SO2对小鼠多脏器脂质过氧化作用的研究

目的　探索二氧化硫 (SO2 )对小鼠不同脏器脂质过氧化作用的影响 ,进一步了解SO2 的毒作用机制。方法　采用SO2 动态染毒实验技术 ,使小鼠吸入不同浓度的SO2 气体后 ,用荧光分光光度法测定小鼠不同脏器中脂质过氧化产物丙二醛 (MDA)含量。结果　 (1)随SO2 浓度的增加 ,小鼠多个脏器氧化损伤加剧 ,呈明显的剂量 -效应关系 ;(2 )在低浓度SO2 (2 2± 2 )mg/m3 吸入情况下 ,对不同脏器引起的氧化损伤不同 ,有器官差异性 ;但随SO2 浓度升高 ,器官间的差异减小 ;(3 )SO2 对雌雄小鼠造成的氧化损伤作用 ,在不同脏器间存在性别差异。结论　SO2 可引起多种脏器氧化损伤 ,是一个全身性毒物 ;SO2 通过活性氧自由基引起组织器官损伤 ,可能是SO2 毒理作用的主要机制之一。     

二氧化硫对小鼠胃组织氧化损伤的作用

目的　了解二氧化硫 (SO2 )对哺乳动物胃组织的毒理作用及其机制。方法　采用SO2 动态吸入SO2 技术 ,使昆明小鼠吸入SO2 ,浓度为 (2 2± 2 ) ,(6 4± 3) ,(1 4 8± 2 3)mg/m3 ,每天 6h ,连续 7d ,分析该小鼠胃组织氧化损伤及抗氧化状态。结果　在SO2 浓度为 2 2mg/m3 时 ,雄鼠胃组织的超氧化物歧化酶(SOD)、过氧化氢酶 (CAT)活力及雌鼠胃组织的脂质过氧化 (LPO)水平显著升高 ;在SO2 浓度为 6 4mg/m3和 1 4 8mg/m3 时 ,雌、雄鼠胃组织的LPO水平显著升高 ,SOD酶活力和还原型谷胱甘肽 (GSH)含量显著下降。结论　吸入SO2 可引起小鼠胃组织多种抗氧化指标发生显著变化 ,表明SO2 对小鼠胃组织产生了氧化损伤作用 ;SO2 的毒理作用与其诱发产生过量自由基有关     

氧化应激效应与SO2全身性毒作用研究

目的　探讨二氧化硫 (SO2 )能否引起多种脏器氧化损伤 ,以及SO2 是否是一个全身性的毒物。方法　小鼠经SO2 吸入染毒 (56mg/m3 ,6h/d× 7d)后 ,测定其 9种脏器 (脑、肺、心、肝、胃、肠、脾、肾及睾丸 )组织的脂质过氧化(LPO)水平和抗氧化状态的变化。结果　SO2 引起 :(1)所有测试器官组织的LPO水平显著升高 ;(2 )抗氧化酶超氧化物歧化酶和谷胱甘肽过氧化物酶活性显著降低 ,但是过氧化氢酶活性除肝下降外 ,其他脏器无显著变化 ;(3 )抗氧化物质谷胱甘肽显著降低。结论　 (1)SO2 能够引起小鼠全身多种器官的氧化损伤 ,是一种全身性有毒物质 ;(2 )氧化损伤是SO2 毒性作用的机制之一。为了阐明SO2 对人和哺乳动物多种器官甚至全部器官的毒作用 ,进一步研究是必要的。     

2-乙氧基乙醇染毒对大鼠某些脂质过氧化相关指标的影响

目的：观察2－乙氧基乙醇（EE）染毒大鼠与脂质过氧化过程有关的某些生化指标的变化,并探讨EE染毒是否诱发血清脂质过氧化（LPO）升高及其可能机理。方法：选取雄性Wistar大鼠,随机分为4组：对照组、EE分别为200、400、800mg/kg组,每组30只。每天染毒1次,每周6次,持续6周。分别于染毒每周后,将各组动物随机处死5只,对血液及肝脏中的脂质过氧化相关指标进行测定。结果：血清LPO水平显著升高;血清铜蓝蛋白（CP）、血清超氧化物歧化酶（SOD）和肝脏SOD活性显著升高;肝脏过氧化氢酶（CAT）活性显著下降,肝脏GSH－Px活性变化不明显。结论：EE长期染毒可诱发大鼠LPO水平升高,这可能是EE诱发大量活性氧（ROS）产生和影响大鼠抗氧化机制共同作用的结果。     

SO2对雄性小鼠睾丸组织的氧化损伤作用

目的了解SO2对哺乳动物和人雄性生殖系统有无氧化损伤作用,探讨SO2污染对生殖的影响.方法SO2染毒剂量分别为(22±2)mg/m3,(64±3)mg/m3,(148±23)mg/m3,采用SO2动态吸入实验技术,使昆明小鼠吸入不同浓度的SO2,每天染毒6 h,共7 d,染毒后,测定小鼠睾丸组织氧化损伤和抗氧化状态的变化.结果SO2吸入能够引起小鼠睾丸中GSH-Px、SOD和CAT酶活性改变,GSH含量减少,脂质过氧化产物丙二醛含量显著增高,并且随着SO2熏气浓度的升高,氧化损伤程度愈加严重.结论SO2可对雄性小鼠生殖系统产生损伤作用.     

刺梨汁对高氟摄入大鼠肝肾脂质过氧化作用的影响

利用自由进食含氟320mg／kg饲料和饮用刺梨汁水喂养大鼠6个月的动物模型，探讨刺梨汁对高氟摄入大鼠肝肾脂质过氧化损害的影响。结果发现：刺梨汁能拮抗高氟引起的肝肾组织抗氧化能力降低，使肝肾还原型谷胱甘肽（GSH）含量和谷胱甘肽过氧化物酶（GSH—Px）、超氧化物歧化酶（SOD）活性降低显著回升；拮抗肝肾组织脂质过氧化增强，使肝肾脂质过氧化物（LPO）含量升高程度显著回降；从而拮抗肝肾损害，使肝甘油三脂（TG）含量和尿γ－谷氨酰转移酶（γ—GT）活性升高显著回降。表明刺梨汁对高氟摄入大鼠肝肾脂质过氧化损害具有明显的拮抗作用。     

二氧化硫吸入对小鼠心脏脂质过氧化和抗氧化指标的影响

二氧化硫 (SO2 )吸入可诱导体内产生自由基和活性氧 ,造成血红细胞[1] 、脑[2 ] 、肺[3 ] 、气管和支气管等处脂质过氧化水平升高 ,并改变它们的抗氧化状态 ,因而SO2 对机体的氧化损伤是其毒作用的重要方面[4] 。由于心脏是循环系统的枢纽 ,它的规律收缩不仅可以保持血液在血管中循环流动 ,而且具有传导兴奋的功能 ,如果心脏受损则危害巨大。为此 ,我们通过研究不同浓度SO2 吸入对雌雄小鼠心脏脂质过氧化作用(LPO)以及还原型谷胱甘肽 (GSH)、谷胱甘肽过氧化物酶(GSH Px)、超氧化物歧化酶 (SOD)等抗氧化指标造成的影响 ,以期阐明SO2…     

二氧化硫吸入对小鼠各脏器过氧化氢酶活性的影响

[目的]探讨SO2对小鼠不同组织的氧化损伤及其毒作用机制。[方法]对昆明种小鼠采用动式吸入法进行22，64，148mg/m^3SO2三个浓度染毒，用分光光度法测定各器官的过氧化氢酶（CAT）活性。[结果]22mg/m^3SO2吸入时，雌雄小鼠各脏器CAT活性有上升趋势，但统计学上差异不显著；64mg/m^3SO2吸入时，各脏器CAT活性有下降趋势。 在148mg/m^3浓度时，肝，肺，肾，脑中CAT活性下降比较显著，而胃，小肠中的CAT显著升高。[结论]SO2的动式吸入可引起小鼠部分脏器CAT活性下降，对机体造成氧化损伤，且损伤程度随SO2浓度的增大而增强。     

二氧化硫对小鼠肾脏的氧化损伤作用

目的：研究SO2对小鼠肾脏的氧化损伤作用。方法：160只小鼠随机分成4组,每一组又分为对照组和染毒组,染毒组分别吸入不同浓度的SO2(7,14,28,56mg／m^3),每天4h,连续染毒7d。染毒结束后立即进行还原性谷胱甘肽(GSH)含量、谷胱甘肽过氧化物酶(GSH—Px)和超氧化物歧化酶(SOD)酶活力、脂质过氧化物产物丙二醛(MDA)含量的测定。结果:雄鼠吸入SO2浓度为7mg／m^3时,肾脏组织GSH含量显著增加,吸人SO2浓度为56mg／m^3时,GSH含量显著降低;雌鼠吸入SO2浓度为56mg／m^3时,GSH含量也显著降低。随着SO2吸入浓度的增加,雌雄小鼠GSH—Px酶活力显著降低,雄鼠变化大于雌鼠。吸入SO2浓度为7,14,28mg／m^3 SO2时,小鼠肾脏组织SOD酶活力没有明显变化,吸入SO2浓度为56mg／m^3时,SOD酶活力显著降低。吸入SO2浓度为7,14,28mg／m^3时,小鼠肾脏组织MDA含量没有明显变化,吸入SO2浓度为56mg／m^3时,MDA含量显著升高。结论:肾脏可能是SO2毒理作用的重要靶器官之一,脂质过氧化作用可能是SO2肾脏毒性的机制之一。     

低浓度混苯对作业工人血脂质过氧化的影响

低浓度混苯对作业工人血脂质过氧化的影响叶榕张琪瑛张国军胡国灿曹京杭近年来，国内外学者运用脂质过氧化理论对苯中毒机理进行研究，发现苯接触工人及实验动物体内超氧阴离子自由基（Ｏ－·２）浓度增高，引起脂质过氧化，并认为这可能是苯细胞毒性作用的一个重要因素〔...     

Oxidative damage of sulfur dioxide inhalation on lungs and hearts of mice

Effects of sulfur dioxide (SO2) on concentrations of thiobarbituric acid-reactive substances (TBARS) and reduced glutathione (GSH), activities of Cu,Zn-superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were investigated in lungs and hearts of Kunming albino mice of both sexes. The mice of SO2 groups were exposed to various concentrations (22, 56, and 112 mg/m3) of SO2 in separate exposure chambers for 6 h/day for 7 days, whereas control groups were exposed to filtered air under otherwise the same conditions. Our results show that SO2 caused lipid peroxidation and changes of antioxidative status in both lungs and hearts of mice. Exposure to SO2 at all concentrations tested caused a significant increase of TBARS and a significant decrease in GSH content in lungs and hearts of mice, with the exception of GSH content in the hearts of female mice. For lungs, SO2 at low concentrations significantly increased SOD and GPx activities, whereas at high concentrations it significantly decreased these same activities in mice of both sexes. For hearts, SO2 at all tested concentrations significantly decreased activities of SOD from mice of both sexes, as well as that of GPx from male mice, but the decrease of GPx activities in hearts from female mice was statistically insignificant. SO2 inhalation tended to decrease activities of CAT in lungs and hearts from mice of both sexes, whereas only the decrease of CAT activities caused by SO2 in lungs from male mice was statistically significant, at 112 mg/m3. The results also show a gender difference in oxidative stress and antioxidation status caused by SO2 exposure. These results lead us to conclude that SO2 exposure can cause oxidative damage to lungs and hearts of mice, and SO2 is toxic not only to the respiratory system, but to the heart as well. Additional work is required to understand the toxicological role of SO2 on many or even all mammalian organs.     

Effect of ozone on the agglutination of erythrocytes by concanavalin A. I. Studies in rats.

A decrease in the agglutination of rat erythrocytes by the lectin concanavalin A was observed after in vitro exposure to ozone (1 ppm for 2 hr) and after inhalation of 0.5–2.0 ppm ozone for 2 hr. Agglutination was inhibited by α-methyl-d-mannopyrannoside demonstrating that it is specific for the lectin. Studies with radioactive concanavalin A indicated that ozone exposure did not significantly affect the number of membrane sites available for lectin binding. Further studies revealed that erythrocytes incubated with malonaldehyde, a decomposition product of lipid peroxidation, also showed a decrease in agglutination as did erythrocytes obtained from rats injected with the oxidizing agent, acetylphenylhydrazine. These findings are consistent with a possible causal role for malonaldehyde in mediating extrapulmonary effects observed after ozone exposure.     

SO2吸入对小鼠骨髓细胞微核的诱发效应

目的 探讨空气中SO2污染物遗传毒理效应。方法 采用SO2吸入染毒法，对SO2吸入诱发小鼠骨髓嗜多染红细胞（PCE）形成微核（MN）的效应进行研究。结果 （1）SO2吸入可引起小鼠骨髓PCE微核率和微核细胞率显著升高；（2）随着吸入的SO2浓度的增高，单微核细胞率、双微核细胞率均显著升高。结论 随SO2浓度增加，细胞遗传物质损伤加重，且有明确的剂量-效应关系，表明SO2空气污染物是染色体断裂剂和基因毒性因子。     

Changes in somatosensory evoked potentials,lipid peroxidation,and antioxidant enzymes in experimental diabetes: effect of sulfur dioxide

The effect of sulfur dioxide (SO2) on brain antioxidant status, lipid peroxidation, and somatosensory evoked potentials (SEPs) was investigated in diabetic rats. A total of 40 rats were divided into 4 equal groups: control (C), SO2 + C (SO2), diabetic (D), and SO2 + D (DSO2). Experimental diabetes mellitus was induced by i.v. injection of alloxan at a dose of 50 mg/kg body weight. Ten ppm SO2 was administered to the rats in the sulfur dioxide groups (SO2 and DSO2) in an exposure chamber. Exposure occurred 1 hr/day, 7 days/wk, for 6 wk; control rats were exposed to filtered air during the same time periods. Although SO2 exposure markedly increased copper, zinc Superoxide dismutase activity, it significantly decreased glutathione peroxidase activity in both the diabetic and nondiabetic groups, compared with the C group. Brain catalase activity was unaltered; however, brain thiobarbituric acid reactive substances (TBARS) were elevated in all experimental groups with respect to the C group. SEP components P1, N1, P2, and N2 were significantly increased in all experimental groups, compared with the C group, and these components were also prolonged in the DSO2 group with respect to the other groups. The authors' findings suggest that exposure to SO2, because it increases lipid peroxidation, can change antioxidant enzyme activities and affect SEP components in diabetic rats.     

几处无机粉尘对红细胞脂质过氧化作用的试验研究

This paper reports on the effects of erythrocytes when incubated with three kinds of inorganic dusts, i.e. quartz (free SiO2 content 97%), alpha-Al2O3 and TiO2. Malonaldehyde as a product of lipid peroxidation was determined as it reacted with thiobarbituric acid, and haemolytic activity was analysed spectrophotometrically. The results showed that quartz presented a stronger stimulative effect on lipid peroxidation of erythrocyte at doses of 1-8 mg than the control (P less than 0.01). No change was observed with alpha-Al2O3 and TiO2 at doses of 1-9 mg. The results suggest that the effects of dusts on lipid peroxidation of erythrocyte are similar to hemolytic reaction, directly reflecting the degree of their damage to the cell membrane. Therefore lipid peroxidation on cell membrane caused by dusts was one of the parameters of cytotoxic effects, and could be considered as one of the measures used in the assessment of cytotoxicity of dusts.     

The effects of diazinon on lipid peroxidation and antioxidant enzymes in rat erythrocytes: role of vitamins E and C

Reactive oxygen species caused by organophosphates may be involved in the toxicity of various pesticides. Therefore, in this study, we aimed to investigate the effects of acute exposure to organophosphate insecticide diazinon (DI) and possible ameliorating role of vitamins E and C, with the following parameters: lipid peroxidation (LPO) and the activity of the glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in rat erythrocytes. The experimental groups were arranged as control group, DI-treated group (DI) and DI + vitamin E + vitamin C-treated group (DI + Vit). DI + Vit groups were treated orally with a single dose of 335 mg/kg DI body weight. Vitamins E and C were injected at doses of 150 mg/kg body weight intramuscular (in) and 200 mg/kg body weight intraperitoneal (ip), respectively, 30 min after the treatment of DI in DI + Vit group. Blood samples were taken 24 h after the DI. The results showed that DI administration caused to increase in LPO and the activities of SOD and GSH-Px enzymes in erythrocytes. Also, the combination of vitamins E and C decreased LPO and the activities of GSH-Px and SOD compared with the DI group. In conclusion, although treating rats with single dose DI increases LPO and antioxidant enzyme activities in erythrocytes, vitamins C and E combination can reduce LPO caused by DI.     

Erythrocyte lipid peroxidation, glutathione and vitamin E levels in cholesterol-fed rats

Erythrocyte cholesterol and phospholipid levels, the susceptibility of erythrocytes to lipid peroxidation as well as erythrocyte glutathione and vitamin E levels were determined in rats fed a high cholesterol (2%, w/w) and high cholic acid (0.5%, w/w) diet for 3 months. Cholesterol feeding caused an increase in erythrocyte cholesterol levels, but no change was observed in erythrocyte phospholipid levels. Dietary cholesterol did not alter the susceptibility of erythrocytes to lipid peroxidation as well as erythrocyte glutathione and vitamin E levels in rats.     

Lipid peroxidation and antioxidants status in patients with papillary thyroid carcinoma in India

The levels of lipid peroxidation products (TBARS), non-enzymatic antioxidants and enzymatic antioxidants activity were investigated in plasma and erythrocytes of twenty clinically diagnosed stage II papillary thyroid cancer patients and an equal number of age and sex matched healthy subjects. An increase in the levels of lipid peroxidation products, decrease in non-enzymatic antioxidants levels and enzymatic antioxidant activities in plasma and erythrocytes were detected in papillary thyroid cancer patients as compared to healthy subjects. Impairment in antioxidant defence mechanisms are responsible for enhanced lipid peroxidation observed in plasma and erythrocytes of papillary thyroid cancer patients.