不同浓度一氧化碳对大鼠脂质过氧化及谷胱甘肽过氧化物酶的…

不同浓度一氧化碳对大鼠脂质过氧化及各胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的影响研究结果表明：大鼠在５００ｍｇ／ｍ＾３ＣＯ染毒下，第２０天血液中的脂质过氧化物及第３０天心脏组织的脂质过氧化物均明显升高，而５０、２５ｍｇ／ｍ＾３ＣＯ染毒则未见上述变化。但自２５ｍｇ／ｍ＾３浓度开始，ＧＳＨ－Ｐｘ活性即发生明显变化。提示ＣＯ能诱发自由基导致脂质过氧化；也说明ＧＳＨ－Ｐｘ是ＣＯ对机体影响的早期敏感指标之一。本研     

不同浓度一氧化碳对大鼠脂质过氧化及谷胱甘肽过氧化物酶的影响

不同浓度一氧化碳对大鼠脂质过氧化及各胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的影响研究结果表明：大鼠在５００ｍｇ／ｍ３ＣＯ染毒下，第２０天血液中的脂质过氧化物及第３０天心脏组织的脂质过氧化物均明显升高，而５０、２５ｍｇ／ｍ３ＣＯ染毒则未见上述变化。但自２５ｍｇ／ｍ３浓度开始，ＧＳＨ－Ｐｘ活性即发生明显变化。提示ＣＯ能诱发自由基导致脂质过氧化；也说明ＧＳＨ－Ｐｘ是ＣＯ对机体影响的早期敏感指标之一。本研究可为室内ＣＯ卫生标准的制订提供部分新的资料。     

三硝酸铈致大鼠肝脏脂质过氧化损伤

ＳＤ成年大鼠随机分为２组,每组３０只,另设对照组（６０只）。一次性腹腔注射１５０ｍｇ／ｋｇＣｅ（ＮＯ３）３,分别于３、６、１２、２４、４８ｈ处死,测定其肝脏蛋白质浓度、ＭＤＡ、ＧＳＨ含量及ＳＯＤ、ＣＡＴ、ＧＳＨ、Ｐｘ、ＧＳＨ、ＳＴ酶的活性。结果显示,注入Ｃｅ（ＮＯ３）３以后,大鼠肝脏内蛋白质浓度、ＭＤＡ含量明显增加,而ＧＳＨ含量及ＳＯＤ、ＧＡＴ、ＧＳＨ－ＰＸ、ＧＳＨ－ＳＴ酶的活性则显著降低。提示Ｃｅ（ＮＯ３）３进入大鼠体内后,早期能够引起肝脏脂质过氧化损伤,使大鼠肝脏抗氧化能力、抗诱变能力降低,估计脂质过氧化损伤可能是由于Ｃｅ３＋与ＧＳＨ作用导致ＧＳＨ耗竭所致。     

原油蒸气吸入引起大鼠肺脂质过氧化损伤的研究

给予大鼠吸入原油蒸气１５ｇ／ｍ３×８ｈ（急性染毒Ⅰ组）、３０ｇ／ｍ３×８ｈ（急性染毒Ⅱ组）、３ｇ／ｍ３×８ｈ／ｄ×３０ｄ（亚急性染毒组），观察血液和肺组织ＧＳＨ、ＭＤＡ含量和ＧＳＨ－Ｐｘ活性变化。结果３个染毒组大鼠血ＧＳＨ含量均明显减少；肺ＧＳＨ－Ｐｘ活性均有所下降，尤以２个急性染毒组酶活性下降显著（Ｐ＜０．０１），急性染毒Ⅱ组大鼠肺ＧＳＨ－Ｐｘ活性仅约为对照组的１／３；急性染毒Ⅱ组大鼠肺ＭＤＡ含量轻度增高，血ＭＤＡ含量显著增高（Ｐ＜０．０５）。本研究提示原油蒸气吸入，可削弱机体氧自由基清除系统的抗脂质过氧化损伤的活性，并引起一定程度的生物膜脂质过氧化损伤。表明脂质过氧化损伤反应可能是原油蒸气吸入引起肺损伤的机理之一。     

二氧化氮对大鼠肺脂质过氧化,抗氧化酶及花生四烯酸代谢的影响

本研究观察了二氧化氮对大鼠肺脂质过氧化，抗氧化酶及花生四烯酸代谢的影响，实验选用Ｗｉｓｔａｒ雄性健康成年大鼠，体重１５０￣１７５ｇ，设计浓度：自然空气，０．１５、１．５，１５ｍｇ／ｍ＾３ＮＯ２组。暴露方法：静式染毒，每天２小时，每周６天，染毒４周，实验结果表明：（１）随着ＮＯ２浓度的递增，大鼠尿中血栓烷素Ｂ２与６－酮－前列腺素Ｆ１ａ比值逐渐升高，且存在剂量－反应关系。（２）１．５ｍｇ／ｍ＾３ＮＯ２     

3－硝基丙酸脂质过氧化作用的实验研究

９只雄性大鼠以８０ｍｇ／ｋｇ３－硝基丙酸（３－ＮＰＡ）经口染毒后１５、３０和４５ｍｉｎ时，在肝脏中用电子自旋共振仪可检测到较强的自由基信号。肾上腺素红法测定发现５×１０－３～１０－２ｍｏｌ／Ｌ３－ＮＰＡ可明显促进肝与脑微粒体和线粒体产生自由基。８０ｍｇ／ｋｇ３－ＮＰＡ灌胃染毒大鼠肝和脑中ＳＯＤ和ＧＳＨ－Ｐｘ活性上升，ＭＤＡ含量升高。因此３－ＮＰＡ在体内和体外均有诱发脂质过氧化作用的能力。     

3－硝基丙酸脂质过氧化作用的实验研究

９只雄性大鼠以８０ｍｇ／ｋｇ３－硝基丙酸（３－ＮＰＡ）经口染毒后１５、３０和４５ｍｉｎ时，在肝脏中用电子自旋共振仪可检测到较强的自由基信号。肾上腺素红法测定发现５×１０－３～１０－２ｍｏｌ／Ｌ３－ＮＰＡ可明显促进肝与脑微粒体和线粒体产生自由基。８０ｍｇ／ｋｇ３－ＮＰＡ灌胃染毒大鼠肝和脑中ＳＯＤ和ＧＳＨ－Ｐｘ活性上升，ＭＤＡ含量升高。因此３－ＮＰＡ在体内和体外均有诱发脂质过氧化作用的能力。     

谷胱甘肽及VitB6对CS2染毒大鼠的保护作用研究

目的：为探讨金属离子络合及ＶｉｔＢ６代谢障碍在二硫化碳（ＣＳ２）神经毒作用中的作用；方法：测定ＣＳ２染毒大鼠脑组织中微量元素铜的含量，并用ＶｉｔＢ６及谷胱甘肽（ＧＳＨ）进行干预。以ＳＤ雄性大鼠为中毒模型，检测不同浓度（０，３００，６００，１２００，２４００ｍｇ／ｍ３）染毒两个月后脑组织铜的含量；同时在高浓度（２４００ｍｇ／ｍ３）组给予两种干预药物：ＧＳＨ（１００ｍｇ／ｋｇ，腹腔注射，一次／日），ＶｉｔＢ６（灌胃，一次／日，０．４ｍｇ／日），观察对大鼠行为及酶活性的影响。结果：ＣＳ２染毒大鼠脑组织铜含量无明显改变；ＧＳＨ，ＶｉｔＢ６对ＣＳ２致运动协调能力障碍无明显改善，对反映学习记忆能力的指标（步下法）有改善作用；ＧＳＨ对Ｎａ＋－Ｋ＋－ＡＴＰ酶活性有升高作用。结论：ＣＳ２所致中枢神经系统与外周神经系统毒性在机制上可能有所不同。     

NO2和LPG燃烧产物对大鼠肺脂质过氧化,胶原含量和尿HOP的影响

本研究分别观察了ＮＯ２染毒和ＬＰＧ燃烧产物自然暴露对Ｗｉｓｔａｒ雄性成年大鼠肺脂质过氧化、肺胶原含量和尿ＨＯＰ排泄的影响及其相互关系。结果发现７．５２ｍｇ／ｍ＾３的ＮＯ２对三者均有一定影响，染毒剂量不同大鼠尿ＨＯＰ排泄也有相应的变化。尿ＨＯＰ的变化早于肺胶原含量，且两者有一定的相关关系。ＬＰＧ燃烧产物暴露期间，尿ＨＯＰ含量一直高于对照组，但未见肺胶原含量的变化，８周时尿ＨＯＰ与肺脂质过氧化物之间有     

车间空气中多次甲基多苯基多异氰酸酯卫生标准的制定研究

ＰＭＰＰＩ分子式中含多个－ＮＣＯ基团,对眼、皮肤等有轻微刺激和潜在致敏作用。小鼠经口ＬＤ５０为７２６６．１ｍｇ／ｋｇ,表明ＰＭＰＰＩ属低毒化合物。２小时吸入染毒小鼠ＬＣ５０大于１２６．９ｍｇ／ｍ＾３,大鼠ＬＣ５０大于５７．２ｍｇ／ｍ＾３。亚慢性吸入染毒实验表明４．４９ｍｇ／ｍ＾３可视为无可见作用浓度。Ａｍｅｓ、ＵＤＳ试验和小鼠骨髓微核试验表明ＰＭＰＰＩ在很高剂量时有一定致突变性。安全系数拟取１０。     

口服谷胱甘肽对氟所致大鼠脂质过氧化的影响

目的 探讨口服不同剂量的谷胱甘肽（GSH）对氟所致大鼠质过氧化的影响。方法 对事先饮用10天150mg/L氟化钠（NaF）的雄性Wistar大鼠分别给予60、300和600mg/kg GSH灌胃12周,同时设对照组（饮蒸馏 水）和单纯氟染毒组（150mg/LNaF ）,测定血清（全血）、肝、肾、心、睾丸和脑组织中超氧化物歧化酶（SOD） 活性和丙二醛（MDA）含量。结果 单纯氟染毒可使大鼠血清、肝、肾、脑MDA含量显著增加,全血、肝、肾、心、睾丸SOD活性显著降低;口服GSH后,血清、肝、肾、脑MDA的生成减少,肝、肾、心、睾丸和SOD活性显著上升,同是300mg/kgGSH可显著促进尿氟的排出。结论 氟可使大鼠脂质过氧化作用增强,抗氧化能力降低,口服GSH可拮抗氟致脂过氧化作用,增加抗氧化能力。     

茶多酚对铅脂质过氧化损伤拮抗作用的研究

目的 探究茶多酚（TP）对铅（Pb）致细胞脂质过氧化损伤的拮抗作用。方法 Wistar雄性大鼠60只随机分为6组,分别给予0、50、100、300mg/kg不同浓度TP灌胃、第6、8、10天分别给予乙酸铅40mg/kg腹腔注射,对照组给予蒸馏水灌胃,腹腔注射生理水。第11日眶静脉采血,继续TP灌胃1周后处死动物,取股动－静脉混合血、肝、脑组织实验。结果 （1）单纯染铅组大鼠体重较非染铅组明显降低,差异有显著性（P＜0．05）,而同时予TP100、300mg/kg灌胃可明显拮抗铅对大鼠生长抑制,末次染铅24h、1周的大鼠体重与TP相关系数为r＝0．973（P＜0．01）和r＝0．9979（P＜0．01）,呈正相关。（2）末次染铅24h、1周的染铅大鼠较非染铅大鼠血、肝、脑丙二醛（MDA）含量明显升高,差异有显著性（P＜0．05）;超氧化物歧化酶（SOD）活力抑制,差异有显著性（P＜0．05）,TP100、300mg/kg灌胃可拮抗铅的上述作用;同时染铅大鼠血、肝、脑谷胱甘肽（GSH)水平、谷胱甘肽－S－转移酶（GST）活力亦发生明显改变,而TP100、300mg/kg灌胃可拮抗铅的作用。结论 TP可明显拮抗铅致大鼠血、肝、脑脂质过氧化损伤而具有防治、拮抗铅中毒的重要功能。     

砷与铅与人及大鼠红细胞脂质过氧化作用的影响

The authors observed the joint effects of arsenic and lead on lipid peroxidation(LPO) in vitro and in vivo. In vitro, the authors used the extracted erythrocyte membrane of health adult men and divided them into three exposed groups. The first group was exposed to As2O3 (0, 0.4, 2.0 and 10.0 mmol/L). The second group was exposed to PbAc2 (0, 0.08, 0.4 and 2.0 mmol/L). The third group was exposed to As(10 mmol/L) + Pb (0.08 mmol/L). The results show that there is interaction between As and Pb on LPO of erythrocyte membrane. In vivo, the authors measured LPO levels of rat's plasma, blood glutathione(GSH) and superoxide dismutase(SOD) activity. By using 2 x 2 factorial design, Wistar rats were gavaged with As2O3 2.4 mg/(kg.d) and PbAc2 30 mg/(kg.d) as well as both arsenic and lead in water for 10 days. The results show that in the As-Pb treated rats, the levels of LPO did not change significantly, the GSH levels and SOD activity decreased significantly. The results of factorial analysis revealed a synergic effect of As-Pb on SOD activity.     

模拟400m氦氧饱和潜水对大鼠抗氧化能力的影响

[目的]观察模拟400m氦氧饱和潜水对大鼠抗氧化能力的影响。[方法]将大鼠在加压舱4．1MPa氦氧环境中饱和暴露24h,以常压和4．1MPa常氧高氦环境作为对照。出舱后测定大鼠肝、脑和肺中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—px）活性和还原型谷胱甘肽（GSH）、丙二醛（MDA）及8-羟基脱氧鸟苷（8-OhdG）含量。[结果]4．1MPa氦氧饱和暴露后大鼠脑SOD活性和肝、脑和肺GSH—Px活性降低（P〈0．05）,脑和肺GSH含量减少（P〈0．05）。4．1MPa常氧高氦暴露后大鼠各指标未见明显改变（P〉0．05）。各组MDA和8-OhdG含量差异无统计学意义（P〉0．05）。[结论]模拟400m氦氧饱和潜水24h使大鼠产生了氧化应激反应,抗氧化能力降低,其原因可能与该环境中的高分压氧有关。     

Peanuts improve blood glutathione,HDL-cholesterol level and change tissue factor activity in rats fed a high-cholesterol diet

Background The inverse association of peanut consumption and risk markers of CHD (lipids) has been reported however health professionals are still concerned whether hyperlipidemic subjects advised to eat peanuts will have increased serum lipid levels. Tissue factor (TF), the major regulator of normal haemostasis and thrombosis, plays a critical role in haemostasis in all tissues. Aim of the study To investigate the effects of peanut consumption on lipid profile, blood Glutathione (GSH), thiobarbituric acid reactive substances (TBARS), haematologic parameters and TF activities in rats fed a high-cholesterol diet. Methods 32 Wistar Albino rats were divided into 4 groups of 8 rats each: 1-Control 2-Control+peanut 3-Hyperlipidemic and 4-Hyperlipidemic+peanut group. At the end of 12 weeks, blood samples were used to evaluate lipid profile, haemostatic parameters, GSH, TBARS and tissue samples were used for the determination of TF activities. Results Peanut consumption increased blood GSH both in the control and hyperlipidemic groups; increased HDL-cholesterol and decreased TBARS in the hyperlipidemic group. The addition of peanut to the diet did not change blood lipids, protrombin time, activated partial thromboplastin time or fibrinogen levels significantly both in the control and hyperlipidemic groups. It affected TF activities differently in both groups. It decreased brain and aorta TF activity but increased spleen and kidney TF activity in the control group. It led to significant increases in the TF activity of kidney, spleen and aorta and a significant decrease in the TF activity of brain in the hyperlipidemic group. Conclusion Peanut consumption improved GSH and HDL-C levels and decreased TBARS, without increasing other blood lipids in experimental hyperlipidemia. Nevertheless the mechanism of the effect of peanut consumption on the TF activity of tissues remains to be determined.     

砷与铅对人及大鼠红细胞脂质过氧化作用的影响

通过体内体外实验探讨了砷与铅对机体脂质过氧化（ＬＰＯ）的联合作用。用离体人红细胞膜染毒，砷（Ａｓ２Ｏ３）在体系中浓度分别是０，０．４，２．０，１０．０及２０．０ｍｍｏｌ／Ｌ；铅（ＰｂＡｃ２）在体系中浓度分别是０，０．０８，０．４及２．０ｍｍｏｌ／Ｌ；联合染毒采用２×２析因设计，各取其剂量的最低无作用剂量，３７℃孵育６０ｍｉｎ测定ＬＰＯ水平。结果显示，砷与铅对离体人红细胞膜ＬＰＯ的影响具有联合作用，其作用形式为相加作用。为观察砷与铅对整体动物的影响，我们采用２×２析因设计，分别取ＬＤ５０的１／５剂量以灌胃的方式染毒，砷为２．４ｍｇ／ｋｇ，铅为３０ｍｇ／ｋｇ，连续１０天。结果显示，砷与铅对大鼠血浆ＬＰＯ作用不明显，但引起红细胞超氧化物歧化酶（ＳＯＤ）活性的明显抑制，红细胞谷胱苷肽（ＧＳＨ）含量下降；析因分析表明，砷与铅对大鼠红细胞ＳＯＤ活性抑制具有联合作用，联合作用形式为相加作用     

孕期和哺乳期母鼠饮水砷暴露对子代大鼠脑组织神经递质代谢酶的影响

目的了解砷对神经递质代谢酶的影响,探讨砷对学习、记忆能力影响的机制。方法选取清洁级Wistar大鼠,按雌∶雄为2∶1合笼。将64只孕鼠随机分为3个暴露组（分别为10、50、100mg/L剂量组）和1个对照组（蒸馏水）。暴露组于妊娠第6天（胎鼠器官分化开始）开始用NaAsO2溶液进行饮水染毒。仔鼠出生后,母鼠继续染毒。仔鼠出生后28d断乳,染毒至出生后第42天。在仔鼠出生后第0、28、42天,测量其大脑皮质和海马中谷氨酰胺合酶（GS）、乙酰胆碱酯酶（AChE）活力。结果出生后第0、28、42天,各暴露组子鼠脑皮质和海马中GS活力与对照组比较,经方差分析,差异均无统计学意义（P〉0.05）。出生后第0天,各组仔鼠的脑组织中AChE活力比较,经方差分析,差异无统计学意义（P〉0.05）。出生后第28、42天,100mg/L组子鼠脑海马中AChE活力高于对照组,差异均有统计学意义（P〈0.05）;且AChE活力均随染毒剂量的增加而增强,相关系数分别为0.408和0.374,呈统计学正相关（P〈0.05）,有明显的剂量-效应关系;其他各组仔鼠脑皮质AChE活力比较,经方差分析,差异均无统计学意义（P〉0.05）。结论砷暴露能够引起发育中的仔鼠脑组织AChE活力改变,可能会导致相应的中枢神经系统的一些改变。     

Melatonin protects rat liver against irradiation-induced oxidative injury

The aim of this study was to investigate the antioxidant roles of different doses of melatonin (5 and 10 mg x kg (-1) ) against gamma-irradiation-caused oxidative damage in liver tissue after total body irradiation (TBI) with a single dose of 6.0 Gy. Fifty adult rats were divided into 5 equal groups, 10 rats each. Groups I and II were injected with 5 and 10 mg x kg (-1) of melatonin, and group III was injected with an isotonic NaCl solution. Group IV was injected with only 5 mg x kg (-1) of melatonin. Group V was reserved as a sham control. Following a 30-min-period, 6.0 Gy TBI was given to groups 1, 2 and 3 in a single fraction. The liver malondialdehyde (MDA) levels, super oxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were measured in all groups. TBI resulted in a significant increase in the liver tissue MDA levels and a decrease of SOD and GSH-Px activities. The results demonstrated that the liver tissue MDA levels in irradiated rats that were pretreated with melatonin (5 or 10 mg x kg (-1) ) were significantly decreased, while the SOD and GSH-Px activities were significantly increased. Decreasing the MDA levels by melatonin was dose dependent, but the liver tissue SOD and GSH activities were not. The data obtained in this study suggest that melatonin administration prior to irradiation may prevent liver damage by irradiation.     

Influence of sesame oil on blood glucose, lipid peroxidation, and antioxidant status in streptozotocin diabetic rats

The present study was carried out to assess the influence of sesame oil on blood glucose, lipid peroxidation, and status of antioxidants in normal and streptozotocin (STZ) diabetic rats. Diabetes was induced in adult female albino Wistar rats weighing 180-200 g by administration of STZ (40 mg/kg of body weight) intraperitonially. Both normal and diabetic rats were fed with a commercial diet containing 2% oil supplemented with 6% sesame oil for 42 days. Diabetic rats had elevated levels of blood glucose (322.61 +/- 9.49 mg/dL), glycosylated hemoglobin, vitamin E, thiobarbituric acid-reactive substances (TBARS), and lipid hydroperoxides and decreased levels of hemoglobin, vitamin C, and reduced glutathione (GSH). An increase in glucose-6-phosphatase and fructose-1,6-bisphosphatase activities and a decrease in hexokinase activity were observed in liver and kidney tissues. When diabetic rats fed with sesame oil were compared with diabetic rats, a significant reduction in levels of blood glucose (222.02 +/- 8.27 mg/dL), glycosylated hemoglobin, TBARS, and lipid hydroperoxides and glucose-6-phosphatase and fructose-1,6-bisphosphatase activities and an elevation in hemoglobin, vitamin E, and GSH levels and hexokinase activity were observed. Thus, sesame oil consumption influences beneficially the blood glucose, glycosylated hemoglobin, lipid peroxidation, and antioxidant levels in diabetic rats.     

大气混合污染物对大鼠呼吸系统氧化损伤作用

目的 探讨大气混合污染物所致大鼠呼吸系统的氧化损伤。方法 48只Wistar大鼠随机分为3个实验组（1，7，30d组）和1个对照组。气管注入可吸入颗粒物（PM10）后，静态吸入sch、N02、CO的空气混合气，分别吸入1，7及30d。检测血清和支气管肺泡灌洗液（BALF）中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—Px）的活力及谷胱甘肽（GSH）、丙二醛（MDA）的含量。结果 1d组对与对照组比较，血清SOD活力显著降低（P〈0．05），GSH和MDA含量显著增高（P〈0．01）；30d组与对照组比较，BALF中SOD、GSH—Px活力及GSH含量显著降低（P〈0．05或P〈0．01）。结论 大气混合污染物对大鼠呼吸系统产生氧化损伤作用。