异丙肾上腺素性心肌缺血大鼠全身重要脏器自由基系统的改变及其意义

本文以异丙肾上腺素性心肌梗塞为模型系统地观察了全身重要脏器及血清脂质过氧化产物丙二醛(MDA)含量及抗氧化酶如超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力的改变。结果表明,心肌缺血大鼠全身重要脏器MDA含量增加,且缺血心肌SOD及GSH-Px活力增强。由此说明,心肌缺血大鼠全身重要脏器均存在着严重的自由基损伤效应,同时抗氧化酶活力亦随之代偿性增强。     

天然抗氧化剂对抗晶状体氧化损伤作用的实验研究

目的:探讨五味子乙素(SchB)、水飞蓟宾(SIB)、没食子酸丙酯(PG)、阿魏酸钠(SF)和沙棘总黄酮(TFH)5种天然抗氧化剂对抗实验性晶状体氧化损伤的作用。方法:将兔眼透明晶状体温育在Fenton氧化反应模型中造成晶状体氧化损伤,同时分别加入上述5种天然抗氧化剂共同温育24h后,测定晶状体总蛋白和可溶性蛋白、SOD、GSH-Px、GSH、VitC、总抗氧化能力和MDA的水平,观察5种抗氧化剂对上述指标的影响。结果:5种抗氧化剂均不同程度地升高氧化损伤晶状体的抗氧化指标,降低脂质过氧化终末产物MDA含量,且优于白内停滴眼液。其中SF和SchB的作用更为显著。结论:5种天然抗氧化剂对实验性晶状体氧化损伤有良好的对抗作用,从天然抗氧化剂中寻找高效的抗白内障药物具有广阔的前景。     

慢性肺疾病早产鼠BALF及肺组织中脂质过氧化的同步研究

目的为探讨高氧致早产儿慢性肺疾病(CLD)发生中支气管肺泡灌洗液(BALF)及肺组织中脂质过氧化的变化规律及相互间关系.方法采用高浓度氧致早产鼠CLD模型为研究对象,应用分光光度计比色法同步测定BALF和肺组织超氧化物岐化酶(SOD)活性及脂质过氧化产物丙二醛(MDA)的含量.结果两组的BALF及肺组织中SOD活性均无差异(P>0.05);而实验组,BALF及肺组织中MDA的水平呈同相变化,即吸高氧3d明显升高(P<0.05),7d达高峰(P<0.01),持续1w后逐渐下降,21d仍高于正常水平(P<0.05).结论肺组织的氧自由基损伤贯穿高氧致CLD发生、发展全过程中;BALF中MDA水平可间接反应肺组织的氧自由基损伤程度.     

慢性乙型肝炎患者血清SF.PDGF水平与脂质过氧化损伤的关系

目的：探讨了慢性乙型肝炎患者血清SF.PDGF与脂质过氧化损伤的关系。方法抽取医院2011年9月~2013年9月收治的慢性乙型肝炎患者68例作为观察组,取同期入院体检正常者35例作为对照组,采用应用放射免疫分析法,酶联法和生化法分析两组患者的血清SF.PDGF和MDA.SOD水平。结果慢性乙型肝炎患者血清SF.PDGF和MDA水平均非常显著地高于正常人组(<0.01),而血清SOD水平又非常显著地低于正常人组(<0.01).血清SF.PDGF水平与MDA水平呈显著正相关(=0.4816.0.6139,<0.01).SF水平与SOD水平呈显著负相关(=-0.2844,<0.01)。结论慢性乙型肝炎患者血清SF.PDGF水平与脂质过氧化损伤有相关性,具有一定的临床参考价值。     

西洛他唑对离体培养大鼠皮层细胞缺血再灌注损伤的保护作用

目的:研究磷酸二酯酶抑制剂西洛他唑对离体培养大鼠皮层细胞缺血再灌注损伤的影响及作用机制。方法:取新生Wistar大鼠皮层细胞进行原代培养,分为5组:正常对照组、西洛他唑组、依达拉奉组、溶剂对照组及缺血再灌注模型组。通过建立糖氧剥离后复糖氧的细胞损伤模型模拟细胞"缺血再灌注损伤",然后进行干预。细胞经4 h糖氧剥离24 h复糖氧培养后,测定培养上清中乳酸脱氢酶(LDH)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、神经元型一氧化氮合酶(nNOS)、诱导型一氧化氮合酶(iNOS)及一氧化氮(NO)的含量;测定细胞内环磷酸腺苷(cAMP)水平,并通过四唑盐(MTT)比色实验测定细胞活力。结果:西洛他唑和依达拉奉均可减少"缺血再灌注"损伤细胞的LDH和MDA漏出量,提高GSH-Px释放量,降低nNOS、iNOS和NO的水平,升高细胞内cAMP水平,使细胞存活率显著提高;西洛他唑与依达拉奉组相比,LDH、MDA漏出量及GSH-Px的释放量无差别,nNOS、iNOS和NO的水平明显降低,细胞内cAMP水平显著升高,细胞存活率明显提高。结论:西洛他唑对大鼠皮层细胞缺血再灌注损伤具有保护作用,其作用机制可能通过抗氧化、降低nNOS及iNOS的水平,从而降低NO的分泌、升高细胞内cAMP水平来实现的。     

新生儿HIE血SOD,MDA的变化及其抗氧化剂的应用

本文测定了40例新生儿缺氧缺血性脑病（HIE）血超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量。发现HIE治疗前血SOD活性明显降低而脂质过氧化反应的产物MDA含量明显升高（与正常对照组比较P＜0．01），抗氧化剂治疗三天后SOD活性升高而MDA含量下降，但未恢复正常，而治疗六天后SOD、MDA均恢复正常。（与正常对照组比较P＞0．05）。说明HIE极其脂质过氧化反应增强，抗氧化功能下降。而应用抗氧化剂复方丹参、维生素C和E、甘露醇、鲁米那、地塞米松治疗能减少脂质过氧化损伤，控制HIE病情的发展，且抗氧化剂的治疗应坚持6天以上。并阐述了各抗氧化剂的治疗作用。     

人红细胞抗氧化酶类的测定

我们曾用H_2O_2处理正常及PNH红细胞,然后测定膜脂质的过氧产物丙二醛(MDA),并发现PNH红细胞产生的MDA远较正常人的为多,共原因可能是:(一)膜脂质组分异常;(二)细胞内抗氧化机能减退。本文报告PNH及正常红细胞中SOD、GSH-Px及过氧化氢酶活性,以探讨红细     

赛庚啶对内毒素血症小鼠氧化损伤的对抗作用

目的:研究赛庚啶对内毒素(LPS)血症小鼠氧化损伤的对抗作用。方法:小鼠尾静脉注射LPS,造成内毒素血症模型,观察赛庚啶能否提高小鼠24h存活率,并测定血浆NO的水平,心、肝、肾和脑组织中SOD和GSH-Px活力以及脂质过氧化产物MDA含量。结果:赛庚啶预防给药能够显著提高致死量LPS攻击后小鼠24h的存活率,使血浆NO2-/NO3-的水平显著降低,其中高剂量组SOD和GSH-Px活力增高,MDA含量降低。低剂量组SOD活力增高,但肝和脑组织中MDA含量下降不明显,肝和肾组织GSH-Px活力无明显增高。结论:赛庚啶预防给药能够防治LPS血症,改善小鼠LPS血症时重要脏器氧化性损伤状态,抑制血浆NO水平过度升高。     

动脉粥样硬化与血浆抗氧化活性

目的:探讨高胆固醇血症所致动脉粥样硬化(AS)发病过程中脂质过氧化激活机制。方法:选择健康雄性家兔，每天定量加胆固醇饲料(0.25 g/kg)饲养。时间 12周，每隔2周从兔耳取静脉血，测量血清铜蓝蛋白-转铁蛋白系统的抗氧化活性及血清胆固醇(Ch)和雨二醛(MDA)含量。结果:饲养12周后，部分兔血清钢蓝蛋白-转铁蛋白系统抗氧化活性明显增强，Ch含量增加 3倍，MDA含量明显下降。其余兔血清铜蓝蛋白-转铁蛋白系统抗氧化活性无明显变化，Ch含量增加 10倍，MDA含量显着提高。结论:高胆固醇血症所致AS的发生过程可能是多种脂质过氧化激活机制综合作用的结果，增强血浆抗氧化活性可在一定程度上抑制Ch和脂质过氧化物(LPO)积累，延缓AS的发生。     

槲皮素对INH诱导的大鼠肝损伤及肝组织Bcl-2和Bax表达的影响

目的探讨槲皮素对异烟肼(INH)致大鼠肝损伤的保护作用。方法将动物随机分为正常对照组、INH组、槲皮素低剂量组、槲皮素高剂量组,灌胃染毒,每天1次,14d后测定大鼠血清中天冬氨酸氨基转移酶(AST)和丙氨酸氨基转移酶(ALT)的活性,肝匀浆中丙二醛(MDA)含量、谷胱甘肽过氧化物酶(GSH-Px)和超氧化物歧化酶(SOD)活性,用Westernblot法检测肝组织中Bcl-2和Bax蛋白的表达。结果与正常对照组比较,INH组大鼠血清AST和ALT的活性增强,肝组织的MDA含量升高,SOD和GSH-Px活性降低,Bcl-2蛋白表达减少,而Bax蛋白表达增加;高剂量槲皮素可减轻INH所致的损伤。结论槲皮素对INH所致的大鼠肝损伤具有保护作用,可能与其抗脂质过氧化作用及调节凋亡相关蛋白Bcl-2和Bax的表达有关。     

银杏叶提取物对大鼠肺纤维化初期肺结缔组织生长因子表达的影响

目的：　研究银杏叶提取物（GbE）对博莱霉素(BLM)性肺纤维化初期大鼠肺内结缔组织生长因子(CTGF)表达的影响。方法： 气管内滴注BLM, 用Western blotting法检测肺组织CTGF含量；用氯胺-T法测定肺组织羟脯氨酸含量；用比色法检测血浆丙二醛(MDA)含量。结果： 注BLM后14 d肺组织CTGF含量和出肺血MDA含量， BLM+NS组均分别高于NS组(P<0.05; P<0.01)。注BLM后30 d肺组织羟脯氨酸含量和出肺血MDA含量，BLM+NS组均分别高于NS组(Both P<0.01)。GbE处理可显著缓解上述变化。结论： GbE缓解BLM性肺纤维化初期肺内CTGF上调; GbE的抗氧化损伤作用可能是其缓解CTGF增多的机制之一。     

姜黄素抑制肝纤维化大鼠脂质过氧化物的生成及肝脏TGF-β1和PDGF的表达

目的： 观察姜黄素对肝纤维化过程中活性氧（ROS）、丙二醛（MDA）的生成及转化生长因子-β₁（TGF-β₁）、血小板源性生长因子（PDGF）表达的影响，探讨姜黄素预防肝纤维化的作用机制。方法: 采用四氯化碳腹腔注射方法，每周3次，共8周制作大鼠肝纤维化模型，同时每只大鼠按每100 g体重分别给予20 mg、10 mg、5 mg姜黄素灌胃处理，每周3次，共8周；设立正常组、肝纤维化组和阳性对照组。8周后处死大鼠，留取大鼠肝脏和血清。比色法检测血清ROS水平；硫代巴比妥酸（TBA）法检测肝组织匀浆中MDA含量；免疫组化方法检测各组大鼠肝组织中TGF-β₁、PDGF的表达水平。结果: 模型组大鼠血清ROS水平明显升高，姜黄素可显著降低ROS水平（P＜0.05）；姜黄素组大鼠肝组织中MDA含量明显低于模型组（P＜0.01）；模型组大鼠肝组织中TGF-β₁、PDGF大量表达，姜黄素可明显抑制上述因子的表达（P＜0.01）。结论: 姜黄素可抑制肝脏脂质过氧化物的形成以及TGF-β₁和PDGF的表达，从而发挥预防肝纤维化的作用。     

甘草酸对博莱霉素诱导的实验性肺纤维化的干预作用

目的:探讨甘草酸(GA)对博莱霉素(BLM)诱导的小鼠肺纤维化的干预作用及其可能机制。方法:将160只雄性C57BL/6J小鼠随机分为生理盐水(NS)组、BLM组、BLM+NS组和BLM+GA组。通过口咽气管吸入法吸入博莱霉素(2.5 mg/kg)建立实验性肺纤维化模型,BLM+GA组及BLM+NS组每天给予40 mg/kg甘草酸或等体积的生理盐水灌胃,于术后第3、7、14、21天取材。采用HE染色和Masson染色观察肺组织病理学变化及纤维化程度,采用流式细胞术检测循环单核细胞和肺泡巨噬细胞的亚群比例变化,采用RT-qPCR检测肺组织中转化生长因子β1(TGF-β1)mRNA的表达水平,采用碱水解法检测肺组织中羟脯氨酸(HYP)含量。结果:与NS组相比,BLM组和BLM+NS组肺组织的炎症浸润及胶原含量明显增多,实验性肺纤维化模型制备成功。与BLM+NS组相比:BLM+GA组肺组织的炎症细胞浸润及胶原纤维沉积较少;第3、7天的Ly6C~(hi)单核细胞亚群比例和第7、14天肺泡巨噬细胞M2表型比例显著降低(P0.01);肺组织TGF-β1 mRNA表达量和HYP含量显著降低(P0.01)。结论:GA可以减轻博莱霉素诱导的小鼠肺组织的炎症反应和胶原纤维沉积,可能与GA对单核巨噬细胞的表型偏移和调控以及肺组织TGF-β1的表达下调有关。     

Antioxidant vitamins and lipid peroxidation status in noncyclic versus cyclic ewes subjected to ram effect,before mating

This study assessed the levels of plasma vitamins A, E, and C and the lipid peroxidation status of cyclic and noncyclic ewes during pre-breeding week after a period of poor nutrition. The study was conducted on 100 crossbred fat-tailed adult ewes with body condition scores of 2.5 to 3.5, grazing on medium-to-low quality forages during summer. During 3 weeks of flushing, the ewes were fed alfalfa hay (40 %) and wheat straw (60 %) ad libitum plus 300 g of barley grain/head/day in addition to the available pasture. The ewes had been isolated for 2 months during summer and, thereafter, were kept in close proximity of the rams for 1 week before ram release. Whole blood samples were collected 7 days (day ?7) and a few hours before ram release (day 1). Plasma progesterone (P4, marker of ovulation) and antioxidant vitamins and hemolysate malondialdehyde (MDA, marker of lipid peroxidation) were measured. Plasma P4 was also measured in an additional sample taken 14 days after ram release. Twenty-eight percent of ewes were noncyclic in both pre-breeding samplings (P4?≤?1 ng/mL). On day ?7, the noncyclic ewes had higher levels of MDA (P?=?0.027), but the antioxidant vitamins were not different between cyclic and noncyclic ewes (P?>?0.05). On day 1, all antioxidant vitamins declined significantly in cyclic ewes, whereas they remained almost constant (P?>?0.05) in noncyclic animals. At this time, MDA concentration increased in the cyclic ewes (P?=?0.014). At day 14, after ram introduction, the proportion of noncyclic ewes reduced to 13 %. Oxidative stress may postpone the ewe’s cyclicity at the beginning of the breeding period but may be alleviated after a while. This may cause delayed conception and extended lambing periods. Ovarian cyclicity is capable of reducing the plasma levels of antioxidant vitamins and increases the level of lipid peroxidation.     

Determination of serum and organ malondialdehyde (MDA) concentration, a lipid peroxidation index, in Trypanosoma brucei-infected rats

Lipid peroxidation was assessed in the sera and various organs of rats experimentally infected with Trypanosoma brucei. Thirty-six adult albino rats divided into 2 groups of eighteen rats each were used in this study. In experiment one, a group of 18 rats were used and they were divided into three groups (A, B and C) of six rats each. Groups B and C rats were infected with 1.54 × 10⁵ trypanosomes per rat intraperitoneally, whereas group A served as uninfected control. The rats were bled on day 0 and subsequently at 7-day intervals for packed cell volume (PCV), sera peroxidation index and parasitaemia. Also, temperature and weight were taken on day 0 and subsequently at 7-day intervals. In experiment 2, 18 rats were also used. Six rats each were sacrificed on days 0, 14 and 28-postinfection. Five rats each were sacrificed on day 14 and day 28 post-infection (PI) from group B, and their organs were promptly collected and washed with normal saline and used for organ malondialdehyde (MDA) concentration. The infection led to an increase in lipid peroxidation index (MDA concentration) of sera samples. The serum MDA concentration of the infected rat group was significantly (p < 0.01) higher than in the uninfected group on days 21 and 28 PI. The increase was however reversed by diminazene aceturate (Berenil; Hoechst, Ireland) treatment at the dosage of 7 mg/kg body weight administered on day 14 PI. The organ lipid peroxidation index also increased significantly (p < 0.05) in the eye, lung and spleen. However, there was no significant (p > 0.05) increase of lipid peroxidation index in the kidney, heart, liver, testes and brain. Also, the mean weekly MDA concentration increased as the disease progressed, the mean weekly temperature and parasitaemia also increased, but the reverse was the case with the mean weekly body weight and PCV which declined as the disease progressed. The findings are indication that oxidative stress plays an important role in the pathology of trypanosomosis.     

The oxidant and antioxidant effects of 25-hydroxyvitamin D3 in liver, kidney and heart tissues of diabetic rats

Previous studies have implicated protective effects of vitamin D on insulin secretion and pancreas beta cell function. The goal of the present study is to determine if a combination therapy of 25-hydroxyvitamin D3 and insulin had any advantage over insulin therapy alone on lipid peroxidation and antioxidant activity in the streptozotocin (STZ)-induced diabetic rat. The lipid peroxidation product, thiobarbituric acid-reacting substances (TBARS), was measured to assess free radical activity in the heart, kidney and liver tissues. The enzymatic activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) were measured as indicators of antioxidation in these tissues. Sprague-Dawley rats were made diabetic with a single injection of STZ (75 mg/kg i.p.). Rats were separated into three groups, each containing 10 animals: Group 1, non-diabetic and no drug treatment was given; Group 2, diabetic rats were treated with 3 IU/day subcutaneous (s.c.) insulin; and Group 3, diabetic rats were treated with 3 IU/day (s.c.) insulin plus 1 mg/kg/day per oral (p.o.) 25-hydroxyvitamin D3 for a period of 4 weeks. At the end of the study, TBARS contents of the liver, kidney and heart tissues in Groups 2 and 3 were found to be significantly increased as compared to Group 1 (P<0.05) and kidney MDA levels in Group 3 were also significantly increased as compared to Group 2 (P<0.05). The SOD and CAT contents of the heart in Group 2 were significantly increased as compared to Groups 1 and 3 (P<0.05). GSH-Px activity was unaltered in all groups (P>0.05). We suggest that a combination of insulin with 25-hydroxyvitamin D3 treatment would not be more beneficial than the use of insulin alone in antioxidant defence of diabetic liver and kidney tissues.     

甘草酸二铵对肝纤维化大鼠肝脏脂质过氧化与间质性胶原酶活性的影响

目的：探讨甘草酸二铵影响纤维化肝脏脂质过氧化与间质性胶原酶活性的抗肝纤维化作用机制。 方法： 以四氯化碳(CCl4)皮下注射与高脂肪低蛋白饮食复合因素诱导大鼠肝纤维化模型，而后予以甘草酸二铵口服治疗，正常大鼠与模型对照组给予等量生理盐水。HE染色与胶原染色观察大鼠肝组织炎性坏死与胶原沉积病理改变，按试剂盒方法检测血清肝功能（ALT、AST、Alb与总胆红素等）变化，检测肝组织主要过氧化损伤指标：超氧化物歧化酶（SOD）活性, 丙二醛（MDA）含量，谷胱甘肽（GSH）含量与谷胱甘肽过氧化物酶（GSH-Px）活性，水解法测定肝组织羟脯氨酸含量，酶底物反应法分析肝组织间质性胶原酶活性变化，RT-PCR法分析肝组织Ⅰ型前胶原基因表达。 结果： 与正常大鼠相比，模型大鼠肝脏有明显胶原沉积与肝纤维化，伴有不同程度的肝细胞炎性损伤坏死；甘草酸二铵药物组明显减轻模型大鼠肝组织损伤坏死与胶原沉积等病理变化。模型大鼠肝功能指标,包括血清总胆红素含量、ALT与AST活性、白蛋白含量均明显减少（P<0.01）。药物组大鼠血清总胆红素含量、AST与ALT活性显著低于模型组（P<0.05），而白蛋白含量高于模型组（P<0.05）。此外，药物组大鼠肝组织羟脯氨酸含量(151.3±37.3 μg/g)明显少于模型组(170.9±15.3 μg/g，P<0.05)，Ⅰ型前胶原基因表达弱于模型组（P<0.05）；肝组织MDA含量(1.96±0.23 μmol/g)低于模型组(2.44±0.32 μmol/L, P<0.05)，SOD水平(19.60±0.97 NU/g)高于模型组(20.60±0.33 NU/g，P<0.05)，GSH含量(47.0±9.1 g/g)与GSH-Px活性(53.1±4.1 U/g)高于模型组(41.2±3.5 g/g；46.7±6.1 U/g，P<0.05)；肝组织间质性胶原酶活性(43.89±7.74 U)高于模型组(32.01±2.75 U，P<0.05)。 结论： 甘草酸二铵有明显抗肝纤维化大鼠肝脏脂质过氧化损伤与提高肝组织间质性胶原酶活性的作用，该作用是药物抗肝纤维化的重要机制。     

布地奈德对肺纤维化大鼠Smad4、PDGF-A及PAI-1表达的影响

目的:探讨布地奈德(BUD)对肺纤维化大鼠肺组织转化生长因子-β1(TGF-β1)、血小板衍化生长因子-A(PDGF-A)、抗生物皮肤生长因子同源物4母体(Smad4)、纤溶酶原激活物抑制物-1(PAI-1)表达的影响。方法:取健康雌性Wistar大鼠随机分成博莱霉素(BLM)组、生理盐水(NS)组和BUD组,每组15只。NS组气管内灌注NS,BUD组、BLM组气管内灌注BLM,继之0～6 d每天雾化1次,BLM组和NS组雾化吸入NS,BUD组雾化吸入BUD,分别于第7、14、28天处死3组大鼠各5只。用HE、Masson染色观察肺泡炎症和纤维化改变;免疫组化法测定肺组织中TGF-β1、PDGF-A、Smad4、PAI-1的表达。结果:第7、14天,BUD组肺泡炎程度较BLM组减轻(P<0.05);第7、14、28天,BUD组肺纤维化程度均较BLM组减轻(P<0.05)。第7、14、28天,BUD组肺组织中TGF-β1、PDGF-A、Smad4、PAI-1表达较BLM组明显降低(P<0.05)。结论:BUD雾化吸入可降低肺纤维化大鼠肺组织TGF-β1、PDGF-A、Smad4、PAI-1的表达,同时亦可减轻其肺泡炎及肺纤维化程度。     

Roles of macrophage stimulating protein and tyrosine kinase receptor RON in smoke-induced airway inflammation of rats

Objective: To investigate the roles of macrophage stimulating protein (MSP) and its tyrosine kinase receptor RON in smoke-induced airway inflammation of rats. Methods: Inhalation of combustion smoke was administered in rats to induce airway inflammation. Alveolar macrophages (AM) of healthy and smoking rats were isolated at different time points, cultured and then treated with different concentrations of MSP for 24 h. Results: When compared with healthy rats, MSP increased in the serum and bronchoalveolar lavage fluid (BALF) of smoking rats in a time dependent manner. In smoking rats, the RON expression in the lung and AM was higher than in healthy rats, and these increases were time dependent. MSP stimulated the production of malondialdehyde (MDA) and reduced superoxide dismutase (SOD) activity in rat AM cells in a dose dependent manner. MSP also stimulated the release of inflammatory factors TNF-α, IL-8, IL-1β and IL-10 in rat AM in a dose-dependent manner. Moreover, at the same MSP concentration, the contents of MDA, TNF-α, IL-8 and IL-1β in the AM of smoking rates were higher than in healthy rats, while the IL-10 content and SOD activity were lower than in healthy rats. Conclusion: MSP and its receptor RON are involved in the smoke-induced airway inflammation in rats via promoting AM to release inflammatory cytokines and inducing the increase of oxygen free radical.     

Brief communication: omega-3 essential fatty acid supplementation and erythrocyte oxidant/antioxidant status in rats

Fish oil contains large amounts of essential omega-3 fatty acids, such as eicosapentaenoic and docosahexaneoic acids, which are building structures of cell membranes. The goal of this study was to elucidate the effects of dietary omega-3 fatty acid supplementation on the oxidant/antioxidant status of erythrocytes in rats. The malondialdehyde (MDA) and nitric oxide (NO) levels and the catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) activities were assayed in erythrocytes of male Wistar albino rats after 30 days of dietary supplementation with fish oil (0.4 g/kg/day). Erythrocyte CAT activity in the treated group was increased in comparison with the control group. Erythrocyte MDA and NO levels were lower in the treated group than the controls. Erythrocyte GSH-Px and SOD activities did not differ significantly in the 2 groups. Negative correlations were found between SOD and CAT activities, and between SOD and GSH-Px activities in the treated group. In conclusion, omega-3 fatty acid supplementation helps to prevent lipid peroxidation and to safeguard erythrocytes from oxidative injury. Dietary supplementation with omega-3 fatty acids might possibly protect tissues from oxygen free radical injury in the various diseases in which the oxidant/antioxidant defense mechanisms are disturbed.