真菌深黄被孢霉及其提取物对高脂血症的作用

探讨深黄被孢霉菌粉及其提取物对实验性高脂血症小鼠血脂的影响 .用高脂饲料造成昆明小白鼠高脂血症动物模型 ,以力平之为阳性对照 ,测定深黄被孢霉及其提取物灌胃小鼠 6 0d后 ,对高脂血症小鼠的血清总胆固醇(TC)、甘油三酯 (TG)、高密度脂蛋白 (HDL)含量的影响 .结果表明 :深黄被孢霉及其提取物可使小鼠血清TG、TC降低(P <0 .0 5或P <0 .0 1) ,并能显著提高血清中HDL水平 (P <0 .0 1) ,且脂溶性提取物和水溶性提取物之间对TG、TC的降低具有协同效果 .图 1表 1参 6     

水胺硫磷亚急性暴露对小鼠肝脏氧化应激的影响

为探讨水胺硫磷对小鼠肝脏损伤作用机制,设置0.11、1.08、2.16 mg·kg-13个低、中、高不同剂量组,以灌胃方式对昆明种小鼠进行染毒7 d后,测定小鼠肝脏组织超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)2种抗氧化酶的活性,以及抗氧化物质谷胱甘肽(GSH)和膜脂质过氧化物丙二醛(MDA)含量,同时观察肝脏的组织学变化。结果表明,除低剂量组外,中、高剂量组小鼠肝脏SOD和GSH-Px活性与对照组相比均受到显著抑制(P0.05),GSH的含量与对照组相比显著下降(P0.05),MDA含量与对照组相比却呈显著上升趋势(P0.01),同时各指标的变化均呈一定的剂量-效应关系。组织学观察显示中、高剂量组肝细胞出现明显水肿和坏死,肝窦狭窄甚至闭塞。结果表明氧化损伤可能是水胺硫磷致小鼠肝脏毒性损伤的作用机制之一。     

铬在小鼠体内的蓄积效应与毒性

铬的工业用途很广,主要用于金属加工、电镀、制革等行业,这些行业排放的三废导致了环境铬污染,对环境生态和人体健康造成危害。为探究铬对动物的毒性作用,选择昆明种纯系小白鼠作为受试生物,研究六价铬在小鼠体内的蓄积效应及毒性。结果显示,饮用水中一定浓度的六价铬(15~70 mg·L-1)可抑制小鼠体重的正常增长,染毒30 d后,小鼠肝脏和肾脏脏器系数下降,脾脏和脑的脏器系数提高;总铬含量在心脏和脾脏中增高,其他脏器中无明显蓄积效应;铬染毒组小鼠骨髓细胞活性氧水平提高,骨髓嗜多染红细胞微核率显著增高。结果表明,通过饮水摄入六价铬可造成小鼠肝肾损伤,心脏和脾脏内铬蓄积,并通过活性氧损伤效应破坏机体的遗传稳定性。     

双酚A对小鼠肝脏和肾脏细胞的氧化损伤

为探究双酚A(BPA)的氧化毒性,分别以剂量为20、40和80mg·kg~(-1)·d~(-1)的BPA对雄性昆明小鼠灌胃处理1周,并测定了小鼠体内活性氧自由基(ROS)水平、还原型谷胱甘肽(GSH)含量、丙二醛(MDA)含量和DNA-蛋白质交联系数(DPC)。与对照组相比,各BPA暴露组小鼠肝脏和肾脏细胞中的ROS生成量、MDA含量和DPC系数均升高,而GSH含量下降(P<0.05或P<0.01)。ROS生成量、GSH含量和DPC系数均显示出剂量-效应关系。研究表明,BPA可扰乱小鼠肝脏和肾脏细胞的氧化应激平衡,诱导细胞氧化损伤。     

五氯酚钠对雄性小鼠的生殖毒性作用

为研究五氯酚钠(PCP-Na)对雄性小鼠的生殖毒性作用,将100只昆明雄性小鼠随机分为5组:3个染毒组、1个阴性对照组(蒸馏水)和1个阳性对照组(环磷酰胺40mg·kg-1).以不同剂量(13.44、26.88、53.76mg·kg-1)PCP-Na经口染毒,连续染毒5d,每天1次.染毒结束后第2d和第23d分两批处死动物,检测精子数量、精子畸形率以及睾丸、附睾重量及其脏器系数的变化.结果表明,PCP-Na染毒结束后第2d,与阴性对照组相比,高剂量组(53.76mg·kg-1)精子畸形率显著增加(p<0.05),睾丸、附睾重量及附睾系数显著下降(p<0.05),其他指标无显著变化(p>0.05).中、低剂量组(26.88、13.44mg·kg-1)各检测指标与阴性对照组均无显著性差异(p>0.05);PCP-Na染毒结束后第23d,与阴性对照组相比,高剂量组(53.76mg·kg-1)精子畸形率显著增加、精子密度显著减少、睾丸和附睾重量显著下降(p<0.05),中剂量组(26.88mg·kg-1)附睾重量显著下降(p<0.05),其他指标均无显著变化(p>0.05);PCP-Na引起的精子畸形以头部畸形为主,主要为无定形,其次为无钩形、香蕉形和尾折叠.以上结果提示,在本实验条件下,PCP-Na对雄性小鼠具有明显的生殖毒性.     

硫化镉量子点与常规硫化镉对小鼠遗传毒性的比较研究

为比较硫化镉量子点(CdS quantum dots,CdSQDs)与常规硫化镉(CdS)对小鼠的遗传毒性作用,将30只昆明种健康雄性小鼠随机分为对照组、CdSQDs组和常规CdS组,通过经口灌胃法进行染毒,其中CdSQDs组和常规CdS组染毒剂量为100mg·kg-1,对照组为等体积的生理盐水.染毒35d后将小鼠处死,通过单细胞凝胶电泳观察外周血淋巴细胞DNA损伤情况,取小鼠一侧附睾观察精子畸形率,并取双侧肾脏做组织病理学检验.结果表明,与对照组小鼠比较,CdSQDs组和常规CdS组小鼠DNA损伤和精子畸形率均显著升高(p<0.05);CdSQDs组小鼠DNA损伤程度及精子畸形率均显著低于常规CdS组(p<0.05);组织病理切片观察显示,两种材料均可引起小鼠肾脏病变,但CdSQDs组小鼠病变程度明显轻于常规CdS组.以上结果提示,CdSQDs和常规CdS均会对小鼠产生一定程度的遗传毒性作用,但CdSQDs毒性低于相同剂量的常规CdS.     

汽车使用乙醇汽油后排放污染物变化趋势

对汽车使用乙醇汽油后尾气中污染物的变化趋势进行了研究,结果表明使用乙醇汽油后,CO和碳氢化合物含量呈明显降低趋势,平均下降率为56.9%和38.2%;氮氧化物含量有所下降,平均下降率为15.0%;CO2含量有所升高,平均增长率为5.04%;苯系物含量明显降低,平均下降率在45.5%～53.1%;醛类的含量呈明显增加趋势,平均增长率在47.8%～293%;丙酮、丁酮的含量略有增加,增加幅度分别为、16.6%和25.3%。     

基于开场试验的森林环境保健功能研究

对森林环境的保健功能进行研究,可为生态旅游资源的开发提供理论基础。采用开场试验(OFT),对在森林和室内环境中生活的小白鼠行为学指标变化进行分析,研究森林环境对小白鼠自发行为的影响,进而综合评价森林环境的保健功能。结果表明,(1)常绿阔叶混交林和柳杉(Cryptomeria fortunei)林的群落结构组成有很大的不同,但其林分环境对小鼠自发行为的动物验证具有很多类似的规律,试验组和对照组小鼠自发活动指标呈阶段性变化,初期差异不显著,但随环境因子影响的累积,中后期差异明显。(2)以柳杉林和常绿阔叶混交林中的小白鼠与对照组自发活动指标差距最大值来看,其运动总路程比对照组分别要高31.49%(P=0.009)和46.64%(P=0.031),小鼠中央格运动路程、穿越次数、站立次数分别是对照组的2.58倍(P=0.016)和1.98倍(P=0.009)、2.24倍(P=0.011)和1.42倍(P=0.035)、1.41倍(P=0.007)和1.41倍(P=0.019);边角活动时间分别比对照组要少7.1%(P=0.004)和7.81%(P=0.007);小鼠的体质量分别为对照组的1.27(P=0.000)和1.15倍(P=0.029),小鼠的粪便粒数分别比对照组要少30.1%和30.2%,降低幅度都远远大于对照组。(3)福州旗山森林环境对提高小鼠的兴奋性、增加小鼠的探索认知能力、缓解焦虑状态、增强食欲等方面有促进作用。     

溴化1-十四烷基-3-甲基咪唑对小鼠的肝脏毒性及其作用机制

研究离子液体溴化1-十四烷基-3-甲基咪唑盐([C₁₄mim]Br)对小鼠的肝脏毒性及其作用机制。实验设立3个剂量的染毒组(1/16 LD₅₀、1/8 LD₅₀、1/4 LD₅₀)和1个空白对照组，考察昆明种小鼠染毒14 d后，[C₁₄mim]Br对小鼠血清生化指标、肝脏抗氧化酶活性及脂质过氧化产物的影响，并观察肝脏组织的病理变化。与对照组相比，小鼠染毒后，血清中ALT、AST、DBIL和γ-GT明显升高；肝组织受到不同程度的损伤，HSI增大，蛋白质含量降低。当染毒剂量为1/4 LD₅₀时，肝脏中SOD活性和GSH-Px活性显著降低，MDA的含量则明显增加。实验结果表明，[C₁₄mim]Br可损伤小鼠的肝脏功能，破坏机体的抗氧化防御系统，造成氧化损伤和脂质过氧化。     

小鼠肝气乘脾泄泻模型的建立及痛泻要方的疗效

为建立小鼠肝气乘脾泄泻的造模方法,并通过痛泻要方对其疗效进行验证.采用番泻叶加束缚夹尾法制备肝气乘脾泄泻小鼠模型,运用痛泻要方进行治疗,以主观和客观指标进行综合评价.结果显示,番泻叶-束缚夹尾使模型小鼠出现情绪亢奋,腹泻程度严重,进食量减少,体重增长幅度下降,毛发变暗、枯黄,同时甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、5-羟色胺(5-HT)含量升高(P 0.05),D-木糖含量下降(P 0.05),符合脾虚证诊断标准,同时出现肠推进率增高(P 0.05)、胃残留率降低(P 0.05)等小肠功能亢进的表现.经痛泻要方干预后小鼠一般行为接近正常组,腹泻症状明显消失,总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)(P 0.05)、TG、LDL-C相对正常组含量下降(P 0.05),模型组相对自然恢复组的5-HT含量减少(P 0.01),而D-木糖含量出现一定程度的升高(P0.05),痛泻要方能调节模型小鼠的胃肠运动,降低其肠推进率,升高胃残留率(P 0.05).本研究表明通过番泻叶-束缚夹尾法上午灌胃番泻叶造成小鼠脾虚泄泻,下午离心管束缚夹尾模拟小鼠肝旺状态,连续造模7 d,可以建立小鼠肝气乘脾泄泻模型,痛泻要方干预3 d可以治愈,5-HT增高、D-木糖降低、胃动力减缓等能作为小鼠肝气乘脾泄泻的评价指标;结果可为小鼠肝气乘脾泄泻模型的建立提供可靠的实验依据.(表6参22)     

Hepatoprotective effects of taurine against mercury induced toxicity in rats

An attempt has been made to study the influence of taurine on mercury intoxicated rats. The animals were treated with sublethal dose of mercuric chloride (2 mg/kg body wt.) for 30 days. During the mercury treatment, the level ofAspartate transaminase(AST), Alanine transaminase (ALT) and Alkaline phosphatase(ALP) in serum and lipid peroxidation (LPO) in liver tissue significantly increased whereas Glutathione (GSH), Glutathione peroxidase(GPx), Catalase (CAT) and Superoxide dismutase (SOD) were simultaneously decreased in the liver tissue. Present results indicate that the liver tissue was completely damaged, after mercury treatment. In another group of animals, taurine (5 mg/kg body wt.) was administrated for another 15 days. Taurine administration was observed to improve the liver function in mercury intoxicated animal as indicated by the decline in increased levels of AST, ALT and ALP in serum and LPO content in liver tissue. The decreased level of antioxidant system (GSH, GPx, CATand SOD) has been promoted Results suggested that taurine played a vital role in reducing the mercury toxicity in intoxicated animals.     

Response of ultraviolet-B induced antioxidant defense system in a medicinal plant, Acorus calamus

Ultraviolet-B (UV-B) radiation generates an oxidative stress in plant cells due to excessive generation of reactive oxygen species (ROS). ROS can denature enzymes and damage important cellular components. In the present study, an important medicinal plant Acorus calamus (Sweet flag) was subjected to two doses of supplemental UV-B radiation (sUV-B): sUV1 (+ 1.8 kJ m(-2) d(-1)) and sUV2 (+3.6 kJ m(-2) d(-1)) to evaluate the relative response of antioxidant defense potential. Stimulation of activities of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX) and glutathione reductase (GR) was observed at initial growth period while the activities of CAT and SOD decreased at later age of sampling. sUV-B induced lipid peroxidation (LPO) was observed showing alteration of membrane properties. No definite trend of change was observed for ascorbic acid (AsA), while increments in thiol, proline, phenol and protein contents were observed due to sUV-B. Results suggested that sUV-B radiation may stimulate the enzymatic and non-enzymatic defense system of Acorus plants, showing its better adaptation at lower dose of sUV-B.     

十溴联苯醚(BDE-209)对紫红笛鲷鳃抗氧化酶活性的影响

十溴联苯醚(BDE-209)是目前唯一仍在全球范围内广泛使用的多溴联苯醚阻燃剂,其环境行为及生物效应逐渐成为环境污染领域研究的热点。选用2(LD组)、10(MLD组)、50(MHD组)及250μg.L-1(HD组)4个浓度的BDE-209作用于紫红笛鲷,探讨BDE-209对紫红笛鲷鳃抗氧化酶(SOD、CAT及POD)活性和MDA含量的影响。结果显示:BDE-209可以显著促进SOD和CAT活性,且随着暴露时间延长CAT活性呈现逐渐增加的趋势。暴露7d后,MLD组SOD活性达到最高68.31U.mg-1,是对照组(CK)的5.50倍,HD组CAT活性达到6.31U.mL-1,其次为MHD组的5.96U.mL-1。BDE-209对鳃POD活性呈现先促进后抑制的作用,暴露3d时各浓度POD活性均显著高于CK组(P<0.05);7d时各浓度POD活性则受到显著抑制(P<0.05),清水恢复15d后各浓度组与CK组没有显著差异(P>0.05)。暴露期间各浓度组MDA含量均显著高于CK组(P<,并且随暴露时间延长呈现先增加后减少的趋势,7d后HD组MDA含量达到最高,为6.99nmol.mg-1,清水恢复15d后,LD和MLD组MDA含量与CK组没有显著性差异(P>0.05)。以上结果表明:BDE-209可以诱导紫红笛鲷产生氧化应激效应,CAT和SOD则在氧自由基清除中发挥作用。     

Cr(VI)对脊尾白虾(Exopalaemon carinicauda)幼虾暴露和恢复期肝胰脏的SOD活性、MDA及MTs含量的影响

为了探索水体中Cr(VI)对脊尾白虾(Exopalaemon carinicauda)的毒性效应,通过Cr(VI)的暴露(15 d)和清水恢复实验(15 d),研究了Cr(VI)对脊尾白虾肝胰脏的SOD活性、MDA及MTs含量的影响。结果表明,通过15 d的暴露,5 mg·L-1(高浓度)、0.5 mg·L-1(低浓度)实验组肝胰脏的SOD均显著高于对照组水平(p0.05),15 d的清水恢复后,两个浓度实验组均能够恢复到对照组水平(p0.05)。MDA在暴露阶段呈现持续上升的趋势,且在15 d后两个浓度实验组MDA的含量均显著高于对照组水平(p0.05),15 d的清水恢复后,5 mg·L-1实验组的MDA含量依然显著高于对照组水平(p0.05),0.5mg·L-1实验组的MDA含量基本恢复到对照组水平(p0.05)。通过15 d的暴露,两个浓度实验组MTs的含量均显著高于对照组水平(p0.05),15 d的清水恢复后,两个浓度实验组MTs的含量均能够恢复到对照组水平(p0.05)。     

Vitamin E-mediated protection on methomyl-induced alterations in rat liver

The present study was carried out to observe the possible beneficial effects of Vitamin E, a natural antioxidant on methomyl-induced biochemical and histological alterations in rat liver. To carry out the investigations, animals were segregated in four different groups. Animals in Group I served as normal controls. Animals in Group II were given single methomyl dose orally in water (9 mg kg^?1 b.wt). Animals in Group III were injected intraperitoneally with Vitamin E (50 mg kg^?1 b.wt) for 1 week on alternate days. Animals in Group IV were administered Vitamin E 1 week before subjecting them to methomyl treatment. Animals in all the groups were sacrificed 24 h after the end of treatments. Different biochemical estimations were carried out, which included estimation of aspartate aminotransaminase (AST), alanine aminotransaminase (ALT), alkaline phosphatase (ALP) and acetylcholinesterase (AChE). Further, to examine the oxidative damage lipid peroxidation (LPO) and glutathione (GSH) levels as well as antioxidant enzymes such as superoxide dismutase (SOD), catalase, glutathione-S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GSHPx), and glutathione-6-phosphate dehydrogenase were estimated in liver samples. AchE activity was inhibited significantly both in serum and liver following methomyl treatment. Administration of methomyl caused a significant increase in serum AST, ALT and ALP which indicated hepatic damage. LPO was found to be significantly increased, whereas GSH levels were decreased in the liver of methomyl-treated animals. The activities of SOD and catalase were significantly decreased whereas GST and GSHPx activities were found to be elevated significantly following methomyl treatment. No significant change in the enzyme activity of GR and glutathione-6-phosphatase dehydrogenase was observed after methomyl treatment. Vitamin E supplementation was able to attenuate appreciably the methomyl-induced changes in LPO levels along with SOD and GST activities. Histopathological studies following methomyl treatment revealed that hepatocytes, were not very well delineated and nuclei showed degenerative changes. Whereas, following Vitamin E supplementation in combined treatment group nuclei showing degenerative changes become less in number. The study, therefore, concludes that Vitamin E has a potential in mitigating most of the adverse effects induced by methomyl acute toxicity.     

全氟辛酸(PFOA)对菲律宾蛤仔体内酶活性的影响

采用半静态毒性实验方法,将菲律宾蛤仔(Ruditapes philippinarum)分别暴露于0.2、2、20μg·L-1的全氟辛酸(perfluorooctanoic acid,PFOA)中,在处理后第1、3、6、10、15、21天分别取样,测定整体组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、过氧化物酶(POD)、谷胱甘肽-S-转移酶(GST)、7-乙氧基异吩噁唑酮脱乙基酶(EROD)活性和过氧化脂质(LPO)含量。酶活性分析结果显示:PFOA对菲律宾蛤仔组织SOD、CAT和POD活性均呈现先促进后抑制的作用;低浓度组SOD活性在暴露第1天达到最高,显著高于对照组(P<0.01);中高浓度组SOD活性在暴露第6天达到最低;暴露1~15 d,低浓度组CAT活性均显著高于对照组(P<0.05);高浓度组CAT活性在暴露第6天得到显著诱导,其余时间基本处于抑制状态;中浓度组POD活性在暴露第3天即达到最高,高浓度组POD活性基本一直处于抑制状态;随着PFOA暴露时间的延长,菲律宾蛤仔组织LPO含量呈现了先降低后升高的趋势;各浓度组中EROD的活力都显著被诱导(P<0.01),与处理浓度呈正相关;中高浓度组的GST活性在胁迫期间变化比较显著,呈现诱导-抑制的变化规律。研究表明,PFOA暴露能够引起菲律宾蛤仔组织抗氧化酶和生物转化酶的变化,可以与其他敏感性指标一起作为指示早期海洋PFOA污染的生物标志物。     

芘暴露对马氏珠母贝鳃和肝胰腺抗氧化酶活性的影响

在实验生态条件下，采用生态毒理学方法，选用海洋环境中常见的有机污染物多环芳烃芘（Pyrene），以马氏珠母贝（Pinctada martensi）为实验材料进行毒理实验。研究了芘不同质量浓度（8、16、32和64μg·L^-1、不同时间（7，10 d）的胁迫对马氏珠母贝鳃和肝胰腺组织中超氧化物歧化酶（SOD）、过氧化物酶（POD）和谷胱甘肽过氧化物酶（GPx）3种抗氧化酶活性的影响。结果表明：3种酶在不同组织和不同胁迫时间的敏感性有所差异，在芘胁迫马氏珠母贝第7天，鳃组织中 SOD、POD、GPx 3种酶活性主要表现为诱导现象，高质量浓度组对3种酶活性均具有极显著诱导作用（p〈0.01），而芘胁迫对肝胰腺3种酶活性的影响主要表现为抑制作用，且POD酶活性表现最敏感，在较低浓度组就被显著抑制（p〈0.01）；到染毒第10天，鳃组织中SOD、GPx两种酶诱导作用明显，POD诱导现象不显著（p〉0.05），肝胰腺中3种酶活性与对照组相比诱导明显，并表现出一定的剂效关系。两种组织中SOD和GPx活性的变化具有一定的同步性。通过比较最低可观察效应质量浓度（LOEC），发现在第7天，鳃组织中敏感性强弱表现为SOD=POD〉GPx，肝胰腺中表现为POD〉GPx〉SOD，而到第10d，两组织中敏感性又分别表现为GPx〉SOD〉POD，GPx=SOD〉POD。因此，在较短的暴露时间，POD酶活性可作为芘胁迫对马氏珠母贝的生物标志物，而对于较长时间的染毒实验，可选用 GPx 酶作为芘胁迫对马氏珠母贝的生物标志物以监测海洋环境芘污染。     

影响雨生红球藻797株生长和虾青素积累的某些因素

研究了雨生红球藻 (Haematococcuspluvialis) 797株的N源需求和营养盐吸收 ,并利用高光强和乙酸钠处理该藻 ,研究虾青素累积情况以及超氧化物歧化酶 (SOD)活性、营养盐、细胞状态的变化 .NH+ 4 N培养的生长速率明显高于NO-3 N培养 ,平均生长速率分别为 0 .2 79d-1和 0 .190d-1.NH+ 4 N培养所消耗的N、P营养盐比NO-3 N培养的消耗少 .两种N源下强光照处理 1d和 7d均导致雨生红球藻细胞数减少而静细胞比例增加 .在虾青素合成阶段 ,藻液N含量急剧下降而P含量基本保持稳定 ,说明虾青素合成对N的需要量大而对P的需要小 .在NO-3 N培养下 ,乙酸钠的加入则对虾青素的生产无显著影响 .在NH+ 4 N培养下SOD活性下降而虾青素含量升高 ;在NO-3 N培养下SOD活性与虾青素含量同时升高 .图 2表 4参 15     

Mercuric chloride induced proteotoxicity and structural destabilization in marine fish (Therapon jarbua)

The reaction byproducts derived from lipid peroxidation (LPO), as well as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) enzyme activities were measured in tissues of marine fish (Therapon jarbua) exposed to mercuric chloride (HgCl) in water dispersions of 0.125 or 0.25 ppm. LPO was significantly increased in various tissues relative to control values after 96-h exposure. SOD and GPx activities significantly decreased after exposure to first two doses but significantly elevated CAT in Dose II kidney and liver tissues. The elevated levels of LPO, decreased activities of SOD and GPx, and increased CAT activities in all tissues examined in T. jarbua are an index of oxidative stress in fish. Structural analysis by scanning electron microscopy studies revealed the structural deformation in HgCl₂-exposed animals. These observations suggest that HgCl acts as a mediator in free radical generation. The increase in CAT and decrease in SOD and GPx activities in these tissues may be an adaptive response.