不同膳食硒水平对甲基苄基亚硝胺（NMBzA）诱发大鼠食道上皮细胞DNA烷基化和

本文报道了硒对NMBzA诱发大鼠食道上皮细胞DNA加合物的形成，DNA加合物修复酶（甲基转移酶）的活性以及-cmyc的基因表达的影响，一次腹腔注射NMBzA 2.5mg/Kg体重，6小时后测定产食上皮细胞中O6－甲基脱氧鸟嘌呤核甙酸（O6－MedGua)和N7－甲基脱氧鸟嘌呤核甙酸（N7－MedGua)的含量，结果表明饲料中不同硒含量对DNA加合物无明显影响；对O6－MedGua DNA甲基转移酶活性也无明显作用，给大鼠每周一次灌胃NMBzA 3mg/kg体重，共8周诱发大鼠食道上皮细胞c-myc基因表达，结果膳食缺硒（＜0．02ppm)和补硒（2ppm)对 c-myc基因表达亦无影响.     

硒降低亚得利亚霉素毒性的实验研究

60只雄性Fisher断乳大鼠分为6组,第1、2、3组喂以适硒饲料(硒含量0.5ppm),第4、5、6组喂低硒饲料(硒含量0.02ppm)。10周后开始第2、5及3、6组动物分别经尾静脉注射0.5及1mg/kg体重亚得利亚霉素(称低剂量组及高剂量组),每周一次,共12次。第1、4组注射生理盐水为对照。 实验过程中动物无死亡。第2及3组体重增长分别显著高于5、6组。肾病变检出率低剂量组内低硒组显著高于适硒组。病变特点为曲管扩张,内含蛋白管型。高剂量组心肌病变严重程度缺硒组高于适硒组。心肌病变特点为实质细胞空泡变性、溶解和萎缩。超微结构观察心肌细胞最主要病变是由肌浆网扩张所引起的不同程度空泡变性,对照组未见任何异常。本次实验表明适量硒对亚得利亚霉素所致肾病变有明显的保护作用,对心肌病变亦有保护作用。     

多种应激对SD食道肿瘤大鼠细胞免疫及肿瘤标志物表达的影响

目的探讨不同种类应激对食道肿瘤大鼠模型T淋巴细胞免疫及肿瘤标志物CEA、CA19-9、CA724、CY-FRA21-1、SCC表达的影响。方法 60只健康12周龄食道肿瘤SD大鼠通过建立食道肿瘤模型,应激组（50只）以国际通用的五种应激模式每组10只分别进行应激,共4周。对照组（10只）正常饲养。在应激实验开始前、每周应激后以及应激结束后1周分别测定每组大鼠的T细胞亚群CD3＋、CD4＋、CD4＋/CD8＋及食道肿瘤肿瘤标志物CEA、CA19-9、CA724、CY-FRA21-1、SCC表达的变化,进行肿瘤变化评价。结果应激组在实验开始到最终共检测六次。与对照组相比较,从应激三周后开始CD3＋、CD4＋、CD4＋/CD8＋及CEA、SCC差异有统计学意义（P〈0.05）,不同应激组间差异无统计学意义（P〉0.05）。结论慢性复合应激对食道肿瘤大鼠T淋巴细胞免疫及肿瘤标志物的表达有明显促进作用,与应激类型无关。     

哺乳期使用抗生素对大鼠生命后期体重和血液学指标的影响

目的探索哺乳期使用抗生素能否对大鼠生命后期的体重和血糖、血脂等产生影响。方法将24只出生8 d的哺乳期SD大鼠雄性仔鼠随机分为2组,干预组(n=12)给予剂量为150 mg/kg体重的阿莫西林生理盐水溶液灌胃,对照组(n=12)给予安慰剂(生理盐水),干预10 d,仔鼠出生21 d后断乳,改为普通饲料喂养。断乳后每周测1次体重,出生后第4周、第8周、第12周、第20周采空腹血测血糖及血脂。20周时结束实验,测量肝脏、脾、肾周脂肪、睾周脂肪重量及脏器系数。结果干预组大鼠与对照组相比体重显著增加,差异有统计学意义(P0.05)。但肝脏、脾脏、肾周及睾周脂肪、脏器系数及空腹血糖、血脂均未观察到显著变化。结论哺乳期使用抗生素可使SD大鼠生命后期体重增加,但其是否会对脏器系数、脂肪重量及血糖、血脂产生影响还需做进一步的研究。     

维生素E和硒缺乏促进大鼠食管肿瘤发生及氧化应激机制的研究

目的探讨维生素E(VE)和硒(Se)营养缺乏对食管肿瘤发生的影响及其氧化应激机制。方法 110只雄性F344大鼠随机分为3组:VE/Se缺乏组,VE/Se正常组和溶剂对照组。VE/Se缺乏组和VE/Se正常组动物皮下注射N-甲基苄基亚硝胺(NMBzA)染毒,染毒剂量为0.35 mg/kg BW,每周3次,连续5周。溶剂对照组动物皮下注射等体积的20%二甲基亚砜(DMSO)。VE/Se缺乏组给予低VE/Se饲料(VE 46U/kg,Se 0.05mg/kg),VE/Se正常组、溶剂对照组给予正常饲料(VE 80U/kg,Se 0.15mg/kg)。在实验第25周解剖动物,进行食管肿瘤肉眼观察及病理检查。动物血浆VE水平采用高效液相色谱法检测,Se水平采用荧光法检测。食管组织中细胞增殖和DNA氧化损伤分别采用5-溴脱氧尿嘧啶(BrdU)和8羟基脱氧鸟苷(8-OH-dG)免疫组织化学法检测。动物血浆、食管及肝脏谷胱甘肽过氧化物酶(GPX)、谷胱甘肽转移酶(GST)活性采用试剂盒法检测。结果动物血浆VE和Se水平VE/Se缺乏组显著低于VE/Se正常组,VE/Se正常组略低于溶剂对照组。VE/Se缺乏组动物食管肉眼可见肿瘤发生率、平均肿瘤数量及病理损伤数量均显著高于VE/Se正常组(P<0.05);与VE/Se正常组相比,VE/Se缺乏组动物食管组织细胞增殖水平、8-OH-dG水平显著升高(P<0.05);动物血浆、食管及肝脏GPX和GST活性显著降低(P<0.05)。结论维生素E和硒缺乏能够加快细胞增殖,显著促进NMBzA诱发的大鼠食管肿瘤的发生,机体氧化应激、DNA氧化损伤在食管癌变过程中具有重要作用。     

亚慢性饮水砷暴露对发育期大鼠学习记忆与运动能力的影响

目的探讨亚慢性饮水砷暴露对大鼠神经发育行为的影响及砷致大鼠脑病理形态的改变。方法初断乳SD大鼠(雌雄各半)40只,按体重随机分为四组,每组10只,以亚砷酸钠LD_(50)的1/40、1/20、1/4确定大鼠染毒剂量依次为1、2、10mg/kg,大鼠经自由饮水染砷12周,对照组(0 mg/kg)正常饮水。染砷结束时对大鼠进行Morris水迷宫实验、平衡木实验、悬挂实验;以光镜观察小脑神经元、胶质细胞的病理变化;以电镜观察大脑皮质细胞内结构。结果定位航行实验发现,第2天开始,与0 mg/kg组大鼠相比,2、10 mg/kg染砷组大鼠逃避潜伏期时间延长(P0.05);第3天开始,10 mg/kg染砷组大鼠比1 mg/kg染砷组逃避潜伏期时间增加(P0.05);空间搜索结果显示,与0 mg/kg组大鼠比较,10 mg/kg组大鼠记忆能力下降(P0.05);运动能力测试结果显示,2、10 mg/kg组大鼠平衡能力与前肢悬挂能力均有所下降(P0.05)。光镜下发现染砷大鼠小脑神经元坏死、胶质细胞增生。电镜下发现染砷组大鼠大脑皮质神经元内部存在不同程度损伤。结论亚慢性饮水砷暴露损伤大鼠的学习记忆与运动能力。     

亚硒酸钠和硒蛋氨酸的毒性比较

目的　比较亚硒酸钠和硒蛋氨酸毒性差异以及探讨硒中毒的指标。方法　将断乳Wistar大鼠随机分为 7组 ,每组 14只 ,雌雄各半。其中一组为对照组 ,另外六组分别给予含硒 3、6、10mg kg的亚硒酸钠或硒蛋氨酸饲料 ,于第 12周将其处死。结果　当饲料硒水平达到 3mg kg时 ,动物肝脏出现病理变化 ,在Se6mg kg时 ,体重才出现下降。饲料硒水平为 6、10mg kg时 ,同一饲料硒水平的亚硒酸钠组大鼠体重小于硒蛋氨酸组。饲料硒水平为 3、6mg kg时 ,硒蛋氨酸组大鼠的肝脏病理改变轻于亚硒酸钠组 ,雄性大鼠轻于雌性。亚硒酸钠组较硒蛋氨酸组或雌性大鼠较雄性大鼠在肝脏体重比方面变化更为明显。除雌性大鼠肝脏谷胱甘肽过氧化物酶 (GPX)活性随硒水平升高而降低外 ,其它补硒各组肝、红细胞、血浆GPX活性具有随硒水平的升高而升高的趋势。结论　大鼠硒中毒的剂量为Se 3mg kg,硒蛋氨酸的毒性小于亚硒酸钠 ,雌性大鼠对硒毒性更为敏感     

多巴胺受体激动剂对丙烯酰胺诱导大鼠神经损伤的影响

目的 研究丙烯酰胺对大鼠中枢神经系统神经递质多巴胺含量的影响以及多巴胺受体激动剂对丙烯酰胺引起的神经损伤的影响,探讨丙烯酰胺的神经损伤机制以及确定多巴胺受体激动剂对丙烯酰胺引起的神经损伤是否具有保护作用.方法 SD大鼠染毒组腹腔注射丙烯酰胺4周,每周5次(30 mg/kg);溴隐亭给药组在腹腔注射丙烯酰胺的同时灌胃给予多巴胺受体激动剂溴隐亭(低剂量组按1.25 mg/kg给药,高剂量组按2.5 mg/kg给药);正常对照组腹腔注射等量生理盐水.每周给药第6天和第7天对大鼠进行感觉神经功能测定以及自主性行为观察.给药结束后,测定大鼠中枢神经系统多巴胺、肌酸激酶(CK)以及Na -K -ATP酶的含量.结果 染毒组大鼠体重呈下降趋势,与其他3组大鼠体重均存在明显差异,染毒组热反应灵敏度也较差,给药组无论低剂量或高剂量组,热反应灵敏度均比染毒组有所改善.此外,染毒组CK、Na -K -ATP酶以及多巴胺的含量均比正常对照组明显减少,给药组各指标也比阳性对照组有所升高.结论 多巴胺受体激动剂溴隐亭对丙烯酰胺诱导的大鼠神经损伤有一定的保护作用.     

大鼠吸入氯乙烯一年的研究结果

使 Wistar 大鼠吸入氯乙烯单体(VGM),以观察氯乙烯引起的早期变化。将刚断乳大鼠雌雄各124只,按性别和体重分成试验组(VCM5,000ppm)和对照组(0ppm)共4大组进行实验。试验组接触时间为7小时/天,5天/周,共52周。实验期间经常测体重,并于第4、13、26和52周时进行血液检查、血清和尿分析及器官功能试验。于第4、13、26和52周后各组宰杀10只大鼠,进行检查。     

亚硒酸钠与核黄素联合暴露对高脂饮食大鼠血脂及血清肝生化指标的影响

目的研究亚硒酸钠与核黄素联合暴露对高脂饮食雄性大鼠血脂及血清肝生化指标的影响。方法将60只健康SPF级雄性SD大鼠按体重随机分为空白对照组(10只)和高脂组(50只),分别给予基础饲料和高脂饲料;喂养4周后,将50只高脂组大鼠按照血脂水平和体重随机分为5组,分别为高脂对照组、1.84μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组、18.40μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组、1.84μg/kg亚硒酸钠+3.50 mg/kg核黄素干预组和18.40μg/kg亚硒酸钠+3.50 mg/kg核黄素干预组,每组10只。采用灌胃方式进行染毒,同时,空白对照组和高脂对照组给予相同体积的生理盐水,染毒容量为10 ml/kg,每天1次,连续60 d。分别于第0(染毒前)、20、40、60天,测定大鼠血清中总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)水平;并于第60天,检测大鼠血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转氨酶(AST)的水平。结果与空白对照组比较,染毒期间高脂对照组及各干预组大鼠血清TC、TG、LDL-C的水平均升高,除第60天时1.84μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组大鼠血清TG水平外,差异有统计学意义(P0.05);而血清HDL-C水平均未见显著变化。与高脂对照组相比,第20、40天时1.84μg/kg亚硒酸钠+0.70mg/kg核黄素干预组大鼠血清TC、TG的水平及1.84μg/kg亚硒酸钠+3.50 mg/kg核黄素干预组大鼠血清TG的水平以及第60天时1.84μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组大鼠血清TC、TG、LDL-C的水平及18.40μg/kg亚硒酸钠+0.70mg/kg核黄素干预组大鼠血清TC的水平均下降,差异有统计学意义(P0.05);而各干预组大鼠血清HDL的水平均无明显改变。与空白对照组比较,高脂对照组、18.40μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组和1.84μg/kg亚硒酸钠+3.50mg/kg核黄素干预组大鼠血清ALT的水平以及高脂对照组、18.40μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组和18.40μg/kg亚硒酸钠+3.50 mg/kg核黄素干预组大鼠血清AST的水平均升高,差异有统计学意义(P0.05)。与高脂对照组相比,仅1.84μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组大鼠血清ALT的水平降低,差异有统计学意义(P0.05);1.84μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组、18.40μg/kg亚硒酸钠+0.70 mg/kg核黄素干预组以及1.84μg/kg亚硒酸钠+3.50 mg/kg核黄素干预组大鼠血清AST的水平降低,差异均有统计学意义(P0.05)。结论适量亚硒酸钠与核黄素联合暴露可以拮抗高脂饮食所致雄性大鼠血脂及血清肝生化指标的升高。     

Lack of effects of selenium on N-nitrosomethylbenzylamine-induced tumorigenesis, DNA methylation, and oncogene expression in rats and mice.

The effects of dietary selenium deficiency and excess on N-nitrosomethylbenzylamine-(NMBA) induced esophageal neoplasia in rats and forestomach tumors in mice and the effects of dietary selenium on DNA adduct formation and on the activities of DNA adduct-repairing enzyme and oncogene expression in rat esophagus were investigated. The esophageal and forestomach tumors were induced by administration of NMBA by gavage with a total dose of 39 mg/kg body wt in rats and 12 mg/kg body wt in mice. Neither selenium dietary deficiency (Se < 0.02 ppm) nor selenium excess (2.0 ppm) showed any significant effect on the incidence of tumors or number of tumors per tumor-bearing animal. For the DNA adduct formation studies, rats were given a dose of NMBA intraperitoneally after six weeks on the different selenium-containing diets. No significant difference in the amount of the DNA adduct O6-methyldeoxyguanosine was found among the different selenium-treated groups. In a parallel group of rats that did not receive NMBA, the levels of esophageal O6-methyldeoxyguanosine DNA methyltransferase were not significantly altered by dietary selenium levels. The c-myc oncogene expression in rat esophagus was induced by the administration of NMBA (3 mg/kg body wt) by gavage once a week for eight weeks. Dietary selenium did not show any effects on its expression. On the basis of the results of these studies, dietary selenium has no effects in the NMBA-induced tumor model.     

苯和硒对小鼠淋巴细胞端粒酶活力的影响

目的 研究苯和硒对小鼠淋巴细胞端粒酶活力的影响,评价端粒酶作为苯刺激淋巴细胞的早期效应标志物的可能性.方法 健康雄性昆明种小鼠随机分为阴性对照组,溶剂对照组,100、200、400 mg/kg苯组,200 mg/kg苯+0.75 ms/ks亚硒酸钠组,200 mg/kg苯+1.50 mg/kg亚硒酸钠组,200 ms/kg苯+3.00mg/kg亚硒酸钠组,每组5只.各组分别给予不同处理,共5 d,每天1次.最后1次染毒48 h后,分离淋巴细胞,用端粒重复扩增一酶联免疫吸附(TRAP-ELISA)法检测端粒酶活力.结果 各剂量苯组的端粒酶活力均增加,与阴性对照组和溶剂对照组比较,其中,100mg/kg苯组差异有统计学意义(P＜0.01).各剂量苯联合硒组的端粒酶活力均增加,与阴性对照组和溶剂对照组比较,200 mg/kg苯+0.75mg/kg亚硒酸钠组差异有统计学意义(P＜0.01);与相应的200 mg/kg苯组比较,200 mg/kg苯+0.75 mg/kg亚硒酸钠组差异有统计学意义(P＜0.05).结论 不同浓度的苯刺激的端粒酶活力均增加,表明小鼠淋巴细胞得到激活和增殖.端粒酶可能是苯刺激淋巴细胞的一种敏感的早期效应标志物.硒可以上调小鼠淋巴细胞端粒酶活力.     

Influence of selenium on the metabolism of bromobenzene and a possible relationship to its hepatotoxicity

When male Sprague-Dawley rats were treated with sodium selenite (1 mg/kg, sc) 24 hr prior to or simultaneously with bromobenzene (2.5 mmol/kg, ip) and sacrificed 48 hr after the bromobenzene dose, increased levels of the activities of serum transaminases (serum glutamic-oxaloacetic transaminase (SGOT) and serum glutamic-pyruvic transaminase (SGPT) induced in the bromobenzene-treated rats were significantly reduced in the presence of selenium. However, no such reduction in the transaminases activities were observed when rats were either pretreated with selenite for 48 hr or pretreated with 0.1, 0.2, or 0.5 mg/kg of selenite. Although selenium alone had no effect on the hepatic microsomal drug metabolism, simultaneous treatment of selenite (1 mg/kg) with bromobenzene resulted only an increase in the activity of aniline hydroxylase after 48 hr as compared to that in the bromobenzene-treated group. When rats were given 2.5, 10, and 20 ppm of selenite in drinking water daily for 4 weeks prior to an ip injection of 2.5 mmol/kg of bromobenzene and were sacrificed 48 hr after bromobenzene administration, a reduction in the SGOT activities in all the pretreated groups and a reduction of SGPT activity in 20 ppm selenite-treated group were observed when compared with those in the bromobenzene-treated groups. A dose-dependent increase in hepatic GSH concentrations were observed due to such chronic selenium treatment. Treatment with selenite (1 mg/kg) 24 hr prior to bromobenzene injection (2.5 mmol/kg) increased initially both o and p-bromophenols in the rat urine at 0-7.5 hr without affecting urinary thioethers. On the contrary, the ratio of thioethers to p-bromophenol was significantly higher in both 2.5 and 10 ppm selenite-pretreated (4 weeks) rats as well as a significant increase in the ratio of thioethers to total phenolic metabolites in 10 ppm and an increase close to significant in 2.5 ppm selenite-treated rats were observed initially at 0-7.5 hr urine samples. These results indicate that acute selenium pretreatment under certain conditions, favors increased hydroxylation of the intermediate bromobenzene epoxides, whereas higher detoxification of the epoxides involving hepatic glutathione (GSH)/GSH transferases pathway is more favored due to increased biosynthesis of GSH in certain chronic selenium treated rats.     

Lack of effect of selenium on induction of tumors of esophagus and bladder in rats by two nitrosamines

The effect of differences in level of dietary selenium on the induction of esophageal and bladder tumors in rats by two nitrosamines was investigated. Groups of 20 female F344 rats were given a synthetic diet containing less than 0.05 ppm Se to which selenium (as sodium selenite) was added at the concentration of 0.35, 0.7, 1.4 and 2.1 ppm selenium. These four groups, plus one without added Se, were treated with 20 ml per rat per day, 5 days a week, of a solution of nitrosomethylcyclohexylamine containing 5 mg/liter. A parallel five groups were treated in the same way with a solution of nitrosomethyl-3-carboxypropylamine in drinking water containing 600 mg per liter, as drinking water. Treatment lasted 28 weeks, at which time some animals had developed tumors. A group of 20 rats fed 0, 1.4 and 2.1 ppm Se was not treated with carcinogen. Rats consuming 1.4 ppm or 2.1 ppm Se gained weight more slowly than other groups. There was no significant difference in survival between the five groups treated with each carcinogen but receiving different dietary levels of selenium. Neither was there any significant difference between groups receiving each carcinogen in the incidence of tumors of the esophagus induced by nitrosomethylcyclohexylamine or of tumors of the urinary bladder induced by nitrosomethylcarboxypropylamine. Control rats on the synthetic diets did not survive as well as untreated rats eating regular chow diet. In these conditions there was no effect of dietary selenium levels on the induction of tumors in female rats by the two carcinogenic nitrosamines we used.     

Iron in neoplastic disease

Promotion of chemically induced esophageal cancer by ethanol may include the generation of highly reactive free radicals and thus may be preventable by the antioxidant vitamin E. In the present study, female C57BL/6 mice received N‐nitrosomethylbenzylamine (NMBzA, 0.2 mg/kg ig) three times a week for three weeks. After this esophageal carcinogenic treatment, mice were fed a nutritionally adequate liquid diet with 30% of the calories supplied by ethanol or an isocaloric carbohydrate with or without supplemental α‐tocopherol (142 mg/kg diet). As a marker of in vivo lipid peroxidation, exhaled ethane was collected and measured 24 hours “before”; the mice were killed after 20 weeks of dietary treatment. Hepatic malondial‐dehyde, lipid fluorescence, and conjugated dienes were determined as markers of products of lipid peroxidation and serum aminotransferases as indexes of liver toxicity. Hepatic liver concentrations of vitamins A and E and the size and frequency of esophageal tumors were also assessed. Ethanol consumption after NMBzA administration significantly increased (p < 0.05) the size and frequency of esophageal tumors. These ethanol‐promoted effects were accompanied by increases in indexes of in vivo and accumulated products of lipid peroxidation. Similarly treated animals that received supplemental dietary vitamin E showed significant reductions (p < 0.05) in mean tumor size and frequency of tumors as well as a decrease in the indexes of hepatic lipid peroxidation. The results suggest that promotion of NMBzA‐induced esophageal tumors by ethanol may in part result from increased lipid peroxidation and that vitamin E reduces carcinogenicity of NMBzA or ethanol promoter effects by inhibiting lipid peroxidation.     

茶叶对N—甲基苄基亚硝胺诱发大鼠食道肿瘤的影响

Five groups of rats were given different varieties of Chinese tea as drinking water and on additional two groups of rats were given water with or without N-nitrosomethylbenzylamine (NMBzA) as controls. Except the control group, all the animals were intubated with NMBzA (5 mg.kg-1/wk) for 6 or 12 weeks. After 6 weeks, the incidence of oesophageal mucosa lesions was significantly lower in the tea-treated rats (16-59%) than the control group with NMBzA (100%). After 12 weeks, the incidence of oesophageal tumor was also significantly lower in the tea-treated groups (42-67%) than the control group with NMBzA (90%). Similar results were obtained in the tumor size and the number of tumors developed. The anti-carcinogenic effects of the 5 varieties of Chinese tea were also not the same the Fujian Oolong tea and Jasmine tea had the strongest effect. The results suggest that Chinese tea can inhibit the carcinogenesis caused by N-nitroso compound.     

硒激活Nrf2对镉致小鼠肝脏氧化损伤保护作用的研究

摘要:目的　研究硒对镉暴露小鼠肝脏转录因子（Nrf2）表达的影响及其保护作用的机制。方法　60只ICR小鼠随机分为5组,对照组采用去离子水灌胃（10 ml/kg）,镉暴露组用氯化镉（7 mg/kg）灌胃,硒处理组分别采用不同浓度的亚硒酸钠（0.05、0.1、0.2 mg/kg）灌胃后用氯化镉（7 mg/kg）灌胃,30 d后颈椎脱臼处死。光镜下观察肝脏形态学变化,测定血清谷丙转氨酶（ALT）和血清谷草转氨酶（AST）、肝匀浆超氧化物歧化酶（SOD）、丙二醛（MDA）、活性氧（ROS）,蛋白印迹法（Western blot）检测肝脏Nrf2表达水平。结果　光镜观察镉暴露组小鼠肝脏结构形态有明显损伤,而硒处理组（0.2 mg/kg）小鼠肝脏形态损伤不明显。镉暴露组AST、ALT、MDA、ROS均高于对照组,有统计学意义（P＜0.05）,硒处理组（0.2 mg/kg）AST、MDA、ROS低于单独镉暴露组,差异有统计学意义（P＜0.05）。镉暴露组和硒处理组肝脏Nrf2的表达量均高于对照组,其中硒处理组Nrf2（0.1、0.2 mg/kg）的表达量明显高于镉暴露组（P＜0.05）。结论　硒可通过抑制ROS和上调Nrf2蛋白表达,对镉暴露小鼠肝脏的氧化损伤具有保护作用。     

不同硒水平饲料对大鼠肝脏谷胱甘肽过氧化物酶和脱碘酶活性的影响

为了解不同饲料硒水平对大鼠肝脏中谷胱甘肽过氧化物酶和脱碘酶活性的影响及确定它们发挥最佳活性时的最低饲料硒水平。５４只体重为５０～６０ｇ的雄性断孔Ｗｉｓｔａｒ大鼠分成９组，分别喂以９种含硒水平为０．０１，０．０２，０．０３，０．０４，０．０５，０．０６，０．１，０．２和５ｍｇ／ｋｇ的不同饲料。实验持续２０周。９组动物２０周的体重增长除５ｍｇ／ｋｇ饲料组与０．１、０．２ｍｇ／ｋｇ饲料组之间有差异外，其余均没有显著性差异。谷胱甘肽过氧化物酶的活性随着饲料硒水平的升高而升高，当饲料硒含量为０．１，０．２和５ｍｇ／ｋｇ饲料时，活性达到最高。因此它发挥正常活性范围的最低饲料硒需要量为０．１ｍｇ／ｋｇ。９个组脱碘酶的活性（ｎｍｏｌ／ｍｉｎ．ｇ）在０．０５至０．２ｍｇ／ｋｇ饲料时活性最高，在５ｍｇ／ｋｇ饲料时酶活性降低，发挥最佳活性最低饲料硒需要量为０．０５ｍｇ／ｋｇ。