3-甲基-4-硝基酚对大鼠肾脏氧化损伤作用的研究

为了探讨3-甲基-4-硝基酚(PNMC)对大鼠肾脏的氧化损伤作用,选择SPF级雄性SD大鼠,随机分为4组(每组10只),设立3个染毒组和1个对照组。染毒组采用皮下注射的途径分别给予每天剂量为1 mg/kg体重、10mg/kg体重和100 mg/kg体重的PNMC,连续5 d。对照组采用同样的途径给予溶剂(PBS+0.05%tween80),最后一次染毒后第24小时剖检取材。称量体重和器官重量,观察肾脏组织病理学变化,检测血清中肌酐和尿素氮的含量,以及超氧化物歧化酶、谷胱甘肽过氧化物酶、总抗氧化能力及丙二醛等抗氧化指标的含量。结果显示,染毒组大鼠体重和日增重出现不同程度的下降;各剂量组大鼠肾脏均有不同程度的病理损伤;100 mg/kg体重组大鼠肌酐浓度显著升高,所有染毒组大鼠超氧化物歧化酶的含量均显著下降,10 mg/mg体重染毒组大鼠总抗氧化能力也显著低于对照组。综上所述,PNMC染毒后血清中超氧化物歧化酶的活性降低,同时伴有总抗氧化能力下降,提示大鼠体内抗氧化系统遭到破坏,导致过多的过氧化物在体内蓄积,从而对大鼠肾脏造成氧化损伤。     

铅、镉染毒对SD大鼠的氧化损伤及乙酰半胱氨酸的保护作用

为了研究铅、镉单独或联合慢性暴露引起SD大鼠的氧化损伤和肾脏组织结构变化,以及抗氧化剂乙酰半胱氨酸(NAC)对其的保护作用,用不同剂量的铅、镉连续灌服大鼠4周后,测定肾脏和血浆SOD、GSH-Px活性及脂质过氧化主要终产物MDA含量,并用光学显微镜观察肾脏组织学变化。结果显示,与对照组比较,铅、镉单独染毒肾脏和血浆SOD、GSH-Px活性及MDA含量均显著升高(P<0.05);铅、镉联合染毒血浆和肾脏SOD、GSH-Px的活性较对照组显著下降(P<0.05),MDA含量显著升高(P<0.05);添加NAC组与铅、镉联合染毒组相比GSH-Px活性显著升高(P<0.05),MDA含量显著下降(P<0.05)。组织切片观察显示,铅、镉单独或联合染毒均导致肾小管管腔内蛋白渗出,管腔变窄甚至闭合,肾小管上皮细胞肿胀、浑浊等病变。由此可见,机体脂质过氧化作用增强是铅、镉引起机体损伤的主要机制之一,可能也是铅、镉引起肾脏组织病变的原因之一。NAC能有效缓解铅、镉引起的氧化损伤,但对肾脏组织病变无明显的保护作用。     

锰致鸡睾丸DNA-蛋白质交联的研究

目的:探讨锰致鸡睾丸DNA-蛋白质交联效应。方法:在饲料中添加500、800、1 700 mg/kg MnCl2建立亚慢性锰中毒模型,分别在试验30 d、60 d、90 d剖杀鸡只取睾丸组织,进行DPC(DNA-蛋白质交联)的检测,并在90 d进行生精细胞的凋亡检测。结果:与对照组相比,各染毒组睾丸组织DPC系数显著增大,凋亡指数升高。结论:锰能使睾丸组织DPC系数增大,生精细胞凋亡指数升高,导致DNA损伤,进而引起细胞凋亡。     

铅镉联合暴露对大鼠肾脏的氧化损伤

采用饮水对大鼠进行铅(Pb)300 mg/L、镉(Cd)50 mg/L单独和联合(Pb+Cd)300 mg/L+50 mg/L染毒8周,通过检测肾脏皮质组织抗氧化指标和超微结构的变化来探讨铅镉对大鼠肾脏的毒性损伤及其机理.结果表明,Pb、Cd单独或联合染毒使肾脏皮质组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性和还原型谷胱甘肽(GSH)含量显著或极显著低于对照组(P<0.05或P<0.01),以铅镉联合组降低幅度最大(P<0.01);3个染毒组丙二醛(MDA)含量显著或极显著高于对照组(P<0.05或P<0.01),联合组升高幅度最大而极显著高于单独染毒组(P<0.01).超微结构发现,铅镉染毒导致线粒体肿胀、膜损伤、嵴断裂或消失,联合组损伤程度重于单独染毒组.表明氧化损伤是Pb、Cd肾脏毒性的机制之一,其联合毒性表现为协同效应.     

微量元素锰的营养功能及其在家禽生产中的应用

锰是家禽的必需微量元素，分布于动物体内所有组织中，以骨骼、肝脏、肾脏及脑垂体中的浓度最高。在鸡体含量很少，仅为2-3mg／kg，在禽蛋中以蛋黄为最高，其浓度比蛋白高5倍，蛋锰浓度常被作为评定家禽锰营养水平的指标。     

高蛋白质日粮对肉鸡生长性能和肾脏组织及相关血液指标的影响

为研究日粮中不同含量的蛋白质对肉鸡生长性能、肾脏组织及相关血液指标的影响,试验采用单因素试验设计,将1200只1日龄白羽肉鸡随机分为4组,每组5个重复,每个重复60只。I组饲喂基础日粮（蛋白质含量为19%）,II～IV分别在日粮中添加豆粕使粗蛋白质含量分别为22%、25%和28%,试验为期21?d,观察不同蛋白质含量对肉鸡生长性能、肾脏组织及相关血液指标的影响。试验结果表明,（1）随着日粮蛋白质水平的提高,肉鸡平均日增重（ADG）明显降低（P＜0.05,P＜0.01）,F/G显著增加（P＜0.05）|（2）高蛋白质日粮显著提高了肉鸡血清中Cr和BUN的浓度（P＜0.05）,加重了肾脏组织损伤。（3）随着日粮中蛋白质水平的增加,肉鸡血清中MDA含量显著增加（P＜0.05）,GSH-Px活性、SOD活性与T-AOC含量显著降低（P＜0.05）,表明高蛋白质日粮打破了氧化与抗氧化系统的稳态,引起氧化应激,造成氧化损伤。 [关键词]高蛋白质|肉鸡|生长性能|肾脏|血液指标     

固始鸡组织器官中微量元素锰(Mn)沉积量的动态研究

用原子吸收分光光度计法测定了固始鸡0、2、4、6、8周龄时各组织器官(胸肌、腿肌、肝脏、肾脏、心脏、胰脏、胫骨、趾骨、跖骨、法氏囊)锰沉积量,并对其进行方差分析。结果表明：(1)胰脏和肝脏中锰的沉积量随着周龄的增加差异不显著(P＞0．05),肾脏和腿肌中锰的沉积量随周龄的增加差异显著(P＜0．05),其他各组织器官中锰的沉积量随周龄的变化差异极显著(P＜0．01);(2)胫骨、趾骨、跖骨、心脏、肾脏、肝脏、胸肌内锰沉积量随周龄的增加变化规律一致;不同组织器官中锰含量各不相同,肝脏中锰的沉积量最大,肾脏、骨骼(趾骨、跖骨、胫骨)次之,心脏和胸肌中含量最低。(3)法氏囊中锰的沉积量在0-2周龄有小幅度降低,从2周逐渐增加,并且差异极显著(P＜0．01)。     

肉仔鸡日粮中不同形态锰源的相对生物学利用率评定

为评价肉仔鸡日粮中不同形态锰源的相对生物学利用率,采用2×5完全随机试验设计,选择玉米—豆粕型基础日粮(锰含量为37.66mg/kg),添加2种锰源(复合氨基酸螯合锰和硫酸锰)和5个锰添加水平(0、45、90、130、180mg/kg),构成10个日粮处理组,将540只1日龄健康艾维茵肉仔鸡随机分为10个处理组,每个处理组3个重复,每个重复18只鸡,公母各半,开展为期42d的肉仔鸡饲养试验。分别于21、42日龄时,取各组试验鸡的肝脏、肾脏及左侧胫骨,采用原子吸收分光光度计测定肝脏、肾脏组织以及胫骨的锰浓度。将各组织锰含量与日粮锰进食量进行多元线性回归方程拟合,采用斜率比法计算复合氨基酸锰相对无机硫酸锰的生物学利用率。结果表明,饲粮中添加锰可显著增加肝脏、肾脏和胫骨锰含量,尤以胫骨锰含量反映最敏感,呈明显的剂量效应(P<0.01);相比肝脏锰和肾脏锰含量,21日龄胫骨锰含量可作为评价锰利用率的有效指标;采用斜率比法估测的复合氨基酸螯合锰的相对生物学利用率要略高于饲料级硫酸锰。研究结果为有机锰添加剂在禽生产上的合理应用提供了基础数据。     

饲料和饮水对肉牛体内微量元素锰含量的影响

试验旨在研究饲料和饮水对肉牛机体组织微量元素锰含量的影响。采用电感耦合等离子体质谱法对黑龙江省哈尔滨、鹤岗、齐齐哈尔及伊春4个地区的8个肉牛场饮用水、所有饲料原料和配合饲料中锰元素含量进行测定;每个地区选取1个牧场,每个牧场选取5头肉牛,检测血液、肌肉、肝脏、肾脏及粪尿中锰元素含量。结果表明,所检测的8份饮水中锰含量为0~2.17 mg/l,玉米秸秆锰含量为54.60~176.99 mg/kg,精饲料锰含量为7.14~209.2 mg/kg,精料补充料锰含量为125.2~370.9 mg/kg;肌肉、肝脏、肾脏中锰含量分别为0.034~0.156、2.146~3.638 mg/kg和0.444~1.141 mg/kg。肉牛肝脏、肾脏、肌肉、血液中锰含量与饲料锰含量呈正相关,按相关度大小排序是:肌肉、肝脏、肾脏、血液。试验表明,机体组织锰含量不同程度地受饲料锰含量的影响。     

母鼠围产期铅暴露对仔鼠组织微量元素含量的影响及乙酰半胱氨酸的保护效应

为观察母鼠围产期铅暴露对仔鼠各组织微量元素含量的影响及N-乙酰半胱氨酸(NAC)的保护效应,采用电感耦合等离子体质谱法(ICP-MS)测定低水平铅暴露后的仔鼠血液、大脑、骨骼、肝脏和肾脏等组织中的铅、锌、铜、铁、锰和硒等微量元素的含量。结果表明,与对照组相比,染铅组所测组织铅含量均极显著升高(P<0.01),锌含量均极显著降低(P<0.01);肝脏铁含量、肾脏硒含量及骨骼铁、铜、硒含量均显著降低(P<0.01或P<0.05)。NAC拮抗组与染毒组比较,各组织铅含量显著降低(P<0.01或P<0.05),血液和肾脏锌含量显著升高(P<0.05),其他元素含量无明显差异(P>0.05)。     

Protective Effects of Proanthocyanidins on the Liver and Kidney Oxidative Damage Induced by Zearalenone in Mice

The experiment was conducted to study whether the proanthocyanidin (PC) had the protective effects on the liver and kidney oxidative damage induced by zearalenone in mice.40 8 to 9 week-old healthy clean grade Kunming mice with the 45 g body weight were chosen and randomly divided into four groups: control group was given normal saline,PC group was given 100 mg/kg PC,ZEA group was given 40 mg/kg ZEA and PC＋ZEA group was fed 100 mg/kg PC＋40 mg/kg ZEA.Liver and blood sampls were taken after cervical vertebra to death.AST、ALT、MDA、SOD were measured to determine the degree of liver damage and antioxidant capacity,and UA and BUN were used to determine the kidney damage.The results showed that: Compared with the control group,the indexes of PC group were not significant changed (P>0.05),indicating that there was no obvious oxidative damage in the liver and kidney.Compared with control group,ALT,MDA and AST content were significantly or extremely significant increased in ZEA group (P<0.05;P<0.01),SOD content was extremely significant decreased (P<0.01),UA and BUN were extremely significant increased in serum (P<0.01),indicating that the liver and kidney of ZEA group had a serious oxidative damage.The indexes of the PC＋ZEA group (except SOD)were significantly or extremely significant lower than ZEA group (P<0.05;P<0.01),indicating that the oxidative damage of the liver and kidney in PC＋ZEA group was lower than that in the ZEA group.In conclusion,the liver and kidney oxidative damage of mice induced by ZEA was eased to some extent by PC.     

原花青素对玉米赤霉烯酮致小鼠肝脏、肾脏氧化损伤的保护作用

试验旨在研究原花青素(PC)是否对玉米赤霉烯酮(ZEA)中毒的小鼠肝脏及肾脏具有保护作用.选取40只日龄为8~9周、体重约为45 g的健康清洁级雄性昆明系小鼠,随机分为4组,对照组灌喂生理盐水,PC组灌喂100 mg/kg PC,ZEA组灌喂40 mg/kg ZEA,PC＋ZEA组灌喂100 mg/kg PC+40 mg/kg ZEA,眼球采血,颈椎处死后采取肝脏样本.测定肝脏组织中谷丙转氨酶(ALT)、谷草转氨酶(AST)、丙二醛(MDA)、超氧化物歧化酶(SOD)含量及血清中尿酸(UA)、尿素氮(BUN)含量.结果显示,与对照组相比,PC组各项指标差异均不显著(P>0.05),提示肝脏及肾脏没有明显的氧化损伤;与对照组相比,ZEA组的小鼠组织中谷草转氨酶、谷丙转氨酶及丙二醛含量显著或极显著升高(P<0.05;P<0.01),超氧化物歧化酶含量极显著降低(P<0.01),血清中尿酸、尿素氮含量极显著升高(P<0.01),提示肝脏及肾脏有严重的氧化损伤;PC+ZEA组的小鼠各项指标(除超氧化物歧化酶外)均显著或极显著低于ZEA组(P<0.05;P<0.01),提示其肝脏及肾脏氧化损伤程度低于ZEA组,PC对ZEA中毒小鼠的肝脏及肾脏氧化损伤有一定的保护作用.     

Effects of acute cold exposure on oxidative balance and total antioxidant capacity in juvenile Chinese soft‐shelled turtle,Pelodiscus sinensis

Acute cold exposure may disturb the physiological homeostasis of the body in ectotherms. To date, there has been no information on the effects of cold exposure on homeostasis of reactive oxygen species (ROS) or antioxidant defense response in the Chinese soft‐shelled turtle, Pelodiscus sinensis. In this study, P. sinensis juveniles were acclimated at 28 °C, transferred to 8 °C as cold exposure for 12 h, then moved back to 28 °C rewarming for 24 h. We measured the ROS level and total antioxidant capacity (TAC) in the brain, liver, kidney and spleen at 2 and 12 h cold exposure, and at the end of the rewarming period. Malonaldehyde (MDA) and carbonyl protein were used as markers of oxidative damage. Turtles being maintained simultaneously at 28 °C were used as the control group. Cold exposure did not disturb the ROS balance in all 4 tissues, while rewarming raised the ROS level in the brain and kidney of P. sinensis. Cold exposure and rewarming decreased the TAC in the brain, liver and spleen but did not change the TAC in the kidney. MDA and carbonyl protein levels did not increase during the treatment, indicating no oxidative damage in all 4 tissues of P. sinensis. Our results indicated that extreme cold exposure did not impact the inner oxidative balance of P. sinensis, but more ROS was produced during rewarming. P. sinensis showed good tolerance to the harsh temperature change through effective protection of its antioxidant defense system to oxidative damage. This study provides basic data on the stress biology of P. sinensis.     

Effect of dietary α‐tocopherol + ascorbic acid,selenium, and iron on oxidative stress in sub‐yearling Chinook salmon (Oncorhynchus tshawytscha Walbaum)

A three‐variable central composite design coupled with surface‐response analysis was used to examine the effects of dietary α‐tocopherol + ascorbic acid (TOCAA), selenium (Se), and iron (Fe) on indices of oxidative stress in juvenile spring Chinook salmon. Each dietary factor was tested at five levels for a total of fifteen dietary combinations (diets). Oxidative damage in liver and kidney (lipid peroxidation, protein carbonyls) and erythrocytes (erythrocyte resistance to peroxidative lysis, ERPL) was determined after feeding experimental diets for 16 (early December) and 28 (early March) weeks. Only TOCAA influenced oxidative stress in this study, with most measures of oxidative damage decreasing (liver lipid peroxidation in December and March; ERPL in December; liver protein carbonyl in March) with increasing levels of TOCAA. We also observed a TOCAA‐stimulated increase in susceptibility of erythrocytes to peroxidative lysis in March at the highest levels of TOCAA. The data suggest that under most circumstances a progressive decrease in oxidative stress occurs as dietary TOCAA increases, but higher TOCAA concentrations can stimulate oxidative damage in some situations. Higher levels of TOCAA in the diet were required in March than in December to achieve comparable levels of protection against oxidative damage, which may have been due to physiological changes associated with the parr‐smolt transformation. Erythrocytes appeared to be more sensitive to variation in dietary levels of TOCAA than liver and kidney tissues. Using the March ERPL assay results as a baseline, a TOCAA level of approximately 350–600 mg/kg diet would provide adequate protection against lipid peroxidation under most circumstances in juvenile Chinook salmon.     

Antioxidant capacity and oxidative damage determination in synovial fluid of chronically damaged equine metacarpophalangeal joint

In order to determine oxidative stress in equine joints with degenerative processes, we analyzed synovial fluid (SF) antioxidant capacity and the concentration of oxidative damage biomarkers in healthy and chronically damaged metacarpophalangeal joints. SF samples were collected from joints of thirty 2–5 year-old crossbreed male equine, macroscopically classified at post mortem inspection and later histologically confirmed. The antioxidant capacity was determined measuring uric acid and the concentration of sulfhydryl groups and the total radical trapping antioxidant potential (TRAP). The oxidative damage was determined by assessing malondialdehyde (MDA) and carbonyl protein concentration. TRAP was significantly higher (p < 0.05) in the group with chronic damage (CD). The sulfhydryl groups and concentration of uric acid did not show significant difference between the groups (p > 0.05). Although carbonyl concentration did not show significant difference between groups, it was slightly higher in the group with CD (p = 0.05009). Concentration of MDA did not show significant difference (p > 0.05) between groups. The observed significant increase in TRAP in the group with CD could be related to the participation of components other than protein, sulfhydryl groups, or uric acid coming from degenerating joint tissues. These findings could be helpful for a better understanding of the oxidative stress role in equine joints with chronic degenerative process.     

日粮三聚氰胺对产蛋鸭组织氧化损伤的影响

采用单因子试验设计,研究了日粮三聚氰胺(MEL)对产蛋鸭组织氧化损伤的影响。选用体重和产蛋率相近的19周龄金定鸭648只,随机分成6个处理,每个处理6个重复,每重复18只。6种日粮的MEL添加水平分别为0、1、5、25、50mg/kg和100mg/kg。试验期21d。结果表明:与对照组相比,100mg/kg处理组血清中谷胱甘肽过氧化物酶(GSH-Px)活性显著降低(P0.05),丙二醛(MDA)含量显著升高(P0.05);50mg/kg和100mg/kg处理组肾脏中GSH-Px活性显著降低(P0.05);100mg/kg处理组肝脏中过氧化氢酶(CAT)和超氧化物歧化酶(SOD)活性显著降低(P0.05),MDA含量显著升高(P0.05);50mg/kg处理组肝脏中SOD活性显著降低(P0.05);胸肌中各抗氧化指标均未见显著差异(P0.05),表明MEL可引起产蛋鸭血清、肾脏和肝脏组织的氧化损伤。     

Oxidative stress and hypoxia observed in the kidneys of mice after a 13-week oral administration of melamine and cyanuric acid combination

Both melamine and cyanuric acid have low toxicity, but together they may cause serious lesions to the kidney, via an unknown mechanism. This study was aimed to estimate whether lesions to the kidney were relative to oxidative damage and hypoxia in the kidney after mice exposed to 1 mg/kg/day, 5 mg/kg/day or 25 mg/kg/day of a mixture of melamine and cyanuric acid for 13 weeks. Pathological changes to the kidneys, oxidative stress and energy parameters and hypoxia-inducible factor-1α (HIF-1α) change in the kidneys were evaluated. Pathological changes were found in the distal tubules of kidneys, such as crystals, proteinaceous casts and compensatory expansion, indicating that the mixture induced toxicity to the kidney. The activities of total antioxidant capacity (TAC) and superoxide dismutase (SOD) and the concentration of glutathione (GSH) decreased, while the concentrations of lipid peroxidation (MDA) and protein carbonyl groups (PC) increased after exposure to the mixture, demonstrating that the mixture resulted in imbalance of antioxidant and reactive oxygen species (ROS) and excessive ROS induced oxidant damage to lipid and proteins in kidneys. The activities of malate dehydrogenase (MDH) and succinate dehyrogenase (SDH) decreased, however, the activity of lactic dehydrogenase (LDH) and the concentration of HIF-1α increased after exposure to the mixture. Accordingly, it was concluded that the mixture resulted in a hypoxic state in kidneys and that both oxidative stress and hypoxia contributed to the lesion of kidneys. The exact cause of oxidative damage and hypoxia is not clear, it might be caused by either a direct effect or by an indirect effect, which is secondary to substantial renal damage caused by tubular obstruction due to crystal formation.     

Antioxidant Activity of Tocotrienol Rich Fraction Prevents Fenitrothion-induced Renal Damage in Rats

Fenitrothion (FNT) is an organophosphate compound widely used as pesticide in Malaysia. The present study aims to investigate effects of palm oil tocotrienol rich fraction (TRF) on the renal damage of FNT-treated rats. A total of 40 male Sprague Dawley rats were divided into 4 groups randomly, the control, TRF, FNT and FNT+TRF groups. FNT (20 mg/kg b.w.) and TRF (200 mg/kg b.w.) were given orally for 28 days continuously. Rats from the FNT+TRF group were supplemented with TRF 30 minutes prior to administration of FNT. Rats were sacrificed after 28 days, and the kidneys were removed for determination of oxidative stress and histological analysis. Plasma was collected for determination of blood creatinine and urea level. Statistical analysis showed that palm oil TRF has a protective effect against renal oxidative damage induced by FNT. In the FNT+TRF group, malondialdehyde and protein carbonyl levels were significantly lower, while the glutathione level as well as superoxide dismutase and catalase activities were significantly higher compared with the FNT-treated group (p<0.05). As for renal function, there was a markedly lower urea level (p<0.05) in the FNT+TRF group compared with the FNT-treated group, but there was no significant difference in creatinine level. Besides, total protein also showed no significant difference for all groups of rats (p>0.05). Histological evaluation also revealed that the FNT+TRF group had less glomerulus and renal tubule damage than the FNT-treated group. In conclusion, palm oil TRF was able to reduce oxidative stress and renal damage in FNT-treated rats.     

Effect of mercury chloride on oxidative stress and nuclear factor erythroid 2‐related factor 2 signalling molecule in liver and kidney of laying hens

This study investigated the effects of mercury chloride (HgCl₂) on the deposition of mercury (Hg), histopathology and oxidative stress in liver and kidney of laying hens. The gene expressions of antioxidant enzymes and nuclear factor erythroid 2‐related factor 2 (Nrf2)‐Kelch‐like ECH‐associated protein 1 (Keap1) were further studied to uncover the molecular mechanism. A total of 960 40‐week‐old Hyline brown laying hens were randomly allocated to five treatments with eight pens per treatment and 24 hens per pen. The hens were fed with five experimental diets containing graded levels of Hg at 0.270, 1.250, 3.315, 9.405 and 27.230 mg/kg respectively. Results revealed that both deposition of Hg and score of injury in liver and kidney were significantly increased as dietary Hg dosage up to 27.230 mg/kg diet. Deposition of Hg was positively related to score of injury in liver and kidney of laying hens. Besides, the activities of superoxidative dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GSH‐Px), and glutathione (GSH) content all significantly decreased (p < 0.05), while malondialdehyde (MDA) content significantly increased (p < 0.05) after Hg exposure in liver and kidney of laying hens. In addition, positive relationships occurred between antioxidant enzyme activities and antioxidant enzyme gene expressions except between SOD activity and manganese superoxide dismutase (MnSOD) gene expression in liver. Meanwhile, Nrf2 gene expression was positively related to antioxidant gene expressions and negatively connected with Keap1 gene expression. Negative relationships occurred between Nrf2 and Keap1 protein levels in liver and kidney. In conclusion, Hg could dose‐dependently damage liver and kidney and induced hepatic and renal oxidative stress by means of suppressing Nrf2‐Keap1 signalling molecule in laying hens.