys,” handled) conditions. Animals were then sacrificed, the brains Golgi impregnated, and CA1 pyramidal cell apical and basilar spine densities quantified. Among isolated animals there were no significant differences between control and alcohol-exposed groups. In general, environmental enrichment increased apical or basilar spine densities in untreated and sucrose controls. However, in prenatal alcohol-exposed animals, environmental enrichment did not increase spine densities. Because the environmental enrichment acted postnatally, these findings suggest that the effects of prenatal alcohol exposure include decreased neural plasticity enduring into early adulthood. Such a reduction in neuroanatomical plasticity in Hppocampus may be associated with cognitive impairments found following prenatal alcohol exposure.     

Responses to ethanol challenge in long- and short-sleep mice prenatally exposed to alcohol

Individual sensitivity to alcohol may influence the severity of functional deficits due to prenatal alcohol exposure. To examine this hypothesis, Long-Sleep (LS) and Short-Sleep (SS) mice, selectively bred for differences in ethanol-induced narcosis, were intubated with either 2.9 g/kg ethanol (E) or an isocaloric amount of sucrose (S) twice per day on days 7 through 15 of pregnancy. An untreated control group (C) was maintained for each line. Offspring were fostered to lactating Rockland-Swiss mice at birth. Males and females from each litter were challenged with an acute dose of ethanol (3.8 g/kg) at 30 days of age. Measures of sleep time duration, waking blood ethanol concentrations (BEC), rectal temperatures, heart rate, and ethanol clearance were obtained to examine whether the acute effects of ethanol are altered by prenatal alcohol exposure. Prenatal alcohol exposure did not differentially affect responses to ethanol challenge within either genotype. Ethanol-induced hypothermia, heart-rate depression, and sleep time did differ between genotypes, with LS more affected than SS mice. Ethanol clearance rates were faster for SS than LS mice. These results suggest postnatal pharmacological responses to acute ethanol challenge are not altered by prenatal alcohol exposure in LS and SS mice. Prenatal alcohol-exposed offspring of both mouse genotypes showed lower average heart rate responses than controls, suggesting this measure may be a sensitive indicator of prenatal alcohol effects in mice.