高钼对小尾寒羊肾脏蛋白含量和代谢酶活性及微核率的影响

采用透射电镜、比色法、姬姆萨染色和流式细胞术来探讨高钼对小尾寒羊肾脏蛋白含量、代谢酶活性、微核率及凋亡等的影响。试验采用雄性健康小尾寒羊12只,随机分成3组,分别饲喂含有5.61mg/kg Mo(对照组)、30mg/kg Mo(高钼Ⅰ组)和60mg/kg Mo(高MoⅡ组)的日粮120d(以Na2Mo4·2H2O形式)。随着钼剂量的增加,血清肌酐、血尿素氮、尿酸、肾脏细胞钼含量、微核率以及凋亡率都呈增加的趋势,且显著高于对照组(P0.01);高钼组小尾寒羊肾脏细胞铜含量、蛋白含量与代谢酶的活性与对照组相比极显著显著降低(P0.01);透射电镜的结果表明,高钼组肾脏细胞出现不同程度的空泡变性和线粒体肿胀,与肾脏生化指标的观察变化结果相符。结果表明,高钼引起的蛋白含量和代谢酶活性的降低能够影响肾脏细胞的正常功能。     

钼暴露对雌性小鼠肾脏脂质过氧化损伤及 Smac蛋白表达的影响

试验旨在观察钼暴露对雌性小鼠肾脏脂质过氧化损伤及Smac蛋白表达的影响。选用60只35日龄健康雌性昆明小鼠,随机分成3组(对照组、补钼Ⅰ组、补钼Ⅱ组),分别饮用含钼浓度为0、200、400 mg/L的去离子水,连续染毒90 d后取样检测肾脏组织SOD活性和MDA含量,免疫组化法检测肾脏组织Smac蛋白表达。与对照组比较,补钼Ⅰ组SOD活性显著降低(P＜0.05),补钼Ⅱ组SOD活性极显著降低(P＜0.01);补钼Ⅱ组MDA含量较对照组显著升高(P＜0.05)。补钼Ⅰ组、补钼Ⅱ组小鼠肾皮质Smac蛋白表达极显著高于对照组(P＜0.01)。结果表明,钼暴露对小鼠肾脏能产生脂质过氧化损伤,钼可以通过上调线粒体促凋亡蛋白Smac蛋白表达参与肾脏的损伤过程。     

钼对小鼠后代肾脏的损伤作用

为探讨长期钼暴露对子代小鼠肾功能的影响,采用2月龄清洁级小鼠60只(雌雄比2∶1),随机分为4组(每组10只雌鼠,5只雄鼠),雌雄分开饲养。饮水中加入不同剂量Na2MoO4.2H2O组成空白对照组、低钼组(100mg/L)、中钼组(200mg/L)和高钼组(400mg/L),4周后雌雄合笼饲养,待其产仔。妊娠期和哺乳期母鼠仍按原分组给予不同剂量的钼。仔鼠断奶后,同样按原分组给予不同剂量的钼。饲养8周后,再从每组后代中随机选取雌性小鼠10只和雄性小鼠5只合笼饲养,待其产仔。如此反复,使小鼠繁殖4代。选取第3代(F2)、第4代(F3)小鼠眼球摘除法采血并分离血清,测定血清肌酐和尿素氮。采集肾脏测定微核率和肾组织切片。结果表明,当饮水中Na2MoO4.2H2O达到200mg/L以上时,可显著增加后代小鼠肾细胞微核率(P<0.05)和血清肌酐浓度(P<0.05),降低血清尿素氮含量(P<0.05)。说明钼制剂可对小鼠后代肾脏产生损伤作用。     

锌、铜对实验性钼中毒绵羊肝脏、肾脏中钼含量的影响

小尾寒羊20只,随机分为5组,分别口服钼、铜和锌(mg/kg),Ⅰ组30mg/kg钼、Ⅱ组30mg/kg钼+15mg/kg铜、Ⅲ组30mg/kg钼+15mg/kg锌、Ⅳ组30mg/kg钼+15mg/kg铜+15mg/kg锌,Ⅴ组去离子水。试验90d期满,采取肝脏和肾脏,硫酸-高氯酸消化,原子吸收法测定钼、锌、铜含量,结果显示,Ⅰ组肝脏钼含量与第Ⅱ、Ⅲ、Ⅳ、Ⅴ组差异极显著(P<0.01),Ⅱ、Ⅲ组与Ⅳ、Ⅴ组差异极显著(P<0.01);Ⅳ组肝脏铜含量与Ⅰ、Ⅲ、Ⅴ组差异极显著(P<0.01),与Ⅱ组差异显著(P<0.05),Ⅱ组肝铜含量与Ⅰ、Ⅲ、Ⅴ组差异极显著(P<0.01);组间肝脏锌含量均差异极显著(P<0.01)。Ⅰ、Ⅲ组肾钼含量显著高于Ⅱ、Ⅳ、Ⅴ组(P<0.01);Ⅱ与Ⅳ、Ⅴ组差异极显著(P<0.01);肾铜含量Ⅲ组与Ⅰ组差异极显著(P<0.01);Ⅱ、Ⅲ、Ⅳ组与Ⅰ、Ⅴ组差异极显著(P<0.01);各组肾脏锌含量差异均极显著(P<0.01)。结果表明,30mg的钼可使肝脏钼含量显著增加(P<0.01),锌、铜含量降低。锌对肝脏钼有很好的颉抗作用,铜、锌有效地降低了钼在组织中的蓄积。     

高钼低铜对小鼠肾脏结构及其表达TNF-α蛋白的影响

为研究高钼低铜对小鼠肾脏结构及TNF-α蛋白表达的影响,选用80只雄性昆明种小鼠随机分为4组,在饮水中添加不同浓度的钼(600 mg/L)及铜(3mg/L),建立动物模型。在试验处理第90天时采样,研究高钼低铜对小鼠肾脏组织病理学及TNF-α表达的影响。结果显示,高钼组小鼠肾脏组织肾小体聚集,部分肾小球发生萎缩,间质中有大量炎性细胞浸润,有新月体出现。与对照组相比,高钼组肾脏TNF-α蛋白表达量上升15.60%(P0.01);与低铜组相比,高钼低铜组肾脏TNF-α蛋白表达量上升24.60%(P0.01);与高钼组相比,高钼低铜组肾脏TNF-α蛋白表达量上升7.14%(P0.05)。表明高剂量钼导致肾脏发生明显的病理组织学损伤,显著提高了小鼠肾脏TNF-α的表达,低铜加剧了钼的毒性作用。     

钼和铜对雏鸡肾脏抗氧化能力的影响

为研究饲料中不同剂量钼和铜对雏鸡肾的影响,试验用2日龄海兰褐壳蛋公雏鸡80只,随机平均分为Ⅰ空白对照组、Ⅱ(Cu 800 mg/kg,Mo 400 mg/kg)、Ⅲ(Cu 800 mg/kg,200 mg/kg)、Ⅳ(Cu 800mg/kg,100mg/kg)组。试验60d,每15d每组随机处死5只测定肾脏总超氧化物岐化酶(T-SOD)、过氧化物酶(POD)、黄嘌呤氧化酶(XOD)、谷胱甘肽过氧化物酶(GSH-Px)含量。结果表明,试验组T-SOD第15天最高,随后呈下降趋势(P0.05);POD、GSH-Px和XOD随时间延长呈上升趋势(P0.05),Ⅲ组GSHPx第30天时最高,最后回归正常,Ⅱ组XOD第30天最高,Ⅲ组POD随时间延长先下降后上升(P0.05),第45天时最高,Ⅳ组POD随时间延长先下降后上升再下降(P0.05)。说明日粮中以2∶1的比例关系添加Cu 800mg/kg、Mo 400mg/kg,随时间的延长可提高肾脏抗氧化能力。     

钼对F1代雌性小鼠雌激素的影响

本试验主要探讨金属元素钼(Mo)对F1代雌性小鼠雌激素的影响。试验选择健康昆明系ICR F1雌性小白鼠20只,体重30~40 g,适应5 d后,随机分为4组。基础日粮相同,试验组分别在其饮水中加入100、200和400 mg/L钼酸钠,对照组给予正常饮水。喂养7周后,测量其体重并记录。采用眼球摘除采血法采集血液制备血清,测定小鼠的肝脏、肾脏、脾脏,计算肝脏、肾脏、脾脏的脏器指数。采用发光免疫技术测定小鼠血清雌二醇水平。     

C57BL/6J小鼠亚慢性镉中毒模型的建立

为了建立小鼠亚慢性镉中毒模型,本研究将20只C57BL/6J雄性小鼠随机分为4个剂量组和溶剂对照组,每组隔天分别腹腔注射含0.25、0.5、1和2 mg/kg剂量的氯化镉溶液和等量去离子水(溶剂),共染毒4周,观察不同剂量的镉离子对雄性小鼠肝脏、肾脏、睾丸的损伤情况.结果各处理组小鼠体质量增长要比对照组慢,脏器系数与对照组相比也有显著差异,处理组小鼠肝脏、肾脏、睾丸中镉含量显著高于对照组.病理组织切片结果表明,各处理组中小鼠的肝脏、肾脏、睾丸组织均出现不同程度的损伤.氯化镉可以显著地抑制小鼠体质量增长,并对小鼠的脏器系数产生影响,腹腔注射后在肝脏、肾脏、睾丸组织中产生蓄积,并对其造成一定损伤.隔天腹腔注射2 mg/kg剂量的氯化镉,4周可建立较理想的小鼠镉中毒模型.     

亚急性铜、镉暴露对鲤肝脏Hsp60表达的影响

试验通过实时定量PCR和Western blot技术,检测重金属铜、镉单一及联合急性暴露后鲤肝脏中Hsp60基因和蛋白水平。鲤随机分为7组,两个Cu2+处理组(0.05 mg/l和0.1 mg/l),两个镉处理组(0.63 mg/l和1.26 mg/l),两个混合处理组(0.045 mg/l和0.09 mg/l)和对照组。结果表明铜、镉单一及联合急性暴露对鲤有毒性作用,经过96 h的暴露,除混合低浓度组之外,其余各组肝脏中Hsp60基因表达水平显著提高(P0.05)。受重金属暴露的影响,初期鲤肝脏中Hsp60蛋白水平下降,随着时间推移,蛋白水平逐渐上升,混合低浓度组显著高于对照组水平(P0.05)。     

不同剂量钼对绵羊肝脏细胞的损伤作用

选用18只2月龄小尾寒羊,体质量约为（20±1.34）kg,随机分为3组,分别在基础日粮（Mo 5.61mg/kg）中添加不同剂量的钼（mg/kg）构成加钼日粮（Ⅰ组Mo 0、Ⅱ组Mo 30、Ⅲ组Mo 60）,试验周期120d,定期采血,剖杀取样,以化学比色法、流式细胞术和透射电镜的方法观察钼对绵羊肝脏细胞损伤的影响。与Ⅰ组相比：Ⅱ、Ⅲ组肝脏超氧化物歧化酶（SOD）和黄嘌呤氧化酶（XOD）活性显著下降（P〈0.01）,丙二醛（MDA）和NO含量显著升高（P〈0.01）,血清NO含量和相应抗氧化酶活性变化与肝脏中的一致;Ⅱ、Ⅲ组肝脏细胞G0/G1期和凋亡细胞百分数显著升高（P〈0.01）,S期、G2＋M期和增殖指数（PI）显著降低（P〈0.01）。与Ⅲ组相比：Ⅱ组需要更长的作用时间引起机体抗氧化酶活性、NO含量和细胞周期发生相应变化。电镜观察,Ⅱ组肝细胞出现空泡变性及线粒体肿胀,Ⅲ组细胞线粒体数目减少,严重空泡化。结论：日粮钼含量30mg/kg及其以上可引起绵羊肝脏抗氧化功能降低和NO含量升高,导致细胞增殖分化受阻,细胞受损程度与机体钼暴露剂量和时间有关。     

Comparison of cupric and sulfate ion effects on chronic selenosis in rats

The ameliorating effects of Cu++ and SO4--ions on concurrent selenite toxicity were compared in two factorial experiments using 60 weanling rats each. In the first experiment, 0, 500 and 1,000 mg Cu (as CuCl2)/kg diet were fed in conjunction with 0, 5, 10 and 20 mg Se (as Na2SeO3)/kg diet. In the second experiment, the treatments were 0, 500 and 1,000 mg SO4 (as Na2SO4)/kg fed in conjunction with 0, 5, 10 and 20 mg Se/kg diet. A paired-feeding experiment using 10, 15 and 20 mg Se/kg diet was also conducted with 28 rats to compare the influence of inanition in control and selenite-fed rats. Cupric++ ion, but not SO4--ion, prevented mortality among selenite-intoxicated rats. There were significant Cu X Se interaction effects on feed intake, daily gain, packed cell volume (PCV), serum Cu and Fe, sperm counts, and weights of liver, kidney and testis. There were main effects of Cu and Se on serum Se and liver Cu. In Exp. 2 there were significant SO4 X Se interaction effects on feed intake, daily gain, serum Cu and testis weight. There were main effects of Se on PCV, sperm count, serum testosterone, liver Se, liver Cu and the absolute weights of liver and kidney. The only main effect of SO4 was that of increased liver Cu concentrations. Among the pair-fed rats, the selenite-fed rats, with one exception, died before their paired rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of ammonium tetrathiomolybdate intake on tissue copper and molybdenum in pregnant ewes and lambs

Pregnant ewes (d 32 of gestation) were allocated to three treatments and given intraruminal controlled-release devices designed to deliver 0, 20 or 60 mg diammonium tetrathiomolybdate (TTM) per day. Ewes given 20 or 60 mg TTM/d also received an oral drench of 120 or 360 mg TTM twice weekly commencing on d 86 of gestation. Liver and kidney samples were taken from lambs 48 h after birth and from ewes on d 18 postpartum. Trichloroacetic acid soluble Cu, ceruloplasmin and superoxide dismutase activities in the plasma of ewes were decreased (P less than .05) by TTM. Liver Cu concentrations were decreased (P less than .05), but kidney Cu concentrations increased (P less than .05) by 16-fold in ewes given the higher dose of TTM. Liver and kidney Mo concentrations were elevated (P less than .05) 9- and 30-fold, respectively, in ewes given TTM. Plasma glucose concentrations in ewes were decreased (P less than .05) by the highest level of TTM treatment. Lambs of ewes given TTM had a fivefold increase (P less than .05) in liver Mo concentration, but kidney Mo concentration was not affected (P greater than .05) and liver Cu concentration was reduced (P less than .05). In ewes, Mo apparently caused Cu to be mobilized from the liver and a Cu and Mo complex accumulated in the kidney. Some Mo crossed the placenta, but only limited Mo accumulated in the fetal livers. When given to pregnant ewes, TTM reduced liver Cu levels in the lambs but did not affect the concentration of Cu in colostrum.     

Using sodium molybdate to treat chronic copper toxicity in dairy cows: A practical approach

Abstract

CASE HISTORY: A Jersey herd of 350 cows and 70 heifers located in the Taranaki region of New Zealand ceased milking in June 2011. Ten cows died during the subsequent 14 days. For at least 9 months, the cows had received palm kernel expeller (PKE) and molasses supplements. Additional Cu supplementation was provided through the water system. Total Cu intake was calculated to be 400?mg/day/cow.

CLINICAL AND PATHOLOGICAL FINDINGS: Half of the cows died suddenly while others presented with anorexia, depression and ataxia, which progressed to recumbency and death after 1 to 3 days. Clinical signs were mild dehydration, cyanosis and firm faeces which were covered in dark blood. Mean concentrations of Cu in liver and kidney in three of the dead cows were 3,900 and 440?µmol/kg fresh weight (FW), respectively. Haemorrhages were observed throughout the alimentary tracts and in muscles, and there were ecchymotic haemorrhages on the epi- and endocardia. The livers were swollen and the gall bladder walls were inflamed.

DIAGNOSIS: High concentrations of Cu in the liver and kidney are characteristic findings of chronic Cu toxicity.

TREATMENT: The remaining herd was fed 200?mg Mo, as sodium molybdate, per cow per day and all Cu supplements were removed including those provided by the water supply. This reduced mean concentrations of Cu in liver from 3,100 to 1,320?µmol/kg FW within 26 days in the five live animals that were biopsied. There were no further deaths.

CLINICAL RELEVANCE: In dairy herds where excessive Cu intakes have resulted in high liver Cu concentrations and caused chronic Cu toxicity, the removal of all Cu supplements and provision of high intakes of Mo (200?mg/cow/day) can markedly reduce liver Cu stores within 4 weeks.     

钼暴露对小鼠繁殖性能及血清含铜酶的影响

将60只二月龄的清洁级ICR小鼠随机分成4组,每组雌性10只和雄性5只,雌雄分开饲养,饮水中加入不同剂量的钼（以Na2MoO4.2H2O形式）,分别是空白对照组、低钼组（100mg/L）、中钼组（200mg/L）、高钼组（400mg/L）。4周后雌雄合笼,产仔后从仔鼠中随机挑选雌性30只和雄性15只按原分组给予不同剂量的钼,8周后,再从每组中随机选取雌性10只和雄性5只合笼饲养,产仔至第4代,记录分娩率和每胎产仔数。第3代和第4代小鼠每组选取5只,眼球采血,分离血清,测定血清黄嘌呤氧化酶（XOD）、单胺氧化酶（MAO）、丙二醛（MDA）、一氧化氮（NO）、铜蓝蛋白（CP）和超氧化物歧化酶（SOD）。试验结果表明高剂量钼能够颉抗体内的铜,使部分含铜酶活性下降,降低了小鼠繁殖性能,具体如下：（1）F1和F2代高剂量组分娩率显著低于其他组（P〈0.05）;（2）与对照组相比,试验组小鼠XOD活性、除中钼组外的F2代MAO活性、F2代中钼组SOD活性、F3代中钼组CuZn-SOD活力值和试验组CP活性均显著降低（P〈0.05）。可见高剂量钼可降低小鼠的繁殖性能,其作用机制可能是钼降低部分含铜酶的活性,导致小鼠抗氧化能力降低。     

柴胡多糖通过抑制氧化应激和炎症反应减轻铅诱导小鼠肝肾损伤的研究

本研究旨在探讨柴胡多糖对铅诱导小鼠肝肾损伤的影响。选取150只SPF级雄性健康昆明小鼠,适应性饲养2周后,随机分成5组,分别为对照组,铅处理组,铅处理+柴胡多糖低、中、高剂量组（100、200和400 mg·kg^-1）。铅染毒模型建立：小鼠每天饮铅水（醋酸铅0.5%）,连续4周,建模结束后,试验组（铅处理+柴胡多糖组）每隔1 d灌胃柴胡多糖1次,连续2周,对小鼠血液及组织中铅含量及体质量进行测定,对抗氧化酶活性、脂质过氧化水平及炎症因子进行检测和分析,并从分子水平分析氧化损伤和炎症反应相关因子mRNA相对表达量。结果表明,与铅处理组相比,柴胡多糖可抑制铅中毒小鼠体重的下降和肝、肾脏器系数的升高,添加柴胡多糖使小鼠血液及组织中铅浓度略降低,但效果不显著（P>0.05）;与铅处理组相比,柴胡多糖可使染铅小鼠肝、肾组织的超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）及过氧化物酶（CAT）活性显著提高（P<0.05）,丙二醛（MDA）含量降低;柴胡多糖可显著降低铅诱导小鼠血清和肝组织中丙氨酸转移酶（ALT）和谷草转移酶（AST）活力的升高,使小鼠血清血尿素氮（BUN）、肌酐（Scr）水平降低,肝、肾组织肿瘤坏死因子（TNF-α）、白细胞介素-6（IL-6）、髓过氧化物酶（MPO）活性显著下降（P<0.05）;柴胡多糖能显著提高Nrf2信号通路的表达,使其HO-1、Cu/Zn-SOD、Mn-SOD、CAT mRNA水平上升,降低Keap1 mRNA水平,此外,柴胡多糖能明显降低铅诱导小鼠肝、肾炎症因子NF-κB、IL-1β及TNF-α mRNA水平上升（P<0.05）。综上表明,低、中、高剂量柴胡多糖可以减轻铅诱导小鼠引起的脂质过氧化和炎症反应,对小鼠肝和肾损伤均具有保护作用,其中柴胡多糖高剂量组对小鼠肝肾组织损伤保护作用最显著。     

Impact of molybdenum on the copper status of red deer (Cervus elaphus)

AIM: To determine the effect of increasing molybdenum (Mo) intakes on serum and liver copper (Cu) concentrations and growth rates of grazing red deer (Cervus elaphus). METHODS: Molybdenum- and Cu-amended fertilisers were applied to six 1.1-ha paddocks in a 3 x 2 design. Three levels of Mo were applied on two paddocks at each level in mid April (designated Day 1); levels were: none (control), 0.5 (medium) and 1.0 (high) kg Mo/ha as sodium molybdate. In late May (Day 39), two levels of Cu (none and 3.0 kg Cu/ha, as copper sulphate) were applied to each of the three levels of Mo-treated paddocks. Pasture Mo, Cu and sulphur (S) concentrations were measured at about fortnightly intervals. In late June (Day 74), ten 6-month-old red deer hinds were placed on the six experimental pastures, and serum and liver Cu concentrations were monitored at about monthly intervals for 102 days. The hinds were weighed on four occasions during the trial. RESULTS: Mean pasture Mo concentrations on Day 56 were 2, 4.6 and 11.3 mg/kg dry matter (DM) for the untreated control, medium and high Mo-treated pastures, respectively. Pasture Cu concentration was 95 mg/kg DM on Day 59, 53 mg/kg DM on Day 90, and 9 mg/kg DM by Day 153. Mean S concentration in pasture was 3.3 (range 3.03-3.45) g/kg DM. Copper application to pasture had no significant effect on serum and liver Cu concentrations in deer so data were pooled within Mo treatment. Mean initial (Day 74) serum Cu concentration was 9.2 micromol/L. In the deer grazing the control Mo pasture, this increased to 10.3 micromol/L on Day 112, before decreasing to 6.4 micromol/L on Day 176. In deer grazing the medium and high Mo-treated pastures, mean serum Cu concentrations were 3.8 and 3.9 micromol/L, respectively, on Day 112, and 2.5 and 3.3 micromol/L, respectively, on Day 176. Mean initial (Day 74) liver Cu concentration was 131 micromol/kg fresh tissue. In the deer grazing the control Mo pasture, this declined to 120 and 52 micromol/kg on Days 112 and Day 176, respectively. In deer grazing the medium and high Mo-treated pastures, liver Cu concentrations decreased to 55 and 52 micromol/kg fresh tissue, respectively, on Day 112, and 21 and 20 micromol/kg fresh tissue, respectively, on Day 176. Mean serum and liver Cu concentrations were not significantly different between deer grazing the medium and high Mo-treated pastures, and were lower (serum p=0.003, liver p<0.001) in those groups than in deer grazing the untreated control pastures. No clinical signs of Cu deficiency associated with lameness were observed. Deer grazing pastures that had Mo concentrations >10 mg/kg DM had lower (p=0.002) growth rates (100 vs 130 g/day) than those on pastures containing <2.4 mg Mo/kg DM. CONCLUSION: Increasing pasture Mo concentrations from 2 mg/kg DM to > or =4.6 mg/kg DM significantly reduced serum and liver Cu concentrations in grazing deer. Reduced growth rate was observed at pasture Mo concentrations >10 mg/kg DM.     

The metabolism of 75Se-selenomethionine in sheep given supplementary copper and molybdenum

Four groups of three ram lambs were fed, in group pens, the following diets from 4 to 19 wk of age: 1) control (6 mg Cu/kg and 1 mg Mo/kg); 2) control plus 10 mg Cu/kg; 3) control plus 10 mg Mo/kg and 4) control plus 10 mg/kg of both Cu and Mo. Copper and Mo were added to the diet as copper sulfate and sodium molybdate. The main ingredients of the diets were alfalfa hay (20%), oats (20%) and corn (59%). At 19 wk, the animals were allocated randomly to individual metabolism cages and received a single oral dose of 75Se-selenomethionine. Liver Cu concentrations at slaughter (22 wk) were 77, 259, 68 and 316 mg/kg fresh weight for treatments 1 through 4. There was clinical evidence of Cu poisoning in lambs on treatment 2. Sheep given Cu supplements without additional Mo had reduced (P less than .05) levels of 75Se activity in muscle compared with control animals. This decrease in muscle 75Se in Cu-supplemented lambs was associated with a nonsignificant increase in 75Se content of other tissues and a nonsignificant increase in fecal excretion of 75Se. Apparent absorption and net retention of 75Se was 80% and 74%, respectively. Long-term ingestion of moderate levels of Cu influenced the metabolism of Se fed as selenomethionine, possibly through effects of chronic Cu toxicity on liver function.     

麦麸阿魏酰低聚糖对敌草快致氧化应激大鼠血浆和组织抗氧化能力的影响

本试验以酿酒酵母和枯草芽孢杆菌作为混合菌种发酵小麦麸皮,通过Amberlite XAD-2柱分离纯化制备麦麸阿魏酰低聚糖(feruloyl oligosaccharides,FOs),探讨麦麸FOs对敌草快(diquat)诱导的大鼠氧化应激是否有缓解作用。试验选用体重相近的断奶雄性大鼠48只,随机分为未攻毒组、攻毒组、攻毒+100 mg/kg BW麦麸FOs组、攻毒+200 mg/kg BW麦麸FOs组、攻毒+300 mg/kg BW麦麸FOs组和攻毒+100 mg/kg BW维生素C组,每组8个重复,每个重复1只鼠,各组大鼠均饲喂相同的商业饲料。麦麸FOs和维生素C配制成水溶液,采用灌胃的方式给予,未攻毒组、攻毒组用生理盐水替代,灌胃体积0.2 mL,连续灌胃15 d。灌胃结束当天,未攻毒组大鼠注射0.3 mL生理盐水,其他5组按0.1 mmol/kg BW的剂量腹腔注射0.3 mL敌草快。敌草快攻毒12 h后取样,分析各组大鼠血浆以及肝脏、肾脏和回肠中总抗氧化能力(T-AOC),过氧化氢酶(CAT)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性以及谷胱甘肽(GSH)和8-羟基脱氧鸟苷(8-OHd G)的含量。结果显示:1)通过混菌发酵小麦麸皮制备麦麸FOs,利用Amberlite XAD-2柱进行分离纯化,获得的麦麸FOs浓度为0.059 mmol/g。2)腹腔注射敌草快显著降低大鼠血浆中SOD活性和GSH含量(P0.05),显著降低大鼠肝脏中T-AOC,CAT、GSH-Px活性及GSH含量(P0.05),显著降低大鼠肾脏中T-AOC及CAT、SOD活性(P0.05),显著降低大鼠回肠中T-AOC,CAT、GSH-Px活性及GSH含量(P0.05),并显著提高大鼠血浆和各组织中8-OHd G含量(P0.05)。3)在敌草快引起的氧化应激状态下,灌胃一定剂量的麦麸FOs可以显著提高大鼠血浆中SOD(400 mg/kg BW)、GSH-Px活性(100和200 mg/kg BW)以及GSH含量(100和200 mg/kg BW)(P0.05),显著提高大鼠肝脏中T-AOC(100、200和400 mg/kg BW),CAT(200和400 mg/kg BW)、SOD(100、200和400 mg/kg BW)和GSH-Px活性(100、200和400 mg/kg BW)以及GSH含量(100、200和400 mg/kg BW)(P0.05),显著提高大鼠肾脏中T-AOC(400 mg/kg BW),CAT(200 mg/kg BW)和GSH-Px活性(200和400 mg/kg BW)以及GSH含量(400 mg/kg BW)(P0.05),显著提高大鼠回肠中T-AOC(200 mg/kg BW),SOD(400 mg/kg BW)和GSH-Px活性(100、200和400 mg/kg BW)以及GSH含量(100、200和400 mg/kg BW)(P0.05),显著降低血浆和各组织中8-OHd G含量(血浆、肾脏、回肠:100、200和400 mg/kg BW;肝脏:100 mg/kg BW)(P0.05);且灌胃200、400 mg/kg BW麦麸FOs后,大鼠血浆和组织中部分抗氧化相关指标可恢复到正常生理状态水平。综上所述,本试验制备的麦麸FOs可以通过有效提高大鼠血浆和组织中抗氧酶活性和GSH含量,降低DNA氧化应激代谢产物8-OHd G的含量,有效缓解由敌草快诱导产生的氧化应激。