Mobile phone-induced myocardial oxidative stress: protection by a novel antioxidant agent caffeic acid phenethyl ester

Electromagnetic radiation (EMR) or radiofrequency fields of cellular mobile phones may affect biological systems by increasing free radicals, which appear mainly to enhance lipid peroxidation, and by changing the antioxidant defense systems of human tissues, thus leading to oxidative stress. Mobile phones are used in close proximity to the heart, therefore 900 MHz EMR emitting mobile phones may be absorbed by the heart. Caffeic acid phenethyl ester (CAPE), one of the major components of honeybee propolis, was recently found to be a potent free radical scavenger and antioxidant, and is used in folk medicine. The aim of this study was to examine 900 MHz mobile phone-induced oxidative stress that promotes production of reactive oxygen species (ROS) and the role of CAPE on myocardial tissue against possible oxidative damage in rats. Thirty rats were used in the study. Animals were randomly grouped as follows: sham-operated control group (N: 10) and experimental groups: (a) group II: 900 MHz EMR exposed group (N: 10); and (b) group III: 900 MHz EMR exposed+CAPE-treated group (N: 10). A 900 MHz EMR radiation was applied to groups II and III 30 min/day, for 10 days using an experimental exposure device. Malondialdehyde (MDA, an index of lipid peroxidation), and nitric oxide (NO, a marker of oxidative stress) were used as markers of oxidative stress-induced heart impairment. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status. In the EMR exposed group, while tissue MDA and NO levels increased, SOD, CAT and GSH-Px activities were reduced. CAPE treatment in group III reversed these effects. In this study, the increased levels of MDA and NO and the decreased levels of myocardial SOD, CAT and GSH-Px activities demonstrate the role of oxidative mechanisms in 900 MHz mobile phone-induced heart tissue damage, and CAPE, via its free radical scavenging and antioxidant properties, ameliorates oxidative heart injury. These results show that CAPE exhibits a protective effect on mobile phone-induced and free radical mediated oxidative heart impairment in rats.     

Preventive effect of vitamin E on iron-induced oxidative damage in rabbit

Although iron (Fe), plays an important role in different oxidative steps during the metabolism of the human body, it can cause free radical damage. Iron ions seem to play a major role in initiation and promotion reactions of intracellular lipid peroxidation. The aim of this study was to investigate if vitamin E has a protective effect on oxidative changes in erythrocytes induced by Fe treatment. Thirty male New Zealand white rabbits weighing 1400 +/- 50 g were used in the study. The animals were divided into three groups. The first group (n:10) was given 500 mg/kg iron-dextran through intraperitoneal (ip) injection. The second group was given 500 mg/kg iron-dextran+100 mg/kg vitamin E(ip). The third group constituted the control group and received a saline solution injection. The activities of erythrocyte antioxidant enzymes; Superoxide Dismutase (SOD), Glutatione peroxidase (GSH-Px), Catalase (CAT) and Malondialdehyde (MDA) level, an indicator of lipid peroxidation, were determined. Erythrocyte SOD, GSH-Px and CAT activities were decreased and MDA level was increased in iron-dextran treated animals compared to the control group (P < 0.05). The activities of the three antioxidant enzymes were increased and MDA level was decreased in iron-dextran and vitamin E treated group compared to the control group (P < 0.05). Our data indicate that lipid peroxidation occurs after iron overload in the blood. In the light of our findings, vitamin E administration can prevent the toxic oxidative effects induced by iron-dependent free radical damage in erythrocytes.     

叶黄素对糖尿病大鼠肾损伤的缓解作用

目的研究叶黄素对糖尿病大鼠肾损伤的影响并探讨其可能机制。方法采用四氧嘧啶诱导大鼠糖尿病模型,灌胃给予叶黄素4w,测定大鼠血浆叶黄素水平、肾重、肾脏指数、BUN、SCr、CCr、24h尿蛋白及肾组织SOD、GSH-Px活性、GSH、MDA含量、TNF-α、IL-6水平。结果叶黄素5mg/kg.bw和20mg/kg.bw剂量组大鼠肾重、肾脏指数、BUN、SCr、CCr、24h尿蛋白均低于糖尿病大鼠组,差异有统计学意义(P<0.05);而肾组织SOD与GSH-Px活性、GSH含量高于糖尿病大鼠组(P<0.05),MDA含量低于糖尿病大鼠组(P<0.05),肾组织TNF-α、IL-6低于糖尿病大鼠组(P<0.05)。结论叶黄素能缓解糖尿病大鼠的肾功能损害,其机制可能与叶黄素升高抗氧化酶活性,降低肾组织的氧化应激水平以及减少促炎性细胞因子的表达有关。     

硒对乙醇致大鼠机体损伤的保护作用

目的 :探讨硒对乙醇致体内脂质过氧化的保护作用及机理。方法 :用 3g/kg体重的乙醇给大鼠灌胃 ,同时自由饮用含硒量为 0 .2 5 mg/L 的亚硒酸钠水溶液 ,饲养三个月。结果 :与单给乙醇组比较 ,乙醇 +Se组大鼠组织和血清 MDA含量显著降低 (P均 <0 .0 1) ,GSH- Px、SOD、CAT活性均升高 (P均 <0 .0 5 )。结论 :硒可能通过增加 GSH- Px、SOD、CAT活性从而抑制过量乙醇对机体的损伤     

T-2毒素对低硒大鼠关节软骨抗氧化酶活性及基因表达的影响

目的研究T-2毒素对低硒(Se)大鼠关节软骨抗氧化酶及基因表达的影响。方法新生断乳雄性健康SD大鼠,平均体重60~80g,随机分成两大组即常规组和低Se组喂养30 d,低Se动物模型建造成功后再分成常规组、低Se组、常规+低T-2组、常规+高T-2组、低Se+低T-2组、低Se+高T-2组,再T-2毒素灌胃饲养30 d后,观察低Se、T-2毒素及二者共同作用对各组大鼠关节软骨丙二醛(MDA)含量、总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活性及SOD、CAT、GSH-Px mRNA表达的影响。结果与常规组相比,各组大鼠关节软骨中MDA含量升高,T-AOC、SOD、CAT和GSH-Px活性下降,均有统计学意义(P<0.05);低Se+低T-2组、低Se+高T-2组与低Se组相比,MDA含量升高,T-AOC、SOD、CAT和GSH-Px活性下降(P<0.05);与常规组相比,各组大鼠关节软骨SOD、CAT、GSH-Px mRNA表达降低(P<0.05)。结论低Se或单纯T-2毒素均可减弱大鼠关节软骨抗氧化酶活性,低Se与T-2毒素对机体抗氧化功能有协同作用。     

番茄红素对大鼠体内抗氧化系统功能的影响

目的　观察番茄红素 (lycopene ,LP)对大鼠抗氧化酶系统的影响。方法　大鼠饲喂番茄红素 4周后处死 ,测定血清和肝匀浆的超氧化物歧化酶 (SOD)活性、过氧化氢酶 (CAT)活性、谷胱甘肽过氧化物酶(GSH -Px)活力、总抗氧化能力 (T -AOC)、丙二醛 (MDA)及还原型谷胱甘肽 (GSH)含量。结果　各番茄红素给药组的大鼠血清和肝组织的SOD活性、GSH -Px活力及T -AOC上升 ,MDA含量降低 ,与空白组相比 ,在统计学上差异有显著性 (P <0 0 5 )。结论　番茄红素可以提高大鼠机体的抗氧化能力 ,抑制脂质过氧化     

低聚木糖对摄食高脂饲料的小鼠自由基水平及抗氧化作用的影响

目的研究高脂饲料条件下,不添加和添加中、高剂量(0.0835%和0.1650%)的低聚木糖(XOS)对小鼠体内自由基及抗氧化功能的影响。方法将24只小鼠分成4组,设置对照,通过向高脂饲料中添加XOS,观察对小鼠机体自由基及抗氧化功能的影响。结果与正常对照组相比,高脂饲料可导致小鼠氧化应激,升高体内自由基水平,降低机体抗氧化能力,而添加XOS的饲料能显著降低机体自由基水平,增强血清及组织中SOD、GSH-Px及CAT活性,显著升高血清T-AOC水平,显著降低血清MDA含量。并且,XOS添加量与抗氧化作用呈现量效关系。结论低聚木糖具有较好的清除机体自由基及抗氧化功能。     

EFFECTS OF ENDURANCE TRAINING ON ANTIOXIDANT DEFENSE MECHANISMS AND LIPID PEROXIDATION IN TESTIS OF RATS

Male rats were equally divided into trained rest (TR), trained exhaustive exercise (TE), untrained rest (UR), and untrained exhaustive exercise (UE). Endurance training consisted of treadmill running for 1.5 h/d, 5 days a week for 8 weeks reaching the speed of 2.1 km/h at the fortieth week. For acute exhaustive exercise, graded treadmill running was conducted reaching the speed of 2.1 km/h at 95th min, 10% uphill, continued until exhaustion. Testicular tissue malondialdehyde (MDA), antioxidant potential (AOP) levels, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST), glutathione reductase (GR) and catalase (CAT) activities were determined. There was a slight decrease, but not significant, in the SOD activity in UE group compared to TE and TR groups. Activity of GSH-Px decreased in the UE group compared to UR, TR and TE groups. Acute exhaustive exercise did not affect testicular tissue GSH-Px activity in trained rats. Testicular tissue GST activity of the UE group was similar to TE group, but lower than UR and TR groups. In UE group, testicular tissue AOP values were lower than UR, TR and TE groups. The oxidative effects of acute exhaustive exercise on the rat testis decreased with endurance training. Endurance training prevents oxidative injuries by eliminating oxygen radicals and inhibiting lipid peroxidation via preventing decreases in antioxidant enzyme activities.     

芦荟抗氧化活性成分对老龄鼠抗氧化水平的影响

目的:对芦荟抗氧化活性组分FA进行结构鉴定分析,考察组分FA对老龄鼠体内抗氧化能力的影响。方法:利用高效液相色谱、红外光谱、紫外光谱和质谱等并结合标准品的比较推断FA的分子结构。采用动物体内实验研究FA对不同年龄段(幼龄和老龄)大鼠血液和肝组织中超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px)活性以及脂质过氧化产物丙二醛(MDA)含量的影响。结果:芦荟抗氧化组分FA的分子结构为2-异丙醇基-8-C-D-吡喃葡萄糖-7-羟基-5-甲基对氧萘酮。与对照组动物相比,老龄给药组的血样和肝组织中的SOD、GSH-Px活性均有显著性提高(P<0.05),同时伴随MDA水平的显著降低(P<0.05)。在幼龄鼠中,给药组血样和肝组织中的脂质过氧化产物MDA水平与对照组比较显著降低,然而对抗氧化酶没有显著影响(P>0.05)。结论:FA能有效降低老龄鼠体内的脂质过氧化水平并且防止体内抗氧化酶受自由基诱导的氧化损伤,恢复抗氧化酶的活性。     

Peroxidation in muscle and liver tissues from fish in a contaminated river due to a petroleum refinery industry

In this study, we aimed to investigate the possible effects of the wastewater water contamination of a petroleum industry on the oxidant/antioxidant status of muscle and liver tissues from fish in the Kizilirmak River, Kirikkale, Turkey. The antioxidant/oxidant parameters were analyzed in the muscle and liver tissues from fish in 10 km of the river above and below the industry. Malondialdehyde (MDA) and susceptibility to oxidation (SO) values were measured in the liver and muscle tissues as indexes of oxidation, and antioxidant potential (AOP), superoxide dismutase (SOD), glutathion peroxidase (GSH-Px), and catalase(CAT) activities were measured as indexes of antioxidant status. There was significant oxidation in the muscle tissue of the fish obtained in the river downstream of the industry compared to those obtained upstream of the industry. Although there were no meaningful differences between the SOD and GSH-Px activities, the AOP value and CAT activities were found to be reduced in the muscle tissues from the fish obtained downstream. In the liver tissues, the SOD and GSH-Px activities were found to be increased in the fish obtained downstream but no differences were observed in the MDA, SO, AOP, and CAT values. Our results suggest that some contaminants from the petrochemical industry cause oxidation in fish muscle tissues by impairing the antioxidant system. However, because no peroxidation was observed in the liver tissue from the downstream fish, it is possible that liver tissues have a stronger antioxidant capacity than muscle.     

橙皮素对染矽尘大鼠肺组织氧化损伤的保护作用研究

  目的  探讨橙皮素对染矽尘大鼠肺组织氧化损伤的保护作用。
  方法  将54只Wistar雄性大鼠随机分为阴性对照组,二氧化硅（SiO₂）模型组,橙皮素低、中、高剂量治疗组及吡非尼酮阳性对照组,每组9只。阴性对照组经气管灌注1 mL生理盐水,其他各组均经气管灌注1 mL 50 mg/mL SiO₂,24 h后对各组动物进行药物干预,每天灌胃给药1次。染尘28 d后处死大鼠,观察各组大鼠肺组织病理学改变,检测每组大鼠肺组织丙二醛（MDA）含量、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）活力及总抗氧化能力（T-AOC）。
  结果  组织病理学结果显示,吡非尼酮阳性对照组及橙皮素治疗组大鼠肺组织的损伤程度减轻。与阴性对照组相比,SiO₂模型组大鼠肺系数、MDA含量和SOD活力明显升高（P < 0.05）,CAT、GSH-Px、T-AOC活力未出现明显变化（P > 0.05）;给予药物治疗后,吡非尼酮阳性对照组和橙皮素治疗组的大鼠肺系数、肺泡炎和纤维化评分及MDA含量均出现不同程度的降低（P < 0.05）,CAT、SOD、GSH-Px和T-AOC活力均出现不同程度的升高（P < 0.05）。
  结论  橙皮素可能通过改变各氧化指标水平,增强抗氧化能力,减轻SiO₂对大鼠肺组织的损伤作用。
     

番茄红素对镉损伤大鼠氧化应激的影响

目的:观察番茄红素(lycopene,LP)对镉(Cd)损伤大鼠氧化应激的影响。方法:大鼠饲喂氯化镉(Cd-Cl2)和番茄红素,4周后处死,测定血清和肝匀浆的超氧化物歧化酶(SOD)活性、过氧化氢酶(CAT)活性、谷胱甘肽过氧化物酶(GSH—Px)活力、丙二醛(MDA)及还原型谷胱甘肽(GSH)含量。结果:与镉损伤组相比,番茄红素组的大鼠血清和肝组织的SOD活性、GSH—Px活力上升,MDA含量降低,在统计学上差异有显著性(P<0.05)。番茄红素可以拮抗镉的毒性,提高大鼠机体的抗氧化能力,抑制镉中毒所致的氧化应激。     

白藜芦醇对铅诱导小鼠脂质过氧化的拮抗作用

目的探讨白藜芦醇对铅暴露引起的氧化损伤的拮抗作用。方法铅染毒动物模型用含铅(醋酸铅0.5%)饮用水构建。60只健康雄性昆明种小鼠随机分为6组,每组10只:正常对照组,铅染毒组,铅染毒+白藜芦醇低、中、高剂量干预组,白藜芦醇组。检测小鼠血铅和组织铅含量及肝、肾组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性和丙二醛(MDA)的含量和抗氧化能力指数。结果与铅染毒组相比,白藜芦醇处理组肝、肾组织中SOD、CAT和GSH-Px活性均上升(P<0.01),MDA含量降低(P<0.01)。白藜芦醇使用剂量在800～1 200mg/kg时能够显著地提高机体抗氧化酶的活力,增强机体的抗氧化能力。铅染毒小鼠血浆、肝组织及肾组织中ORAC值均有一定程度的减小,给予白藜芦醇可以拮抗铅毒性引起的ORAC值的下降。结论白藜芦醇通过提高抗氧化酶活性,以减轻铅毒引起的脂质过氧化损伤,提高小鼠机体的抗氧化能力,而实现保护肝、肾组织的作用。     

凹顶藻萜类化合物对酒精暴露大鼠氧化损伤保护作用

目的观察凹顶藻萜类化合物(Laurencia terpenoids extract,LTE)对酒精暴露大鼠的抗氧化水平及HO-1酶活性的影响,并探讨其可能的作用机制。方法60只雄性Wistar大鼠随机分为6组。酒精模型组(B组)给予乙醇4.8g/kgbw·d灌胃;LTE低、中、高剂量干预组(C、D、E组)分别给予LTE25、50、100mg/kgbw·d;甘利欣药物组(F组)给予甘利欣200mg/kgbw·d灌胃。空白对照组(A组)给予等体积蒸馏水。除空白组外,酒精剂量均同模型组。实验进行6w。分别测定血清及肝匀浆中超氧化物歧化酶(SOD)和谷胱甘肽过氧物酶(GSH-Px)活性,丙二醛(MDA)含量。对肝组织切片进行免疫组化染色,观察肝内血红素氧化酶-1(HO-1)免疫阳性细胞的组织分布,并对其灰度值和光吸收密度值进行定量分析。结果与A组比,B、F组血清及肝匀浆SOD活力下降,C、E组血清SOD活力比B组升高,有一定的量效关系。B组大鼠血清及肝匀浆GSH-Px活力较A组下降,而D组较B组显著升高。与A组比,B组血清及肝匀浆MDA含量较A组升高,而D、E组血清和肝匀浆MDA含量较B组显著降低,且有一定的量效关系。与A组比,B组HO-1活力显著降低。D、E、F组HO-1活力比B组升高明显。结论LTE可增强酒精暴露大鼠体内抗氧化的活性,减少脂质过氧化产物的生成,诱导HO-1活性增强,从而对酒精造成的机体氧化损伤表现出相应的保护效应。     

纳米硫化铅对大鼠海马及皮质氧化损伤作用的研究

目的探讨纳米硫化铅对大鼠海马及皮质的氧化损伤作用。方法清洁级SD雄性大鼠60只,随机分为3组,即对照组、纳米硫化铅低、高剂量组,低、高剂量组分别气管灌注15、30mg/kg粒径20nm的硫化铅混悬液1ml,每周1次,连续染毒3个月后测定3个组大鼠体质量变化;检测大鼠血清、海马及皮质中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力和丙二醛(MDA)含量。结果染毒组大鼠血清、海马及皮质中SOD、GSH-Px的活力及MDA含量分别与对照组比较,差异均有统计学意义(P<0.05)。染毒组大鼠血清、海马及皮质中SOD、GSH-Px活力均降低,MDA含量增高。结论纳米硫化铅可能引起海马及皮质中SOD、GSH-Px活力降低,MDA含量增加,可导致海马及皮质抗氧化能力减弱。     

锰烟尘对男工血脂质过氧化和抗氧化酶的影响

目的研究长期高浓度锰烟尘暴露对男工体内脂质过氧化和抗氧化酶的影响。方法用分光光度法测定59名接触锰烟尘男工和59名对照男工的红细胞血红蛋白(Hb)、丙二醛(MDA)含量以及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)和血清谷胱甘肽S-转移酶(GSH-ST)活力。结果作业环境空气中MnO2平均浓度为0.75 mg/m3(0.19~1.60 mg/m3)时,接锰作业组红细胞MDA含量、SOD、CAT、GSH-Px活力与对照组比较,差异无显著性。分层分析显示,接触锰男工红细胞SOD、CAT、GSH-Px的酶活力随接触锰工龄的增加而升高,接触锰工龄>10 a组,SOD、CAT、GSH-Px酶活力均降至对照组水平。结论接触高浓度的锰<10 a,可使体内抗氧化酶活力应激性增强,而脂质过氧化物保持不变。但接触高浓度锰>10 a,可导致男工血脂质过氧化物增加及抗氧化酶活力降低,对机体产生损害作用。     

牛黄及胆红素对三氯乙烯染毒小鼠脂质过氧化的拮抗作用

目的研究牛黄、胆红素对三氯乙烯(TCE)染毒ICR小鼠所致的脂质过氧化的拮抗作用。方法用TCE灌胃染毒ICR小鼠制造脂质过氧化模型,然后分别以牛黄、胆红素灌胃,测定ICR小鼠肝、肾组织中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH Px)、过氧化氢酶(CAT)。结果与阴性对照组比,TCE处理组肝、肾组织GSH Px、SOD、CAT活力降低,MDA含量增加,差异均有显著性(P<0.05);牛黄、胆红素染毒与TCE处理组比较,肝、肾组织GSH Px、SOD、CAT活力显著增强(P<0.05),脂质过氧化产物MDA含量减少。结论牛黄和胆红素均能较好地拮抗TCE所引起的ICR小鼠脂质过氧化。     

维生素C对青春期邻苯二甲酸二丁酯暴露致大鼠卵巢氧化应激的干预作用

目的探讨维生素C(vitamin C,Vit C)对青春期邻苯二甲酸二丁酯(dibutyl phthalate,DBP)暴露致大鼠卵巢氧化应激的干预作用。方法将160只健康初断乳SPF级Wistar雌性大鼠随机分为5组,分别为对照(玉米油)组和低(100mg/kg)、高(500 mg/kg)剂量DBP暴露组及低(100 mg/kg)、高(500 mg/kg)剂量DBP+Vit C(125 g/L)干预组。采用灌胃方式暴露DBP,暴露容量为10 ml/kg,每天1次;采用自由饮水方式暴露Vit C,连续暴露30 d。分别于暴露第5、10、20、30天,测定大鼠卵巢组织中MDA、GSH含量和SOD、CAT、GSH-Px活力。结果与对照组相比,DBP暴露组大鼠卵巢组织中MDA含量均升高,而GSH含量和SOD、CAT、GSH-Px活力均下降;与相同剂量DBP暴露组相比,Vit C干预组大鼠卵巢组织中MDA均下降,而GSH含量和SOD、CAT、GSH-Px活力均升高。且随着DBP暴露剂量的升高,DBP暴露组和Vit C干预组大鼠卵巢组织中的GSH含量和SOD、CAT、GSH-Px活力均呈下降趋势,而MDA含量呈上升趋势。结论 DBP暴露可致青春期雌性大鼠卵巢组织产生脂质过氧化反应,诱导氧化应激,导致卵巢抗氧化能力下降;而抗氧化剂Vit C对于DBP所致生殖系统的氧化损伤具有一定的拮抗作用。     

番茄红素对镉中毒大鼠体内抗氧化酶活力影响

目的　观察番茄红素 (lycopene,LP)对镉 (Cd)中毒大鼠抗氧化酶系统的影响。 方法　大鼠饲喂CdCl2 和番茄红素 ,4周后处死 ,测定血清和肝匀浆的超氧化物歧化酶 (SOD)活性、过氧化氢酶 (CAT)活性、谷胱甘肽过氧化物酶 (GSH -Px)活力、丙二醛 (MDA)及还原型谷胱甘肽 (GSH)含量。结果　与模型组相比 ,番茄红素组的大鼠血清和肝组织的SOD活性、GSH -Px活力上升 ,MDA含量降低 ,有显著性差异 (P <0 0 5 )。结论　番茄红素可以拮抗镉的毒性 ,提高大鼠机体的抗氧化能力 ,抑制镉中毒所致的脂质过氧化。     

Effects of xylene and formaldehyde inhalations on renal oxidative stress and some serum biochemical parameters in rats

In this study, it was aimed to demonstrate the possible renal oxidative stress and some serum biochemical parameters and their alterations caused by the exposure to xylene and formaldehyde (HCHO) in rats. Weighing 150-200g, 12-week-old, 24 female Sprague-Dawley rats were used. The rats were randomly divided into four groups: Group 1 (control), Group 2 (300-ppm technical xylene), Group 3 (6-ppm HCHO) and Group 4 (150-ppm technical xylene + 3-ppm HCHO). The animals were exposed to gases eight hours per day for six weeks. Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities, glutathione (GSH) and malondialdehyde (MDA) levels were measured. In addition, serum total protein, albumin, urea and creatinine levels were evaluated. Compared with the control animals, urea levels increased significantly in all groups (P < 0.001). GSH activities and MDA levels increased in xylene and xylene + HCHO groups (P < 0.05). No statistically considerable differences were found in SOD, CAT and GSH-Px activities, total protein, albumin and creatinine levels among all groups (P > 0.05). The present study indicates but not statistically confirms the renal toxicity of the exposures to xylene, HCHO and a mixture of them.