共查询到20条相似文献，搜索用时 218 毫秒
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《畜牧与兽医》2018,(12)
为探究葛根素(Pur)在镉(Cd)致大鼠大脑皮质氧化损伤中的保护作用,40只雄性SD大鼠随机分为4组,分别为对照组、镉组、葛根素组、镉与葛根素共处理组。试验期间,所有大鼠均自由饮用纯净水,每天按200 mg/kg剂量的葛根素对葛根素组、镉与葛根素共处理组大鼠进行灌胃,同时以相同剂量的纯净水将对照组、镉组大鼠进行灌胃,连续处理5周,镉组、镉与葛根素共处理组大鼠在处理4周后连续一周每天用醋酸镉按2.5 mg/kg剂量进行腹腔注射。5周后,分离大鼠大脑皮质,测定大脑皮质内总抗氧化能力(T-AOC),超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性和丙二醛(MDA)的含量。结果表明,与对照组相比,镉组大鼠大脑皮质T-AOC,SOD和GSH-Px活性显著降低(P0.05),MDA含量显著升高(P0.05);与镉组相比,镉与葛根素共处理组T-AOC,SOD和GSH-Px活性显著升高(P0.05),MDA含量显著降低(P0.05)。说明葛根素在镉致大鼠大脑皮质氧化损伤中具有一定的保护作用。 相似文献
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《黑龙江畜牧兽医》2015,(19)
为了探讨慢性饮水染镉对大鼠睾丸的损伤作用,试验将30只性成熟雄性SD大鼠随机等分为5组,分别饮用Cd(Cd Cl2)浓度为0,25,50,100,200 mg/L的饮水,染毒时间为56 d,定期记录各组大鼠的体质量变化,染毒结束后宰杀大鼠,观察睾丸组织的病理变化。结果表明:与对照组相比,各染毒组大鼠体质量均低于对照组,并且当镉浓度达50 mg/L时差异显著(P0.05),200 mg/L镉组睾丸质量极显著下降(P0.01);用光学显微镜观察睾丸,可见50 mg/L镉组睾丸曲细精管内出现精原细胞和各级精母细胞,精子细胞发生变性、坏死,并且随着镉的浓度升高,变性、坏死程度加重。透镜电镜下观察可见睾丸中生殖细胞随着镉浓度的升高,出现染色质浓缩,胞质中线粒体肿胀,嵴突消失。说明镉能够影响雄性大鼠的生长发育,造成睾丸的病理损伤。 相似文献
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《黑龙江畜牧兽医》2014,(23)
为了研究黄芩素对镉致大鼠肝脏损伤的保护作用,试验将20只雄性SD大鼠随机分为对照组、黄芩素组、镉组、镉+黄芩素组,各组每天分别灌服生理盐水、黄芩素、氯化镉、氯化镉+黄芩素。6周后处死大鼠,采集血清和肝脏,检测血清中天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)活性,肝脏组织中丙二醛(MDA)和还原型谷胱甘肽(GSH)含量。结果表明:镉可极显著提高AST、ALT活性(P0.01),显著升高MDA和降低GSH含量(P0.05);黄芩素能显著降低镉组AST、ALT活性(P0.05),显著降低MDA和升高GSH含量(P0.05)。说明镉可导致大鼠肝脏组织脂质过氧化损伤,黄芩素对镉导致的损伤具有保护效应。 相似文献
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为探究死亡受体Fas在镉暴露致大鼠大脑皮质自噬体形成中的作用,将24只21日龄雄性SD大鼠随机分为4组,分别为对照组、镉组、镉与对照病毒共处理组、镉与Fas基因沉默病毒共处理组。试验期间,对照组大鼠自由饮用纯净水,病毒处理组大鼠于第1天以每只1.4×1011vg的剂量通过尾静脉注射相应病毒,4周后镉染毒组大鼠自由饮用镉水(50 mg·L-1),持续90 d。试验结束后,透射电镜观察大脑皮质中自噬体数量,Western blot检测大脑皮质细胞外信号调节激酶1/2(Erk1/2)、p-Erk1/2、自噬相关蛋白7(ATG7)、自噬相关基因(Beclin-1)、微管相关蛋白1轻链3(LC3)蛋白表达水平,免疫荧光染色检测LC3表达水平。结果显示,镉暴露增加大脑皮质中自噬体数量,极显著激活Erk1/2并上调ATG7、Beclin-1、LC3蛋白表达水平(P<0.01);Fas基因沉默抑制镉引起的自噬体数量增加,极显著抑制镉致Erk1/2激活及ATG7、Beclin-1、LC3蛋白表达水平升高(P<0.01)。结果表明,Fas通过激活Erk1/2参与镉致大鼠大脑皮质自噬体形成。 相似文献
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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. 相似文献
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24只4周龄雄性SD大鼠,分成4组并每天按以下处理:对照组灌服蒸馏水(10 mL/kg);葛根素组每日按照100mg/kg的用量灌服葛根素;镉组按照2mg/kg的Cd2+用量腹腔注射氯化镉溶液(10g/L);镉+葛根素组,在镉组的处理基础上,再按照100mg/kg的用量灌服葛根素。4周后,将大鼠麻醉并处死,摘取睾丸称其质量并计算脏器系数,睾丸制成组织匀浆检测大鼠睾丸中过氧化氢酶(CAT)、还原型谷胱甘肽(GSH)和丙二醛(MDA)的含量,并制作睾丸病理切片显微镜观察。结果显示与对照组相比,镉组大鼠睾丸脏器系数极显著降低(P0.01);睾丸组织中CAT和MDA的含量显著或极显著增加(P0.05或P0.01),GSH含量极显著减少(P0.01);与镉组相比,镉+葛根素组睾丸脏器系数极显著升高(P0.01);睾丸组织中CAT和MDA的含量显著降低(P0.05),GSH含量显著增加(P0.05)。病理切片显示镉组大鼠睾丸组织的细胞出现实化,看不到各级睾丸细胞正常结构,镉+葛根素组与镉组相比,睾丸细胞损坏程度都有所减轻。本试验表明镉对大鼠睾丸有损伤作用,而葛根素能减轻这种损伤,对镉致大鼠睾丸损伤具有保护作用。 相似文献
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富硒植物对大鼠体内镉排泄的影响 总被引：3，自引：0，他引：3
对大鼠日粮添加富硒植物,以促进镉的排出。代谢试验结果证实,富硒玉米、茶叶、黄芪等植物,有较强地加快大鼠体内镉经粪便和尿液排泄的作用。饲料中添加上述几种富硒植物后,第１周内镉排泄总量占４周内排镉总量的５０％以上。４周内添加富硒玉米组大鼠粪镉排泄总量是对照组的２．３７～２．８８倍,茶叶组和黄芪组大鼠粪镉排泄总量分别是对照组大鼠的１．３９～１．４２和１．０５～１．２７倍。尿镉排泄的结果与此类似。富硒植物加入饲料后,尽管饲料中硒含量比亚硒酸钠组低,但促进大鼠体内镉排泄、减少镉在体内沉着的效果却更明显。 相似文献
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饲料中镉含量对蛋鸡生产性能及抗氧化功能的影响 总被引：1，自引：0，他引：1
为研究日粮中低剂量镉对蛋鸡生产性能和血清、肝肾抗氧化能力的影响,将192羽巴布考克B300蛋鸡随机分为4组,每组3个重复。对照组饲喂玉米-豆粕型基础日粮,试验组日粮为在基础日粮中分别添加5、10、20 mg/kg的镉(氯化镉形式,CdCl2.2.5H2O),试验期9周。结果表明:在1～3、4～6、7～9周,试验组的产蛋率、日采食量均低于对照组(P>0.05);各组在第7～9周时的采食量显著低于1～3周(P<0.05);血清中GSH-Px、GST、GR酶活力对镉不敏感(P>0.05),随镉添加量升高肝肾中GSH-Px活力先升后降,试验组肝肾中总巯基含量较对照组有显著升高(P<0.05);血清和肝肾中总SOD、CuZn-SOD、CAT活力随镉添加量升高呈先升后降的趋势;血清和肝肾中MDA、NO含量随着镉添加量的升高显著升高(P<0.05),总抗氧化能力均呈下降趋势。试验结果证实,镉可引起产蛋鸡体内抗氧化功能受损,机体产生氧化应激,并可能由此导致蛋鸡的生产性能下降。 相似文献
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《中国畜牧杂志》2017,(3)
本试验旨在研究约氏乳杆菌对大鼠生长性能、血液指标及脏器指数的影响。试验选取SD大鼠80只,雌雄各半。大鼠按照体重相近的原则随机分为4个剂量组,即阴性对照组、试验Ⅰ(5 000 mg/kg体重)、试验Ⅱ(1 000 mg/kg体重)和试验Ⅲ组(200 mg/kg体重)。试验期为30 d。结果表明:试验剂量为200~1 000 mg/kg体重时,约氏乳杆菌对大鼠体增重、总采食量、饲料转化率、血液学指标和病理学指标的影响无显著性差异(P>0.05);试验剂量为5 000 mg/kg体重时,谷草转氨酶、血糖、总胆固醇差异不显著(P>0.05);与其他剂量组相比,大鼠的体增重和总采食量显著降低(P<0.05),但饲料转化率无显著差异(P>0.05);谷丙转氨酶水平显著降低(P<0.05),白蛋白和总蛋白显著增高(P<0.05);雌性大鼠尿素氮和雄性大鼠肌酐显著增高(P<0.05)。综合分析,约氏乳杆菌剂量低于1 000 mg/kg体重时,对大鼠平均日增重、血液指标及脏器指数无影响;约氏乳杆菌剂量高于5 000 mg/kg体重时,对大鼠脏器指数有影响。 相似文献
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铅镉联合急性中毒对大鼠脏器病理组织学和超微结构的影响 总被引：1，自引：0，他引：1
按照等毒性配比法混合硝酸铅与氯化镉溶液进行急性毒性试验,采用Bliss法和Keplinger标准进行毒性评价,并应用光镜和电镜观察大鼠染毒后各脏器的显微与超微结构变化。探讨硝酸铅（Pb（NO3）2）与氯化镉（CdCl2·2．5H2O）溶液联合经口灌胃对SD大鼠的急性毒性效应。结果显示,铅镉联合作用下大鼠的绝对致死量（LD100）为5062．00mg／kg,最大耐受浓度（MTD）为1436．00mg／kg,半数致死量（LD50）为2696．54mg／kg,95％可信区间是2162．00～3362．89mg／kg。铅镉联合急性中毒的靶器官为肝脏、肾脏和脾脏,光镜下,主要表现为血管发生不同程度的充血和溶血、实质细胞发生不同程度的变性（水泡变性和颗粒变性）和坏死。电镜下,主要表现为细胞器结构破坏。结果表明,硝酸铅和氯化镉联合急性毒性为相加作用,对大鼠肝脏、肾脏和脾脏均有不同程度的急性毒性损伤。 相似文献
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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) 相似文献
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Cisplatin is a chemotherapeutic agent widely used in treatment of several cancers. It is documented as a major cause of clinical nephrotoxicity and hepatotoxicity. The purpose of this study was to investigate the involvement of oxidative stress in the pathogenesis of cisplatin-induced liver and kidney injury. Wistar rats were divided into four groups. Group 1 (control) was intraperitoneally (IP) injected with a single dose of 0.85% normal saline. Groups 2, 3 and 4 were IP injected with single doses of cisplatin at 10, 25 and 50 mg/kg body weight (BW), respectively. At 24, 48, 72, 96 and 120 h after injection, BW, levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), creatinine, malondialdehyde (MDA), and activity of superoxide dismutase (SOD) and histology of the liver and kidney were evaluated. Cisplatin caused a reduction in BW of rats in groups 2, 3 and 4 at all post injection intervals. The levels of serum ALT, AST, BUN and creatinine and MDA of the kidney and liver were markedly increased especially at 48 and 72 h, whereas the activity of SOD was decreased after cisplatin injection. Liver sections revealed moderate to severe congestion with dilation of the hepatic artery, portal vein and bile duct and disorganization of hepatic cords at 50 mg/kg of cisplatin. Kidney sections illustrated mild to moderate tubular necrosis at 25 and 50 mg/kg of cisplatin. Therefore, oxidative stress was implicated in the pathogenesis of liver and kidney injury causing biochemical and histological alterations. 相似文献
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氧化应激在亚慢性镉中毒引起的肝肾细胞凋亡中的作用 总被引：2，自引：0，他引：2
为了探明镉中毒时氧化应激与细胞凋亡的关系，以公鸡为试验动物，在日粮中添加CdCl2 150mg／kg，肝脏、肾脏和血清中谷胱甘肽过氧化物酶（GSH～Px）活性、超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量以及肝、肾细胞凋亡的检测显示镉使鸡血清、肝脏和肾脏中GSH～Px和SOD活性降低，MDA含量增多，并诱导肝肾细胞凋亡的发生。结果表明。镉能够诱发鸡肝肾细胞发生氧化胁迫，并诱导细胞凋亡的发生。提示氧化应激与细胞凋亡存在一定的关系。 相似文献
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Jiang SZ Yang ZB Yang WR Gao J Liu FX Broomhead J Chi F 《Journal of animal science》2011,89(10):3008-3015
Zearalenone (ZEA), an estrogenic mycotoxin, is produced mainly by Fusarium fungi. Previous studies indicated that acute ZEA exposure induced oxidative stress and damage in multiple organs. Therefore, the present study was designed to investigate the adverse effects of dietary ZEA (1.1 to 3.2 mg/kg of diet) on oxidative stress and organ damage in postweaning gilts. A total of 20 gilts (Landrace × Yorkshire × Duroc) weaned at d 21 with an average BW of 10.36 ± 1.21 kg was used in the study. Gilts were housed in a temperature-controlled room, divided into 4 treatments, and fed a basal diet only (control) or basal diet supplemented with purified ZEA at a dietary concentration of 1 (ZEA1), 2 (ZEA2), or 3 (ZEA3) mg/kg of diet for 18 d ad libitum. The actual ZEA contents (analyzed) were 0, 1.1 ± 0.02, 2.0 ± 0.01, and 3.2 ± 0.02 mg/kg for control, ZEA1, ZEA2, and ZEA3, respectively. Gilts fed different amounts of dietary ZEA grew similarly with no difference (P > 0.05) in feed intake. Vulva size increased linearly over the 18 d of feeding in gilts fed diets containing 1.1 mg of ZEA/kg or greater (P < 0.001). Relative weight of genital organs, liver, and kidney increased linearly (P < 0.05) in a ZEA-dose-dependent manner. Serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, γ-glutamate transferase, urea, and creatinine (P < 0.05), and malondialdehyde concentrations in both serum and liver (P < 0.001) were also increased linearly in a ZEA-dose-dependent manner. However, spleen relative weight (P = 0.002) and activities of total superoxide dismutase and glutathione peroxidase (in both serum and liver (P < 0.05) were decreased linearly as dietary ZEA increased. Results showed that besides genital organs, the liver, kidney, and spleen may also be target tissues in young gilts fed diets containing 1.1 to 3.2 mg of ZEA/kg for 18 d. Increased key liver enzymes in the serum suggest progressive liver damage caused by feeding ZEA, and an increase in oxidative stress in gilts is another potential impact of ZEA toxicity in pigs. 相似文献
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小鼠镉的蓄积性毒性试验研究 总被引：2，自引：0，他引：2
选用SPF级昆明种小鼠140只,做急性毒性和蓄积性毒性试验。通过急性毒性试验,得出Cd LD50为94.1 mg/kg体重。蓄积性毒性试验中,试验组小鼠每日灌胃染毒1次,Ⅰ组,1/10 LD50（Cd 9.41 mg/kg体重）;Ⅱ组,1/5 LD50（Cd 18.82 mg/kg体重）;Ⅲ组,1/3 LD50（Cd 31.36 mg/kg体重）;对照组Cd为 0 mg/kg体重,试验期4周。结果显示,染镉组小鼠生长发育落后于对照组（P<0.05或P<0.01）,组织镉残留量高于对照组（P<0.05或P<0.01）,肝细胞和肾小管上皮细胞变性,脾脏瘀血,并有明显的剂量—效应关系。 相似文献
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Jiang SZ Yang ZB Yang WR Wang SJ Wang Y Broomhead J Johnston SL Chi F 《Journal of animal physiology and animal nutrition》2012,96(6):1147-1156
The objectives of this study were to investigate the toxicity of zearalenone (ZEA) on hepatonephric organs, serum metabolites and oxidative stress of piglets and to evaluate the efficacy of Calibrin‐Z (CAZ) in preventing ZEA‐induced adverse effects. The experiment was conducted for 22 days using 36 piglets weaned at 21 days of age (Landrace × Yorkshire × Duroc, 18 females and 18 males; 8.84 ± 0.21 kg average body weight). Piglets of each gender were randomly allocated to the following six dietary treatments: (i) Control (basal diet only); (ii) Control + 1 g/kg CAZ; (iii) Control + 1 mg/kg ZEA; (iv) Control + 1 mg/kg ZEA + 1 g/kg CAZ; (v) Control + 1 mg/kg ZEA + 2 g/kg CAZ; (vi) Control + 1 mg/kg ZEA + 4 g/kg CAZ. Piglets were housed and fed individually for the entire experimental period. Blood samples were taken, and piglets were killed at the end of the experiment to obtain organs for physiological assessment. Results showed that piglets fed the ZEA‐contaminated diet had increased (p < 0.05) activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma‐glutamyltransferase (GGT), creatine kinase and cholinesterase, concentrations of urea, and creatinine in serum, and malondialdehyde (MDA) in serum and liver. Pigs fed the ZEA‐only diet also showed reductions in serum (p < 0.05) globulin, triglycerides and high‐density lipoproteins (HDL), and reductions in total superoxide dismutase (TSOD) and glutathione peroxidase (GSHPx) activity in both serum and liver. Supplementation of CAZ at the dosages of 1–4 g/kg to the diet containing 1.05 mg/kg ZEA linearly increased (p < 0.05) concentrations of triglycerides and HDL in serum, activity of TSOD and GSHPx in serum and liver, but linearly reduced (p < 0.05) all tested serum enzymes and lowered (p < 0.05) the elevated concentrations of urea, and creatinine in serum, and MDA in serum and liver caused by dietary ZEA. Piglets fed the ZEA‐contaminated diet showed increased (p < 0.05) relative weight of liver and kidney compared with the control, whereas only numerical improvement on relative weight of liver and kidney was observed with simultaneous addition of CAZ at 4 g/kg diet and ZEA. However, feeding the diet with CAZ alone at 1 g/kg had no impact on any of the measured parameters when compared to the control. It is suggested that feeding ZEA at 1.05 mg/kg exerted a deleterious effect on piglets, which was totally or partly ameliorated by dietary supplementation of CAZ at concentrations between 1 and 4 g/kg diet. 相似文献
20.
A polybrominated biphenyl fire retardant (Firemaster FF-1) was responsible for the widespread environmental contamination and animal losses in Michigan during 1973 and 1974. In Fischer 344/N rats orally given 30,100,300, and 1,000 mg/kg (5 days/week, 22 total doses) for 4.5 weeks and observed for 90 days after the start of treatment, the LD50 was determined to be 65 mg/kg/day (total 1.43 g/kg) for the female rat and 149 mg/kg/day (total 3.28 g/kg) for the male. All female rats given the dosage of 100 mg/kg/day (22 doses, total 2.20 g/kg) died between 41 and 53 days after the start of treatment, whereas 38% of the males died between 50 and 73 days. Pathologic changes in treated rats were large liver, accentuation of the hepatic lobular markings, and atrophy of thymus and spleen. Microscopically, hepatic changes were characterized by congestion, fatty metamorphosis, and multifocal liquefactive necrosis. Male rats given 100 mg/kg/day and dying after 90 days had subacute to chronic hepatitis with marked focal proliferation of bile ducts. Exposure to Firemaster FF-1 may produce atypical liver nodules in the rat as early as 6 months after they were first given the preparation. Marked hepatotoxic effect persisted in surviving rats when examined after 6 months. 相似文献