Studies on Toxicity,Anti—stress and Hepato—Protective properties of Kombucha Tea

Objective :The objective of the study was to evaluate toxicity,anti-stress activity and hepatoprotective properties of Kombucha tea.Method :Kombucha tea was fed orally for 15 days using three different doses i.e.normal dose,five and ten times the dose,Rats were then sacrficed and various biochemical,and histological parameters were estimated.Anti-stress activity was evaluated either by 1)by exposing animals to cold and hypoxia and estimating the levels of malondialdehyde and reduced glutathione in plasma/blood or 2) by subjecting the animals to restraint stress and recording faecal output.Hepato-toxicity was induced by challenging the animals to an acute dose of paracetamol(1gm/kg)orally and determining the plasma levels of SGPT,SGOT and MDA.REsults:The effect of oral administration of different doses of K-tea to albion rats was examined and the results indicate that K-tea has no significant toxicity as revealed by various biochemical and histopathological parameters.K-tea has been found to prevent lipid peroxidation and fall in reduced glutathione level when rats were exposed to cold and hypoxia in simulated chamber.Further,K-tea has also been found to decrease the Wrap-restraint faecal pellet output in rats.K-tea has also been found to decrease paracetamol induced hepatotoxicity significantly.Conclusion:The study shows that K-tea has anti-stress and hepato-protective activities.     

Ozone Emitted During Copying Process -A Potential Cause of Pathological Oxidative Stress and Potential Oxidative Damage in the Bodies of Operators

INTRODUCTION Copying of references, documents, information and photos plays important roles in social, economic, business, scientific and technological affairs, however, photochemical smog emitted during this process may become risk factors inducing potential oxidative 1Correspondence should be addressed to Prof. Jun-Fu ZHOU, Second Affiliated Hospital of College of Medicine, Zhejiang University, 88 Jiefang R…     

Inhibiting Effects of Achyranthes Bidentata Polysaccharide and Lycium Barbarum Polysaccharide on Nonenzyme Glycation in D-galactose Induced Mouse Aging Model

Objective To investigate the inhibiting effects and mechanism of achyranthes bidentata polysaccharide (ABP) and lycium barbarum polysaccharide (LBP) on nonenzyme glycation in D-galactose induced mouse aging model. Methods Serum AGE levels were determined by AGE-ELISA, MTT method was used to determine lymphocyte proliferation, IL-2 activity was determined by a bioassay method. Spontaneous motor activity was used to detect mouse‘‘s neuromuscular movement, latency of step-through method was used to examine learning and memory abilities of mouse, colormetric assay was used to determine hydroxyproline concentration in mouse skin, pyrogallol autoxidation method was used to determine superoxide dismutase (SOD) activity of erythrocytes. Results Decreased levels of serum AGE, hydroxyproline concentration in mouse skin and spontaneous motor activity in D-galactose mouse aging model were detected after treated with ABP or LBP, while lymphocyte proliferation and IL-2 activity, learning and memory abilities,SOD activity of erythrocytes, were enhanced. Conclusious ABP and LBP could inhibit nonenzyme glycation in D-galactose induced mouse aging model in vivo and ABP has a better inhibiting effect than LBP.     

Potential Oxidative Stress in the Bodies of Electric Arc Welding Operators： Effect of Photochemical Smog

INTRODUCTION Electric arc welding is widely used in many fields such as welding engineering, architectural engineering, automotive industry, boat and ship engineering, aerospace C…     

Effects of SIRPalphal on liver regeneration after partial hepatectomy in rat

BACKGROUND：SIRPalphal is well known as a negative regulator for cell proliferation through the regulation of the activity of receptor tyrosine kinase with ITAM motif. No investigation to data was undertaken on SIRPalphal involving liver regeneration. MATERIALS AND METHODS: Adult male Sprague-Dawley rats underwent approximately 700% partial hepatectomy (PH) or sham operation (SO). Liver specimens were collected at 2，6，12，24，30，48，72，120，168,and 240 h after PH or SO.     

Role of Oxidative Stress in Non—genotoxic Carinogenesis with Special Reference to Liver Tumors Induced by Peroxisome Proliferators

Peroxisome proliferators(POPs),such as hypolipidemic drugs or industrial phthalate ester plasticizers,are widely known as non-genotoxic hepatocarcinogens in rodents.As one of the possible mechanisms of POP-induced carcinogenesis,the“Oxidative Stress” theory has bee postulated.In this review,in order to reconsider the significance of “Oxidative Stress”to POP-induced carcinogenesis,we focus on in vivo studies examining formation of 8-hydroxydeoxyguanosine(8-OH-dG),a marker of oxidative DNA damage with mutagenic potential,after treatment of rodents with POPs.Some studies clearly demonstrated that 8-OH-dG levels in the liver DNA were increased by OPO-treatments.Thee findings suggest that“Oxidative Stress could contribute as one factor to POP-induced carcinogenesis.Furthermore,we refer to other multiple biological changes caused by POP-treatment presumably contributing to the carcinogenic mechanisms,and consider possible roles of “Oxidative Stress” in the carcinogenesis process.     

Injury of Mouse Brain Mitochondria Induced by Cigarette Smoke Extract and Effect of Vitamin C on It in vitro

Objective To investigate the toxicity of cigarette smoke extract (CSE) and nicotine on mouse brain mitochondria as well as the protective effect of vitamin C in vitro. Method Mouse brain mitochondria in vitro was incubated with CSE or nicotine in the absence or presence of vitamin C for 60 minutes, and the changes of mitochondrial function and structure were measured. Results CSE inhibited mitochondrial ATPase and cytochrome C oxidase activities in a dose-dependent manner.However, no significant changes in the peroxidation indices were observed when mitochondrial respiratory enzymes activity was inhibited, and protection of mitochondria from CSE-induced injury by vitamin C was not displayed in vitro. The effect of CSE on mouse brain mitochondria swelling response to calcium stimulation was dependent on calcium concentrations. CSE inhibited swelling of mitochondria at 6.5 μmol/L Ca^2 , but promoted swelling response at 250μmol/L Ca^2 . Nicotine, the major component of cigarette smoke, showed no significant damage in mouse brain mitochondria in vitro. The CSE treatment induced mitochondrial inner membrane damage and vacuolization of the matrix, whereas the outer mitochondrial membrane appeared to be preserved. Conclusion The toxic effect of CSE on brain mitochondria may be due to its direct action on enzymatic activity rather than through oxygen free radical injury. Nicotine is not the responsible component for the toxicity of CSE to brain mitochondria.     

Effects of Lead on pH and Temperature—Dependent Substrate—Activation Kinetics of ATPase System and its Protection by Thiol Compounds in Rat Brain

Lead (Pb) inhibited the activities of Na~+-K~+ ATPase (IC_(50)=2.0×10~(-6) M), K~+-Para-Nitrophenyl phosphatase (PNPPase) (IC_(50)=3.5×10(-6) M) and [~3H]-ouabain binding (IC_(50)= 4.0×10~(-5) M) in rat brain P2 fraction. A variable temperature or pH significantly elevated the inhibition of Na~+-K~+ ATPase by Pb in buffered acidic, neutral and alkaline pH ranges. Noncompetitive inhibition with respect to activation of Na~+-K~+ ATPase by ATP was indicated by a variation in V_(max) values with no significant changes in Km values at any temperature studied. In the presence of Pb, for Na~+-K~+ ATPase at pH 6.5 and 8.5, V_(max) was decreased with an increase in Km values suggesting a mixed type of inhibition. Sulfhydryl agents such as dithiothreitol (DTT) and cysteine (Cyst), but not glutathione (GSH) offered varied levels of protection against Pb-inhibition of Na~+-K~+ ATPase at pH 7.5 and 8.5. The present data suggest that inhibition of Na~+-K~+ ATPase by Pb is both temperature and pHdependent. These re     

肺结核与氧化应激关系的初步探讨

目的探讨肺结核与氧化应激的关系及其可能的机制.方法用分光光度分析法检测50例肺结核患者(PPT)和50例健康成人志愿者(HAV)的血浆维生素C(VC)、维生素E(VE)、β-胡萝卜素(β-CAR)含量和红细胞丙二醛(MDA)含量以及超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性.结果与HAV者比较,PPT患者的MDA平均值显著增高(P<0.001);而VC、VE、β-CAR、SOD和CAT均显著降低(均P<0.001).控制年龄的偏相关分析提示,随着PPT病程的延长,MDA值逐渐增高(r=0.4255,P<0.01),而VC、VE、β-CAR、SOD和CAT值逐渐降低(r分别为-0.3288、-0.3816、-0.4744、-0.3169和-0.3768,P<0.05～0.01).结论肺结核患者体内的氧化应激病理性加剧,且与病程有关.     

高热预处理对PC12细胞氧化应激损伤的保护作用

目的 探讨高热预处理（HPC）对过氧化氢（H2O2）所致大鼠嗜铬细胞瘤株（PC12）细胞氧化应激损伤的影响。方法 体外培养PC12细胞,将细胞分为正常对照组、HPC组、H2O2组、HPC＋H2O2组,采用MTT法测定细胞活力,乳酸脱氢酶（LDH）检测细胞损伤,流式细胞术分析细胞凋亡。结果 与正常对照组相比,H2O2组引起PC12细胞MTT活力明显下降（P〈0．01）,LDH释放量增多（P〈0．01）,凋亡明显;而与H2O2处理组相比,HPC＋H2O2组则表现为MTT活力升高（P〈0．05）,LDH释放量减少（P〈0．05）,且没有出现明显凋亡。结论 高热预处理对H2O2所致PC12细胞氧化应激损伤产生保护作用。     

绿茶多酚对环孢素A所致慢性肾毒性的预防作用研究

目的探讨氧化应激反应在环孢素A（CsA）所致慢性肾毒性中的作用,以及绿茶多酚（GTP）对CsA慢性肾毒性的预防作用。方法将50只SD大鼠随机分为对照组、CsA组和CsA＋1．0％GTP组、CsA＋1．5％GTP组,并分别检测各组大鼠的体重、血肌酐（Scr）、血尿素氮（BUN）和。肾组织丙二醛（MDA）、还原型谷胱甘肽（GSH）、超氧化物歧化酶（SOD）、GSH—S-转移酶（GST）、过氧化氢酶（CAT）、GSH-过氧化物酶（GSH—Px）活性及尿N-乙酰-β—D-氨基葡糖苷酶（NAG）活性,同时观察各组大鼠肾脏组织病理变化。结果CsA组大鼠血清Scr和BUN水平均较对照组增高,而CsA＋GTP各剂量组水平均较CsA组降低（均P〈0．05）;CsA组肾组织GSH、SOD、GST、CAT、GSH—Px活性均较对照组降低,CsA＋GTP各剂量组上述指标均较CsA组增高（均P〈0.05）;CsA组肾组织MDA含量和尿NAG活性均较对照组增高,而CsA＋GTP各剂量组水平则均较CsA组降低（均P〈0．05）;CsA组肾组织中肾小管、间质损伤评分均较对照组增高,而CsA＋GTP各剂量组则均较CsA组降低（P〈0．05）。结论氧化应激反应在CsA慢性肾毒性中具有重要的作用,而各剂量的GTP则可预防CsA慢性肾毒性作用。     

高糖诱导氧化应激对胰岛细胞功能的影响

目的:研究不同浓度葡萄糖对INS-1细胞及胰岛分泌功能的影响,并探讨氧化应激在葡萄糖对INS-1细胞功能损伤中的作用。方法:将不同浓度葡萄糖(11.1、16.7、22.2、33.3mmol/L)作用于INS-1细胞,镜下观察INS-1细胞的形态改变,应用可见分光光度计测定丙二醛(MDA)含量,运用ELISA方法检测葡萄糖刺激的胰岛素分泌(GSIS)。结果:随着葡萄糖浓度的增加,INS-1细胞的凋亡增多,MDA含量逐渐增加,GSIS值逐渐下降,不同浓度葡萄糖组间MDA含量、GSIS值差异有统计学意义(P均<0.01)。结论:高糖可促进INS-1细胞凋亡,在高糖作用下活性氧物质(ROS)代谢产物MDA增多,胰岛细胞胰岛素分泌功能受损。     

辛伐他丁对糖尿病肾病大鼠氧化应激的影响

目的研究辛伐他丁对糖尿病肾病大鼠氧化应激的影响.方法 60只SD大鼠随机分为正常对照组(CG)、糖尿病肾病组(DN)、糖尿病肾病 辛伐他丁组(DN S),模型建立后6、12周时各组分别取10只大鼠称取体重、肾重,测定血糖(GLU)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)、甘油三酯(TG)、肌酐(SCr)及过氧歧化酶(SOD)、谷胱甘肽-S转移酶(GST)、过氧化氢酶(CAT)、血浆丙二醛(MDAp)及红细胞抽提液丙二醛(MDAe),留取尿液测定24h尿白蛋白排泄量(UAE),并作肾组织切片分析肾小球截面积(GV)及系膜区面积(M/T).结果 6周及12周时各组间SCr、LDL、HDL、TG相比差别无显著性意义(均P＞0.05),DN组及DN S组GLU和肾重/体重较CG组明显升高,脂质过氧化产物MDAp及MDAe也均升高(均P＜0.05),抗氧化酶SOD、GST、CAT均下降(均P＜0.05),12周时DN组及DN S组的UAE,GV和M/T均增多(均P＜0.05).DN S组氧化应激指标(MDAp、MDAe、SOD、GST、CAT)改变较DN组轻(P＜0.05),12周时UAE、GV也小于DN组(P＜0.05).Pearson相关性分析发现UAE与MDAp呈正相关,而与SOD、GST、CAT呈负相关.结论血浆中过氧化脂质增多及抗氧化酶水平的下降为糖尿病肾病发生发展的促进因素,辛伐他丁有不依赖于其降脂效果的抗氧化作用,进而起到保护肾脏延缓糖尿病肾病发生发展的作用.     

Overweight and Obesity——Induced Oxidative Stress in Children

Objective To investigate whether overweight and obesity might cause oxidative stress and potential oxidative damage in overweight and obese children, and to explore its possible mechanism. Methods Eighty-five overweight and obese children （OOC）, and eighty-five age-matched healthy children （HC） were recruited in this case-control study. The present study analyzed spectrophotometrically vitamin C （VC）, vitamin E （VE）, and β-carotene （β-CAR） in plasma, as well as the activities of superoxide dismutase （SOD）, catalase （CAT）, and the level of malondialdehyde （MDA） in erythrocytes. Results Compared with those of VC, VE, β-CAR, SOD, CAT and MDA in the HC group, the average values of VC, VE, β-CAR, SOD, and CAT in the OOC group were significantly decreased （P〈0.001）, while the average value of MDA in the OOC group was significantly increased （P〈0.001）. The regression analysis demonstrated that VC, VE, β-CAR, SOD, and CAT were negatively correlated （P〈0.05-0.01）, and MDA was positively correlated with BMI （P〈0.05）. Fitting to the model of multiple stepwise regression of BMI on VC, VE, β-CAR, SOD, CAT, and MDA in 85 OOC was Y = 27.0041 ＋ 0,2541MDA - 2.1448β-CAR -- 0.0090CAr, where F = 43.8088, P〈0.001, r = 0.7866, r^2= 0.6187, adjusted r^2= 0.6046. The findings from the reliability analysis for VC, VE, β-CAR, SOD, CAT, and MDA used to reflect increased oxidative stress and potential oxidative damage in the OOC showed that the reliability coefficients （alpha, 6 items） = 0.7231, P〈0.0001, and that the standardized item alpha = 0.9207, P〈0.0001, Conclusion The present study suggests that there exists an increased oxidative stress in overweight and obese children.     

Alterations in oxidative stress markers in laryngeal carcinoma patients

Background

Data describing how laryngeal cancer affects oxidative stress markers and antioxidants are limited. This study investigated serum antioxidant enzyme activities and oxidative stress markers before and after laryngectomies in patients with laryngeal cancer.

氟伐他汀对糖尿病大鼠心肌组织氧化应激反应的影响

目的探讨氟伐他汀对1型糖尿病大鼠心肌组织氧化应激水平的影响。方法成年SD大鼠43只,随机抽取10只作为正常对照组,其余制备糖尿病模型。将成模大鼠分为糖尿病模型组、氟伐他汀低、中、高剂量（2、6、18 mg/kg）组、胰岛素治疗组（2U/kg）,8周后以半自动生化仪分别测定心肌组织谷胱甘肽过氧化物酶（GSH-PX）、丙二醛（MDA）含量及超氧化物歧化酶（SOD）活力。结果与正常组大鼠比较,模型组及氟伐他汀各剂量组的空腹血糖水平均明显升高（P〈0.01）;氟伐他汀各剂量组与模型组大鼠比较,空腹血糖变化不明显（P〉0.05）。与正常组比较,模型组大鼠心肌组织中SOD、GSH-PX、活力明显下降,MDA含量明显升高（P〈0.01）;氟伐他汀各治疗组与模型组比较,SOD、GSH-PX活力有所增强。结论氟伐他汀可抑制1型糖尿病大鼠的氧化应激水平,对糖尿病大鼠心肌发挥保护作用。     

气管滴注大气可吸入颗粒物对大鼠的系统性氧化应激作用

目的：探讨大气可吸入颗粒物对大鼠的氧化应激作用。方法：将24只体重为320~360 g的雄性Wistar大鼠随机分为4组,即生理盐水对照组和颗粒物低、中、高剂量组（3.75、7.5、15 mg/kg）。染毒采用一次性气管滴注颗粒物,24 h后处死动物,测定血液中的超氧化物歧化酶（superoxide dismutase, SOD）活性和丙二醛（malondialdehyde, MDA）含量,以及心肺组织中SOD活性、MDA和蛋白羰基（protein carbonyl）的含量。结果：与对照组相比,各染毒组大鼠血液中SOD活性降低,中、高剂量组的差异有统计学意义（P<0.05）;血液中MDA含量升高,高剂量组的差异有统计学意义（P<0.05）;各染毒组大鼠心肺组织高剂量组的SOD活性降低,且差异有统计学意义（P<0.05）;肺脏MDA水平升高,中、高剂量组的差异有统计学意义（P<0.05）;心脏MDA水平升高,高剂量组的差异有统计学意义（P<0.05）;肺脏蛋白羰基含量升高,高剂量组的差异有统计学意义（P<0.05）,心脏蛋白羰基含量无明显改变。结论：大气可吸入颗粒物能引起大鼠体内氧化和抗氧化系统的失衡,产生氧化应激效应,膜脂质较蛋白质更易受到氧化应激的作用。     

降压药对高血压患者氧化应激影响的观察

目的：观察不同类别降压药物对高血压患者氧化应激水平的影响。方法：通过比较使用不同降压药（分别为ACEI、AT-Ⅱ、β受体阻滞剂及钙通道拮抗剂）3月后患者的IL-6、CRP和血清微量元素水平的变化，评估机体的氧化应激水平。结果：使用ACEI类和AT-Ⅱ类降压药的患者，3月后血清铜水平下降，锌水平上升，CRP和IL-6水平下降。结论：ACEI和AT-Ⅱ类降压药有调低氧化应激水平的作用，而在其他降压药物中未发现此种改变。