Chronic ethanol and nicotine interaction on rat tissue antioxidant defense system.

Ethanol consumption and cigarette smoking are common in societies worldwide and have been identified as injurious to human health. This study was undertaken to examine the interactive effects of chronic ethanol and nicotine consumption on the antioxidant defense system in different tissues of rat. Male Fisher-344 rats were divided into four groups of five animals each and treated for 6.5 weeks as follows: (1) Control rats were administered normal saline orally; (2) ethanol (20% [wt./vol.]) was given orally at a dose of 2 g/kg; (3) nicotine was administered subcutaneously at a dose of 0.1 mg/kg; and (4) a combination of ethanol plus nicotine was administered by the route and at the dose described above. The animals were killed 20 h after the last treatment, and liver, lung, kidney, and testes were isolated and analyzed. Chronic ingestion of ethanol resulted in a significant depletion of glutathione (GSH) content in liver, lung, and testes, whereas chronic administration of nicotine significantly depleted GSH content in liver and testes. The combination of ethanol plus nicotine resulted in a significant depletion of GSH content in liver, lung, and testes. Ethanol, nicotine, or a combination of ethanol plus nicotine significantly increased superoxide dismutase (SOD) activity in liver and decreased SOD activity in kidney. Ethanol, nicotine, or a combination of ethanol plus nicotine significantly decreased catalase (CAT) activity in liver and increased CAT activity in kidney and testes. Chronic ingestion of ethanol resulted in a significant decrease in glutathione peroxidase (GSH-Px) activity in liver and kidney, whereas a combination of ethanol plus nicotine increased GSH-Px activity in liver and decreased GSH-Px activity in kidney and testes. Ethanol, nicotine, or a combination of ethanol plus nicotine significantly increased lipid peroxidation, respectively, in liver. It is suggested that prolonged exposure to ethanol and nicotine produce similar, and in some cases additive, oxidative tissue injuries in rat.     

Dose- and Time-Dependent Effects of Ethanol on Plasma Antioxidant System in Rat

This study investigates the dose- as well as time-dependent effects of ethanol ingestion on antioxidant system and lipid peroxidation in plasma of the rat. The plasma ethanol concentrations were 154 ± 18, 231 ± 53, and 268 ± 49 mg/dl 1 h after oral ethanol doses of 2, 4, and 6 g/kg, respectively. Superoxide dismutase (SOD) (71%, 56%, and 41% of control) and glutathione reductase (GR) (71%, 66%, and 55% of control) activity in plasma were significantly decreased in a dose-dependent manner. Catalase (CAT)/SOD and glutathione peroxidase (GSH-Px)/SOD ratios were significantly increased whereas GR/GSH-Px ratio was significantly decreased with increasing dose of ethanol. In a time course study, plasma ethanol concentrations were 177± 9.7, 143± 11, 99± 17, and 26± 11 mg/dl at 1.5, 2, 4, and 6 h after an oral dose (4 g/kg) of ethanol in rat indicating time-dependent elimination of ethanol. Plasma SOD and GSH-Px activity significantly increased 4–6 h whereas GR activity significantly decreased 2–4 h after ethanol ingestion. The ratio of GR/GSH-Px and the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG) in plasma decreased at 1.5–6 h after ethanol ingestion. Plasma malondialdehyde (MDA) levels significantly elevated with respect to an increase in time after ethanol ingestion, indicating time-dependent augmentation of lipid peroxidation. The data indicate that ethanol ingestion perturbs the plasma antioxidant system in a dose- and time-dependent manner. The significant changes in the ratios of CAT/SOD, GSH-Px/SOD, GR/GSH-Px, and GSH/GSSG in plasma may be used as an index of alcohol-induced oxidative stress.     

溴氰菊酯对大鼠神经系统的氧化应激作用

目的　观察溴氰菊酯(DM)在大鼠大脑皮层和海马组织诱导的脂质过氧化作用。方法　DM3.12 5、12 .5 0 0mg/kg染毒大鼠,测定其大脑皮层和海马组织丙二醛(MDA)水平和总超氧化物歧化酶(T SOD ,包括Mn SOD和CuZn SOD)、过氧化氢酶(CAT)、谷胱甘肽S 转移酶(GST)、谷胱甘肽过氧化物酶(GSH Px)和谷胱甘肽还原酶(GR)活力。脑组织细胞质碎片γ谷氨酰半胱氨酸合成酶(γGCS)活力和GSH含量用OPA柱前衍生反相高效液相色谱荧光法检测。结果　DM染毒5d ,(1) 12 .5 0 0mg/kgDM组大鼠大脑皮层MDA含量高于3.12 5mg/kgDM组,海马MDA含量高于对照组和3.12 5mg/kgDM组。(2 )两组DM染毒大鼠大脑皮层T SOD和CuZn SOD活力均低于对照组,差异均有统计学意义(P <0 .0 1或P <0 .0 5 )。(3) 12 .5 0 0mg/kgDM组大鼠大脑皮层GSH含量高于对照组,海马GSH含量低于对照组和3.12 5mg/kgDM组;3.12 5mg/kgDM组大鼠大脑皮层GR活力[(11.80±5 .15 )U/mgpro]低于对照组和12 .5 0 0mg/kgDM组[(18.98±3.6 8)、(17.35±2 .4 7)U/mgpro],3.12 5、12 .5 0 0mg/kgDM组大鼠海马GR活力[(2 1.4 6±8.89)、(2 1.6 3±4 .92 )U/mgpro]均低于对照组[(31.2 2±6 .97)U/mgpro];12 .5 0 0mg/kgDM组海马γGCS活力[(1.75±0 .6 0 )nmol·mgpro-1·min-1]低于对照组和     

有机锗-132对乙醇中毒所致大鼠肝脏损伤的保护作用

目的:探讨有机锗-132对乙醇依赖所致大鼠肝损伤的拮抗作用。方法:用市售北京红星牌二锅头(含52%酒精),按5.0g/kg体重剂量连续3个月灌胃形成大鼠酒精依赖,同时给予有机锗-132,观察大鼠肝脏损伤情况,并检测血谷丙转氨酶(GPT)活性、肝组织中脂质过氧化物终末产物丙二醛(MDA)的含量变化及超氧化物歧化酶(SOD)、黄嘌呤氧化酶(XOD)和过氧化氢酶(CAT)的活性。结果:给大鼠喂饲乙醇三个月,其肝组织中的丙二醛含量与对照组比较明显升高(P<0.01),抗氧化酶SOD和CAT活性明显降低(P<0.05),XOD活性明显升高(P<0.01);酒中加锗-132能明显降低肝组织中的丙二醛含量,SOD、CAT及XOD活性亦有所恢复。结论:有机锗-132对乙醇中毒所致大鼠肝脏损伤有一定的保护作用。     

银杏叶提取物对酒精所致大鼠睾丸氧化损伤的保护作用的研究

目的研究银杏叶提取物(EGB)对酒精所致大鼠睾丸氧化损伤的预防保护作用。方法雄性SD大鼠30%酒精灌胃(2.37g/kgbw)前,EGB采用分组(低剂量组48μg/gbw和高剂量组96μg/gbw)预防性给药的方法。于实验90d检测大鼠睾丸组织中超氧化物歧化酶(SOD)、谷胱甘肽转移酶(GST)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、和谷胱甘肽(GSH)、活性氧(ROS)以及丙二醛(MDA)的含量。通过亚细胞分离方法提取大鼠睾丸微粒体,测定微粒体血红素氧化酶-1(HO-1)活性。采用RT-PCR检测睾丸组织中血红素氧化酶-1(HO-1)mRNA表达水平。结果慢性酒精摄入90d后,EGB组睾丸匀浆ROS、MDA较酒精组有明显降低(P<0.05);相反,GST、G-Px、CAT、SOD、HO-1活性以及GSH均有显著性升高(P<0.05);EGB诱导HO-1高表达。结论长期慢性酒精摄入引起大鼠睾丸氧化损伤。EGB可作为一种预防性的抗氧化剂减轻这种氧化损伤;其机制可能与诱导HO-1高表达,清除自由基,抑制脂质过氧化反应有关。     

Antioxidative effects of curcumin, β-myrcene and 1,8-cineole against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced oxidative stress in rats liver

The aim of this study was to investigate the effectiveness of curcumin, β-myrcene (myrcene) and 1,8-cineole (cineole) on antioxidant defense system in rats given a persistent environmental pollutant (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD). Rats (n = 112) were divided randomly into 8 equal groups. One group was kept as control and given corn oil as carrier. TCDD was orally administered at the dose of 2 μg/kg/week. Curcumin, myrcene and cineole were orally administered at the doses of 100 mg/kg/day, 200 mg/kg/day and 100 mg/kg/ day, respectively, by gavages dissolved in corn oil with and without TCDD. The liver samples were taken from half of all rats on day 30 and from the remaining half on day 60 for the determination of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), catalase (CAT), glutathione peroxidase (GSH-Px) and CuZn-SOD levels by spectrophotometric method. The results indicated that although TCDD significantly (p ≤ 0.01) increased formation of TBARS, it caused a significant decline in the levels of GSH, CAT, GSH-Px and CuZn-SOD in rats. In contrast, curcumin, myrcene and cineole significantly increased GSH, CAT, GSH-Px and CuZn-SOD levels but decreased formation of TBARS. Additionally, the antioxidative effects of curcumin, myrcene and cineole were increased at day 60 compared to day 30. In the TCDD groups given curcumin, myrcene and cineole, oxidative stress decreased by time. In conclusion, curcumin, myrcene and cineole showed antioxidant activity and eliminated TCDD-induced oxidative stress in rats in a time-dependent manner.     

不同剂量乙醇对大鼠血清抗氧化系统的动态影响及银杏黄酮的保护效应

目的研究不同剂量乙醇对大鼠血清抗氧化系统的影响及银杏黄酮的保护作用。方法雄性SD大鼠按体重随机分为正常对照组、低、中、高乙醇组(分别为0.8、1.6、2.4g/kg)和低、高干预组(48或96mg/kg银杏黄酮+2.4g/kg乙醇)和黄酮对照组(银杏黄酮96mg/kg)。试验D30、D60、D90取尾血测定血清还原型谷胱甘肽(GSH)、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)、丙二醛(MDA)活性或水平。结果大鼠摄入低剂量乙醇后,血清SOD、CAT和GSH-Px活性逐渐升高;摄入中剂量乙醇后,SOD与CAT在30d时升高,随后降至正常水平,而GSH水平在60、90d时明显下降,MDA水平持续升高;摄入高剂量乙醇后,实验期间抗氧化酶及GSH水平持续下降,MDA不断升高。银杏黄酮干预,尤其是在高剂量干预后,抭氧化酶失活与GSH消耗程度明显下降,MDA升高幅度也相应降低。结论低剂量乙醇摄入激活了机体的抗氧化系统,高剂量则导致严重的氧化应激;银杏黄酮对高剂量乙醇所致的氧化-抗氧化失衡有明显的调节和保护作用     

Protective Effects of Melatonin Against Formaldehyde-Induced Oxidative Damage and Apoptosis in Rat Testes: An Immunohistochemical and Biochemical Study

This study investigated the protective effects of melatonin against formaldehyde-induced oxidative damage and apoptosis in rat testes. A total of 21 male Wistar rats were divided into three groups. Group I was used as a control, Group II was injected every other day with formaldehyde for 1 month, whereas Group III was injected every other day with formaldehyde and melatonin for 1 month. At the end of the experimental period animals were sacrificed and the testes removed and dissected from the surrounding tissues for immunohistochemical evaluation. In addition, the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) were determined. The levels of SOD and GSH-Px decreased significantly, whereas the level of MDA significantly increased in animals treated with formaldehyde compared with the controls. Apoptosis of spermatogenetic and Leydig cells of testicular tissues was observed. In contrast, rats with melatonin SOD and GSH-Px enzyme activity increased whereas MDA levels decreased with formaldehyde exposure along with apoptosis. In view of the present findings, it is suggested that melatonin treatment may prevent formaldehyde-induced oxidative damage and apoptosis in rat testes.     

Protective effects of melatonin against formaldehyde-induced oxidative damage and apoptosis in rat testes: an immunohistochemical and biochemical study

This study investigated the protective effects of melatonin against formaldehyde-induced oxidative damage and apoptosis in rat testes. A total of 21 male Wistar rats were divided into three groups. Group I was used as a control, Group II was injected every other day with formaldehyde for 1 month, whereas Group III was injected every other day with formaldehyde and melatonin for 1 month. At the end of the experimental period animals were sacrificed and the testes removed and dissected from the surrounding tissues for immunohistochemical evaluation. In addition, the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) were determined. The levels of SOD and GSH-Px decreased significantly, whereas the level of MDA significantly increased in animals treated with formaldehyde compared with the controls. Apoptosis of spermatogenetic and Leydig cells of testicular tissues was observed. In contrast, rats with melatonin SOD and GSH-Px enzyme activity increased whereas MDA levels decreased with formaldehyde exposure along with apoptosis. In view of the present findings, it is suggested that melatonin treatment may prevent formaldehyde-induced oxidative damage and apoptosis in rat testes.     

急性百草枯中毒大鼠氧化应激水平及二巯丙磺钠的作用

目的 观察急性百草枯(PQ)中毒大鼠体内氧化应激水平及二巯丙磺钠(Na-DMPS)的作用.方法 80只雄性SD大鼠随机分为正常对照组:8只;Na-DMPS对照组:8只;PQ染毒组:32只(腹腔注射质量分数为1%的PQ溶液20 mg/kg);Na-DMPS保护组:32只.正常对照组及Na-DMPS对照组于1 d处死,PQ组及NA-DMPS保护组于染毒后6h及1、3、7d处死,留取血清、肺泡灌洗液(BALF)及肺组织,检测血清、BALF及肺组织匀浆中丙二醛(MDA)含量、过氧化氢酶(CAT)活力,血清、BALF中谷胱甘肽(GSH)含量,反转录-聚合酶链反应(RT-PCR)检测肺组织Nrf2基因表达水平.结果 与正常对照组相比,PQ中毒组和Na-DMPS保护组血清、BALF、肺组织匀浆中MDA含量均升高,CAT活力和GSH含量均降低,差异有统计学意义(P<0.05或P<0.01);与相应时点PQ染毒组比较,Na-DMPS保护组6 h、1 d时血清、BALF及肺组织匀浆中MDA含量均明显降低,6 h及1、3 d时血清,1、3 d时BALF和肺组织匀浆中CAT活力明显增高,差异有统计学意义(P<0.05或P<0.01).与同时间点PQ染毒组比较,Na-DMPS保护组6 h、3 d时血清中GSH[(730.07±16.23)、(793.66±7.40)mg/L]和1、3 d时BALF中GSH[(609.75±6.74)、(631.83±12.03)mg/L]明显升高,差异均有统计学意义(P<0.05或P<0.01).1、3、7d时PQ染毒组Nrf2mRNA表达分别为(0.710±0.061)、(1.023±0.158)、(0.969±0.046),Na-DMPS保护组Nrf2mRNA表达分别为(1.005±0.060)、(1.464±0.166)、(1.066±0.191),明显高于对照组,差异有统计学意义(P<0.05或P<0.01);与PQ染毒组比较,1、3 d时Na-DMPS保护组Nrf2mRNA表达明显升高,差异有统计学意义(P<0.01).结论 Na-DMPS可降低PQ中毒大鼠体内MDA含量,增加的CAT活力,增加GSH含量及NRF2 mRNA的表达,促进体内氧化-抗氧化系统的平衡,具有保护作用.     

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     

Gastroprotective and Antioxidative Effects of the Traditional Thai Polyherbal Formula Phy-Blica-D against Ethanol-Induced Gastric Ulcers in Rats

Phy-Blica-D is a traditional Thai polyherbal formula that has reduced oxidative stress in non-communicable diseases. However, evidence supporting the gastroprotective effects of Phy-Blica-D has not been previously reported. Therefore, this study aimed to evaluate the gastroprotective effects of Phy-Blica-D against gastric ulcers in rats and investigate the potential underlying mechanism. To estimate the possible mechanisms of action, we examined the levels of oxidative stress markers, such as reactive oxygen species (ROS) and malondialdehyde (MDA), as well as antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH). According to our results, rats treated with only 80% ethanol (vehicle group) exhibited significant increases in their ulcer area and ulcer index (UI). Moreover, the levels of ROS and MDA markedly increased in the vehicle group compared with the normal control group. Daily oral administration of Phy-Blica-D (500 and 1000 mg/kg) for 7 days not only significantly decreased the ulcer area and UI, but also remarkably decreased the ROS and MDA levels in gastric tissue. Gastric ulcers induced by ethanol had significantly decreased antioxidant enzyme activities (CAT and SOD) and non-enzymatic antioxidant (GSH), whereas pretreatment with Phy-Blica-D significantly improved the activities of CAT, SOD, and GSH. Moreover, after exposure to ethanol, the rats exhibited a significantly increased level of inducible nitric oxide synthase (iNOS), which was reduced after treatment with Phy-Blica-D. These findings suggest that Phy-Blica-D potentially exerts its gastroprotective effects by suppressing oxidative stress and stimulating antioxidant enzymes, which is one of the causes of destruction of cell membranes, and it is involved in the pathogenesis of acute gastric ulcers induced by ethanol.     

Differential expression of EC-SOD, Mn-SOD and CuZn-SOD in rat lung exposed to crystalline silica

Superoxide dismutases (SODs) are antioxidant enzymes that catalyze the dismutation of superoxide into hydrogen peroxide. There are 3 kinds of isozymes: extracellular superoxide dismutase (EC-SOD), manganese-containing superoxide dismutase (Mn-SOD) and copper- and zinc-containing superoxide dismutase (CuZn-SOD). To examine the expression of SOD isozymes in lungs injured by crystalline silica, we intratracheally instilled male Wistar rats with 2 mg (8 mg/kg) of crystalline silica and investigated the mRNA, protein level and distribution of SOD isozymes in the rat lungs using RT-PCR, western blot analysis and immunostaining, respectively at from 3 d to 180 d of recovery following the exposure. EC-SOD mRNA levels significantly increased from 3 d to 90 d and the EC-SOD protein level was significantly higher after 90 and 180 d recovery in the crystalline silica exposed groups than in the control groups. Mn-SOD increased in silica treated rat lungs at both mRNA and protein levels, peaking at 30 d post-exposure. CuZn-SOD mRNA levels were decreased at 3, 7 and 30 d, and CuZn-SOD protein levels were also significantly lower than the control group at 90 and 180 d recovery. There was prominent EC-SOD immunostaining mainly in the plasma and alveolar macrophages and strong Mn-SOD staining in alveolar macrophages and interstitial cells of the proximal and distal portions of the alveolar duct following crystalline silica exposure. There was less CuZn-SOD staining in epithelial cells at terminal bronchioles in the crystalline silica-exposed group. These findings suggest that these SOD isozymes may be related to lung injury induced by crystalline silica.     

钒对大鼠肝线粒体微粒体抗氧化酶活力的影响

目的研究钒对大鼠肝脏抗氧化酶活力的影响。方法将70只Wistar大鼠随机分为7组,每组10只,6个实验组,1个阴性对照组。试验组每天分别饮用剂量为1.25、2.5、5、10、20和40mg/kg的偏钒酸铵（ammoniummetavan-adate）;对照组饮用三重蒸馏水,持续饮用20d,测定肝微粒体谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）、肝线粒体超氧化物歧化酶（SOD）活力和丙二醛（MDA）含量。结果GSH-Px、CAT、SOD活力随着偏钒酸铵剂量的增大而降低,MDA含量随着偏钒酸铵剂量的增大而升高。与对照组相比,5、10、20和40mg/kg组的GSH-Px和CAT活力显著降低,差异有统计学意义（P〈0.01）,2.5mg/kg组的GSH-Px活力显著降低,差异有统计学意义（P〈0.05）;10、20和40mg/kg组SOD活力显著降低,差异有统计学意义（P〈0.05）,MDA含量显著升高,差异有统计学意义（P〈0.05）;其他组差异无统计学意义（P〉0.05）。结论偏钒酸铵在5－40mg/kg剂量范围内能显著降低大鼠肝脏线粒体和微粒体抗氧化酶活力。     

槲皮素对大鼠原代肝细胞酒精性氧化损伤的防护作用

目的:观察槲皮素(quercetin)对大鼠原代肝细胞酒精性氧化损伤的防护作用。方法:经二步胶原酶技术分离培养大鼠原代肝细胞,用100mmol/L无水乙醇染毒细胞8h,作为酒精损伤模型。乙醇染毒前经不同剂量槲皮素(25～200μmol/L)预作用不同时间(0～8h),观察槲皮素干预对细胞培养上清液中乳酸脱氢酶(LDH)、谷草转氨酶(AST)活性,丙二醛(MDA)、谷胱甘肽(GSH)水平和超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性的影响。结果:大鼠原代肝细胞经100mmol/L酒精暴露8h后,LDH、AST活性,MDA、GSH含量和SOD、CAT活性与对照组相比,均有非常显著性差异;酒精暴露前1～4h经50～75μmol/L槲皮素干预效果最明显,LDH、AST、MDA和GSH、SOD、CAT水平分别较酒精组非常显著性降低和升高。结论:槲皮素可能通过减少GSH耗竭,提高抗氧化酶活性,抑制脂质过氧化来保护大鼠原代肝细胞抗酒精性氧化损伤,保护作用呈剂量与时间效应关系。     

The effects of chronic ethanol consumption and ethanol withdrawal on serum cholinesterase activity in rats

AIMS: The effect of chronic ethanol consumption and ethanol withdrawal on serum cholinesterase (ChE) activity was investigated in female Wistar rats. METHODS: Ethanol was administered by a modified liquid diet with 4.8% (v/v) ethanol for 3 days followed by 25 days on a liquid diet in which the ethanol concentration was increased to 7.2%. Control rats were pair-fed with an isocaloric liquid diet not containing ethanol. The blood ethanol concentration and serum ChE activity were measured at the end of the 4.8% ethanol consumption period; after 7, 14 and 35 days of ethanol (7.2%) consumption, and at 24 and 72 h after ethanol withdrawal following ethanol consumption of 35 days. RESULTS: Daily ethanol consumption of the rats ranged from 11.5 to 14.9 g/kg. Serum ChE activity was found significantly increased from the 3rd day of ethanol (4.8%) consumption. Serum ChE activities of the rats receiving 7.2% ethanol also increased significantly compared with rats ingesting 4.8% ethanol. Blood ethanol levels were measured as 121 and 0.88 mg/dl on the 35th day of ethanol (7.2%) consumption (just before ethanol withdrawal) and after 24 h of ethanol withdrawal, respectively. Increased serum ChE activity (1968 U/l) was still observed (1942 U/l) after 24 h of ethanol withdrawal. ChE activity returned to control levels (501 U/l) after 72 h of ethanol withdrawal. Audiogenic seizures indicating development of physical dependence on ethanol were also observed after 8 h of ethanol withdrawal in another individual group of ethanol-fed rats. CONCLUSIONS: Our results show that serum ChE activity is increased by chronic ethanol consumption in rats and that this increase is affected by ethanol concentration and duration of ethanol ingestion.     

Intestinal Redox Status of Major Intracellular Thiols in a Rat Model of Chronic Alcohol Consumption

Background: Alcohol consumption is associated with oxidative stress in multiple tissues in vivo, yet the effect of chronic alcohol intake on intestinal redox state has received little attention. In this study, we investigated the redox status of 2 major intracellular redox regulating couples: glutathione (GSH)/glutathione disulfide (GSSG) and cysteine (Cys)/cystine (CySS) in a rat model of chronic alcohol ingestion. Methods: Sprague‐Dawley rats were fed the liquid Lieber‐DeCarli diet consisting of 36% ethanol of total calories for 6 weeks. Control rats were pair‐fed with an isocaloric, ethanol‐free liquid diet. Defined mucosal samples from the jejunum, ileum, and colon were obtained and analyzed by high‐performance liquid chromatography (HPLC) for GSH and Cys pool redox status. Mucosal free malondialdehyde (MDA) was measured as an indicator of lipid peroxidation. Results: In the ethanol‐fed rats, Cys and mixed disulfide (GSH‐Cys) were significantly decreased in all 3 segments of intestinal mucosa. Free MDA was increased in jejunal but not in ileal or colonic mucosa. Chronic ethanol ingestion significantly increased mucosal GSH concentration in association with a more reducing GSH/GSSG redox potential in the jejunum, but these indices were unchanged in the ileum. In the colon, chronic ethanol ingestion increased oxidant stress as suggested by decreased GSH and oxidized GSH/GSSG redox potential. Conclusions: Chronic alcohol intake differentially alters the mucosal redox status in proximal to distal intestinal segments in rats. Such changes may reflect different adaptability of these intestinal segments to the oxidative stress challenge induced by chronic ethanol ingestion.     

Nigerian Bonny Light Crude Oil Disrupts Antioxidant Systems in Testes and Sperm of Rats

Nigerian Bonny light crude oil (BLCO) is commonly used by the local population in folklore medicine for the management of various forms of gastrointestinal problems and male reproductive capacity. The study investigated the effects of BLCO on the antioxidant systems of the testes and epidydimal sperm in rats by oral exposure to 0, 200, 400 and 800 mg/kg BLCO for 7 days. In testes and sperm, BLCO treatment at all doses significantly (p < 0.05) decreased superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST) activities, whereas it markedly increased glucose 6-phosphate dehydrogenase (G6PD) and gamma glutamyl transferase (GGT) activities as well as increased glutathione (GSH), hydrogen peroxide, and malondialdehyde (MDA) levels in all treatment groups. Although epididymal sperm number (ESN), daily spermatozoa production (DSP), and sperm motility were significantly decreased, total sperm abnormalities were significantly increased without affecting sperm viability at all dose levels compared with controls. The adverse effect of BLCO on TSN was noted at the 800 mg/kg dose only. Histopathology results showed treatment-related lesions of the testes characterized by severe congestion of interstitial vessels, decreased germinal epithelium, and increased number of vacuolization. These results suggest that exposure to BLCO, such as its use in ailment management, may promote infertility by altering the function of the testes and sperm, particularly by way of induction of oxidative stress.     

Acute effect of single-dose cadmium treatment on lipid peroxidation and antioxidant enzymes in ovariectomized rats

We investigated the acute effect of single-dose cadmium (Cd) treatment on lipid peroxidation and antioxidant enzymes in liver and kidney of rats following an ovariectomy operation. Twenty-eight female Wistar albino rats were used and were divided into four groups: I, control (n=7); II, cadmium (Cd, n=7); III, ovariectomized (Ovx, n=7); and IV, ovariectomized+cadmium (Ovx-Cd, n=7). Fourteen of the rats were ovariectomized. Twelve weeks later, cadmium chloride (CdCl(2), 5 mg/kg) was administered i.p. as a single dose to the Cd and Ovx-Cd groups. Twenty-four hours after the injection, all rats were sacrificed and had their liver and kidney tissues removed for the measurement of superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) levels. SOD activity showed a significant decrease (P<0.001) in both organs of Ovx and Cd rats in comparison to controls. CAT activity was significantly decreased (P<0.01) in the liver of Ovx and Cd groups but not in the kidneys of both groups compared to control values. MDA concentrations were higher (P<0.05) in both organs of Ovx and Cd rats than those values observed in the control group. Similar patterns of changes were observed in the Ovx-Cd rats, but the increase in the MDA levels and the decrease in the antioxidant enzymes for the Ovx-Cd group were higher than those of the Ovx and Cd groups. Based on the data, it can be stated that cadmium increases the effect of ovariectomy on lipid peroxidation, impairs the antioxidant defense system, and induces oxidative stress.     

乙醇对大鼠神经行为及相关酶的影响

[目的 ]探讨乙醇对大鼠神经行为效应及脑组织中相关酶的影响。 [方法 ]体重 160g左右的雄性SD大鼠2 5只 ,随机分为三组 ,每组为 9、8、8只 ,分别以 0 % (对照组 )、2 5 64 % (低剂量组 )、5 1 2 8% (高剂量组 )乙醇溶液 (浓度以V/V表示 )按 1 0ml/10 0g体重一次性灌胃染毒。 3 0min后 ,进行自发活动、转棒实验和方位水迷宫测试。在染毒 1h后 ,断头处死 ,取血测血中乙醇浓度 (BAC) ,取脑组织测丙二醛 (MDA)、超氧化物歧化酶 (SOD)、巯基化合物 ( SH )和胆碱酯酶活性。 [结果 ]高剂量组自发活动中的行走次数显著高于低剂量组和对照组 ;转棒测试 ,高、低剂量组在棒上停留时间均显著低于对照组 (P <0 0 1) ;水迷宫试验学习次数 ,在染毒前对照组明显高于染毒组 ,而在染毒后各组间差异无统计学意义 ;且上述改变与BAC相关显著。高剂量组SOD活性显著低于低剂量组和对照组。丙二醛、巯基水平及胆碱酯酶活性各组间无明显差异。 [结论 ]乙醇可降低大鼠对新环境的适应性、肌肉运动协调能力下降和学习记忆能力的减退 ,并和脑组织中SOD活性呈一定相关