铅染毒家兔脂质过氧化水平和神经传导速度的变化及关系研究

为观察铅对脂质过氧化水平和神经传导速度(NCV)的影响,并探讨两者关系,1 6只家兔随机分为2组,每组8只,染铅组饮用0 1 %醋酸铅水,对照组予以去离子水,持续8周,测定了两组家兔股神经NCV及血浆和脑组织丙二醛(MDA)、总超氧化物歧化酶(T -SOD)水平,分析了MDA、T -SOD与NCV之间的关系。结果表明,染铅组NCV显著低于对照组(P <0 0 1 ) ,NCV与脑组织MDA之间存在相关关系(r=-0 5 2 1 ,P <0 0 5 ) ,但染铅组MDA、T -SOD与对照组比较未达到显著性差别(P >0 0 5 )。提示铅中毒能引起NCV减慢,这与脂质过氧化水平有关,脂质过氧化损伤可能是铅致中毒性周围神经病的机制之一。     

硒与铅

硒和铅是一对拮抗元素。高秋华发现,喂铅小鼠血和组织中硒浓度显著降低而铅含量显著增加,同时喂硒可使小鼠血、肾、脾中的蓄积铅和MDA显著降低(P<0.01)。阮迪云对发育过程中的大鼠所做的研究也证明,硒可使染铅大鼠肝、脑、血浆和眼球中的铅含量降低到铅处理组的三分之一左右,使肝、脑、血浆的MDA浓度分别下降37％、31％和27％,并可保护铅引起的视觉损伤。高泽宣的研究表明,大鼠醋酸铅[5mg/(kg·d)]染     

TBARS法测定胰岛素口腔喷雾剂中脂质过氧化物研究

采用硫代巴比妥酸反应物法(ThiobarbituricAcidReactiveSubstanceAssay,TBARS)对胰岛素口腔喷雾剂(InsulinBuccalSpray,IBS)中脂质过氧化程度进行了测定,并对IBS前处理方法、稀释倍数、加热作用亦进行了探究。发现在使用丙二醛(Malondialdehyde,MDA)测试盒测量IBS中脂质过氧化物(LipidPeroxide,LPO)实验中,样品应该先用有机溶剂稀释或用含0.8%(m/V)TritonX 100的0.01mol·L-1HCl溶液破乳;而乳剂测量前以稀释10倍为宜。对不同时期的IBS制剂检测,发现在IBS的一年保质期内,其脂质过氧化程度变化不大。     

立得益片对铅中毒小鼠(生殖系统、脑、血液、心脏)促排铅的作用

研究了立得益片对铅中毒小鼠促排铅的作用。给小鼠腹腔注射醋酸铅溶液染毒 7d ,建立铅中毒模型后 ,灌胃给药不同剂量立得益片及阳性对照药物EDTA ,极谱法测定不同时间生殖系统、脑、血液、心脏中的铅含量 ,观察及统计立得益片对铅中毒小鼠上述各脏器的促排铅作用。结果表明 ,铅中毒小鼠给药 6、 1 3d后脑、心脏、血液中的铅含量明显下降 ,生殖系统中仅卵巢和子宫中的铅含量在给药 1 3d后 ,立得益片高剂量组与模型对照组有显著性差异 (P <0 0 1 )。提示立得益片对铅中毒小鼠血液及脏器有明显促排铅作用 ,降低机体的铅负荷且存在时效、量效关系     

长期低剂量YbCl3暴露的神经毒性评价

雌性Wistar大鼠受孕之日起以经口灌胃方式用YbCl3染毒,剂量为0.1,2.0和40 mg Yb·kg^-1体重,对照组灌生理盐水。仔鼠出生后20 d断乳并用相同剂量的YbCl3染毒。用Morris水迷宫评价学习记忆能力,并尝试从大鼠体内微量元素含量变化、大脑海马体中Ca^2＋-ATP酶活性、海马细胞内游离钙水平及脂质过氧化程度等方面评价YbCl3的神经毒性。结果显示,2.0和40 mg·kg^-1体重剂量的YbCl3长期暴露会对大鼠的学习记忆能力产生负面影响,这可能和YbCl3暴露引起的骨骼、血清、肝脏和各脑区中部分微量元素含量发生改变,Ca^2＋-ATP酶活性受到抑制,海马细胞内游离钙水平升高及脂质过氧化程度加剧等因素有关。     

几种螯合剂解镍致小鼠急性肾毒性作用比较

为寻找镍(Ni)新型解毒剂，小鼠腹腔注射氯化镍溶液(5 mg Ni/kg)，观察二乙氨基二硫代甲酸钠(DDTC)，二羟乙氨基二硫代甲酸钠(DHED)，N-苯甲基-D-葡糖氨基二硫代甲酸钠(BGD)，meso-2，3-二巯基丁二酸钠(DMSA)及环己烷二胺四乙酸钠(CDTA)等螯合剂对镍致小鼠肾脏毒性的解毒作用。镍染毒引起小鼠肾脏脂质过氧化(LPO)和钙、铁及锌浓度增加，血清肌酐及血液尿素氮(BUN)升高。镍染毒30分钟和24小时后进行各螯合剂治疗(剂量均为400 μmol/kg     

低剂量硝酸镧对小鼠肾脏自由基防御机能的影响

通过采用肾组织匀浆生化测定法, 观察不同剂量硝酸镧灌胃一个月后, 小鼠肾组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、脂质过氧化物(LPO)、谷胱甘肽过氧化物酶(GSH-PX)含量的变化, 探讨了低剂量硝酸镧的抗氧化作用; 结果表明 雌性、雄性小鼠20.0, 10.0 mg*kg-1 Cu-ZnSOD和CAT的含量均较对照组明显降低; 而GSH-Px和LPO的含量均较对照组显著升高. 雌性、雄性小鼠0.1, 0.2, 2.0 mg*kg-1组Cu-ZnSOD, CAT, GSH-Px和LPO的含量与对照组无显著性差异. 较高剂量(20.0, 10.0 mg*kg-1)的硝酸镧的直接损伤可使小鼠肾脏脂质过氧化反应增强, 清除自由基的能力下降. 较低剂量(0.1, 0.2, 2.0 mg*kg-1)的硝酸镧对小鼠肾脏自由基的生成和清除无影响.     

镁离子、维生素E抗氧化作用的研究

为研究镁离子、维生素E体内外抗氧作用,探讨镁离子抗氧化作用的机制,将3月龄昆明种小鼠70只随机分7组,设正常对照组、氧化对照组、63、42、21mmol／L镁保护组,镁和维生素E保护组,维生素E保护组,饲养10d,腹腔注射0．15％CCl4致小鼠肝损伤,观察镁离子、维生素E对小鼠肝匀浆中MDA、SOD、GSH含量的影响;在肝匀浆中加入FeSO4和H2O2诱导自由基的生成,观察镁离子、维生素E的抗氧化作用。结果表明,镁离子、维生素E能显著降低肝匀浆中脂质过氧化物MDA的含量,对SOD、GSH无明显影响。提示镁离子、维生素E能抑制自由基的生成,促进自由基清除作用。     

有氧运动训练对D-半乳糖诱导的亚急性衰老大鼠血管老化的影响

目的探讨游泳运动对大鼠血管抗衰老的影响。方法 30只健康雄性SD大鼠(180~220g)随机分为3组:溶剂对照组(n=10),D-半乳糖组(n=10)和有氧运动+D-半乳糖组(运动组,n=10)。D-半乳糖组和运动组大鼠每日颈部皮下注射D-半乳糖(125 mg/kg),溶剂对照组大鼠每日颈部皮下注射同体积生理盐水,且运动组大鼠每日进行60 min的无负重游泳运动训练,持续8周。以血浆总一氧化氮合成酶(T-NOS)活力,一氧化氮(NO),内皮素(ET)和NO/ET平衡建立血管衰老指标评价体系,并测量主动脉组织超氧化物歧化酶、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)和丙二醛(MDA)含量。结果与溶剂对照组相比,D-半乳糖组大鼠主动脉MDA和血浆ET含量显著升高,而GSH-Px、SOD活力、血浆NO含量和NO/ET比值显著下降。与D-半乳糖组相比,运动组大鼠主动脉MDA含量和T-NOS活力显著下降,GSHPx、SOD、T-NOS活力、NO含量和NO/ET比值显著升高(P0.05),且与对照组相比上述各项指标无显著差异。结论 D-半乳糖皮下注射可诱导大鼠主动脉脂质过氧化反应,血浆NO/ET失衡;适宜的有氧运动能显著增加大鼠血管的抗氧化能力,减少脂质过氧化反应,改善NO/ET失衡,预防血管衰老。     

HPLC测定雄黄染毒小鼠血浆及肝脏中活性硫的含量

建立了HPLC测定雄黄染毒小鼠血浆及肝中活性硫含量的方法.结果表明,该方法准确、灵敏、可靠、检出限低.研究发现,雄黄可引起小鼠血浆、肝中活性硫水平降低.     

Beneficial effects of THSG on acetic acid-induced experimental colitis: involvement of upregulation of PPAR-γ and inhibition of the Nf-Κb inflammatory pathway

The polyphenolic compound 2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucoside (THSG) has been shown to possess anti-inflammatory effects. Here, we examined the effects of THSG on experimental mice with colitis induced by acetic acid and whether the underlying mechanisms were associated with the PPAR-γ and NF-κB pathways. Mice were randomized into six equal groups: normal, colitis model, THSG (10, 30, 60 mg·kg(-1)) and mesalazine. The mice were administered 10, 30, 60 mg·kg(-1) THSG or 100 mg·kg-1 mesalazine or saline once daily by intragastric administration for 7 days after induction of colitis by acetic acid irrigation. THSG dramatically attenuated acetic acid-induced colon lesions, including reversing the body weight loss and improving histopathological changes. THSG apparently decreased the increase of malondialdehyde (MDA) which is a marker of lipid peroxidation. THSG appears to exert its beneficial effects on acetic acid-induced experimental colitis through upregulation of PPAR-γ mRNA and protein levels and inhibition of the NF-κB pathway, which in turn decreases the protein overexpression of the downstream inflammatory mediators TNF-α, IL-6 and COX-2. The effect of THSG 60 mg·kg(-1) on PPAR-γ mRNA expression was higher than that of mesalazine. THSG may thus be a promising new candidate or lead compound for the treatment of IBD.     

长期低浓度铅暴露对人体微量元素的影响

测定了１５名长时间从事低剂量铅接触的女工血铅、铜、锌、铁、锰及铜锌超氧化物歧化酶活性、脂质过氧化产物二级降解物丙二醛含量,并以同年龄组同地区非铅暴露人群作对照。结果显示：暴露组的血铅、铜、ＭＤＡ含量高于对照组;而血锌Ｃｕ－Ｚｎ－ＳＯＤ活性低于对照组;血Ｍｎ、Ｆｅ两组无明显差异。     

Postadministration Protective Effect of Magnesium-L-ascorbyl-phosphate on the Development of UVB-induced Cutaneous Damage in Mice

The effects of stable vitamin C, magnesium-L-ascorbyl-2-phosphate (MAP), administered after acute and chronic exposure to UVB irradiation were investigated using hairless mice. Intraperitoneal administration of 100 mg/kg of MAP immediately after acute exposure to 15 kJ/m² of UVB significantly prevented increases of UVB-induced lipid peroxidation in skin and sialic acid in serum, an inflammation marker. Administration of 50 mg/kg of MAP immediately after each exposure significantly delayed skin tumor formation and hyperplasia induced by chronic exposure to 2 kJ/m² of UVB. Intraperitoneal administration of 200 mg/kg of MAP produced an increase in ascorbic acid (As) levels in the serum, liver and skin within 15 min. Serum As levels quickly returned to normal, but hepatic and cutaneous levels remained elevated before returning to normal after 24 h, suggesting that MAP was converted to As in the serum and in those tissues. Ultraviolet B-induced hydroxyl radical generation in murine skin homogenates was scavenged by As-Na addition, which was directly detected by electron spin resonance (ESR). These results suggest that postadministration of MAP delays progression of skin damage induced by UVB irradiation. It is presumed that MAP, once converted to As, exhibits such inhibitory effects by scavenging hydroxyl and lipid radicals generated as a direct or indirect result of UVB exposure.     

Glutathione Isopropyl Ester Reduces UVB-lnduced Skin Damage in Hairless Mice

Abstract— The protective effect of administration of glutathione (GSH) isopropyl ester on photodamage, such as lipid peroxidation, inflammation and tumorigenesis induced by UV exposure (290–400 nm, max. 312 nm), was investigated using hairless mice. Pretreatment with 20 mg/kg GSH isopropyl ester prevented the increases of thiobarbituric acid-reactive substance (TBARS) formation in skin and serum sialic acid, indices of lipid peroxidation and inflammatory reaction, respectively, which were caused by a single dose (15 kj/m²) of UV irradiation. The level of epidermal GSH in skins of the GSH ester-treated mice was maintained within normal limits. When mice were exposed to UV at a dose of 2 kj/m², three times weekly, skin tumors developed in all of them after 25 weeks. The formation of skin tumors was significantly inhibited by administration of 10 mg/kg GSH ester prior to each UV irradiation for 25 weeks. Moreover, the increases of cutaneous TBARS and serum sialic acid in the tumor-bearing mice were also prevented by continuous pretreatment with GSH ester. Even after 24 weeks, the epidermal GSH content of the pretreated mice was mostly retained compared to nonirradiated mice. However, administration of GSH prior to acute or chronic UV irradiation had no effect on the UV-induced damage. The present results suggest that the protection from photo-damage afforded by pretreatment with GSH ester is due to maintenance of a normal GSH level.     

Hypoglycemic and hypolipidemic effects of polyphenols from burs of Castanea mollissima Blume

Substantial evidence suggests that phenolic extracts of Castanea mollissima spiny burs (CMPE) increase pancreatic cell viability after STZ (streptozotocin) treatment as a result of their antioxidant properties. In the present study, the hypoglycemic and hypolipidemic activities of CMPE were studied in normal and STZ-induced diabetic rats CMPE were orally administrated at doses of 150 and 300 mg/kg twice a day for 12 consecutive days. Serum glucose, triglyceride, total cholesterol, HDL- and LDL-cholesterol levels, malondialdehyde (MDA) level and SOD activity in liver, kidney, spleen and heart tissues were measured spectrophotometrically. In normal rats, no significant changes were observed in serum glucose, lipid profiles and tissue MDA and GSH levels after orally administration of CMPE. In diabetic rats, oral administration of CMPE at a dose of 300 mg/kg caused significant decreases in serum glucose, triglyceride, total cholesterol, LDL-cholesterol levels, as well as MDA and GSH levels in spleen and liver tissues. However, the 300 mg/kg dosage caused a significant body weight loss in both normal and diabetic rats. The observed effects indicated that CMPE could be further developed as a drug to prevent abnormal changes in blood glucose and lipid profile and to attenuate lipid peroxidation in liver and spleen tissues.     

Protective Effect of Magnesium-L-Ascorbyl-2 Phosphate Against Skin Damage Induced by UVB Irradiation

The protective effect of magnesium-L-ascorbyl-2-phosphate (MAP) on cutaneous photodamage such as lipid peroxidation and inflammation induced by ultraviolet B (UVB) exposure (290–320nm, max. 312 nm) was investigated using hairless mice. When MAP was administered intraperitoneally to mice at a dose of 100 mg of ascorbic acid (AS) per kg body weight base immediately before irradiation (15 kJ/m²), the expected increases in thiobarbituric acid reactive substance (TBARS) formation in skin and serum sialic acid, indices of lipid peroxidation and inflammatory reaction, respectively, were significantly reduced. However, the expected decrease in the level of cutaneous AS was unchanged. Similar results were observed for animals given 100 mg of AS-Na per kg body weight before UVB irradiation. When MAP was administered intracutaneously immediately before irradiation, the expected UVB-induced increases in TBARS and sialic acid were again significantly prevented. Ascorbic acid-Na had a less protective effect than intracutaneous MAP administration. The cutaneous AS level was significantly higher in the MAP-treated mice than in the controls, and the UVB-induced decrease in tissue AS was prevented by intracutaneous MAP administration. These results suggest that MAP protects against UVB irradiation-induced lipid peroxidation and inflammation in cutaneous tissue, regardless of the drug administration route. We found, in an in vitro experiment, that MAP was converted to AS as it crossed the epidermis, but that AS-Na did not pass through the epidermis. Furthermore, MAP was also converted to AS in serum. These results suggest that the protective effect of MAP on UVB-induced cutaneous damage is due to conversion of MAP to AS.     

Effect of X-radiation on lipid peroxidation and antioxidant systems in rats treated with saponin-containing compounds

The aim of this study was to investigate the effect of three saponin-containing plant species extracts (Aesculuc hippocastanum L. seed extract [AHE], Medicago sativa L. extract [MSE] and Spinacia oleracea L. extract [SOE]) on lipid peroxidation and on antioxidant systems in rats exposed to X-rays (XR). The rats were divided into three categories. The first category served as controls and received only a standard diet. The second category served as the radiation group and received 5 and 10 Gy XR dose. The third category (XR+extract-treated) received plant extracts (25.0 or 50.0 mg kg(-1) live weight) and 5 or 10 Gy XR dose. Blood samples were analyzed for their content of malondialdehyde (MDA), reduced glutathione (GSH), plasma vitamin C, beta-carotene and retinol. In animals receiving XR, the plasma MDA (P < 0.001) value significantly increased but the level of GSH (P < 0.01), vitamin C (P < 0.001), retinol and beta-carotene (P < 0.001) decreased significantly with increasing XR doses. In the XR+extract-treated groups, the concentrations of MDA increased significantly with increasing radiation but their concentrations decreased significantly with increasing extract concentrations. Plasma concentrations of GSH, beta-carotene, retinol and vitamin C in XR+extract-treated groups decreased significantly with increasing XR dose but their concentrations increased with increasing extract doses. Further, comparison of blood samples of XR+extract-treated groups with those from the control group showed that GSH, beta-carotene, retinol and vitamin C values increased significantly but that MDA values decreased significantly. The results showed that all extracts have enhanced the antioxidant status and decreased the incidence of free radical-induced lipid peroxidation in blood samples of rats exposed to XR. However, the antioxidant effect of AHE-administered animals was more effective than that of MSE- and SOE-administered whole-body XR rats. We conclude that the supplementation with saponin-containing extracts may serve to reinforce the antioxidant systems, thus having protective effect against cell damage by XR.     

番茄红素对镉诱导睾丸损伤大鼠抗氧化酶活性及生殖激素水平的影响

目的观察番茄红素对镉诱导睾丸损伤大鼠抗氧化酶活性及生殖激素水平的影响。方法将28只雄性SD大鼠随机分为4组,每组7只,分别为空白对照组、5 mg/L镉组、5 mg/L镉+10 mg/kg番茄红素组、5 mg/L镉+20 mg/kg番茄红素组,给药1周后处死,测定睾丸组织超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)活性及血清促黄体生成素(LH)、睾酮(T)水平。结果镉组大鼠体质量、睾丸质量、睾丸组织SOD、GSH-Px活性及血清T水平均显著低于NC组(P0.01),睾丸组织MDA含量和血清LH水平则显著高于后者(P0.01);番茄红素可缓解染镉大鼠体质量和睾丸质量的减轻,并回调抗氧化酶活性和生殖激素水平,且高剂量组效果更为显著。结论番茄红素对染镉大鼠的睾丸损伤具有剂量依赖性的改善作用,可能与清除氧自由基和抗脂质过氧化有关。