氟对大鼠MDA含量、肝功及光镜结构的影响

目的研究不同浓度氟对大鼠丙二醛(MDA)含量、肝功及光镜结构的影响。方法在饮水中加入不同剂量的氟化钠喂饲大鼠1月后,测定血清氟含量、尿氟含量、肝组织中MDA含量、血清门冬氨酸氨基转移酶(AST)及丙氨酸氨基转移酶(ALT)的活力。结果与对照组相比,各剂量组大鼠血氟浓度相应增加,存在剂量-效应关系(R=0.884,P﹤0.01),但各剂量组间血氟浓度差异无统计学意义;各剂量组大鼠尿氟浓度相应增加,与对照组比较差异有统计学意义(P﹤0.01),存在剂量-效应关系(R=0.921,P﹤0.01);各剂量组大鼠MDA含量升高,与对照组比较差异有统计学意义(P﹤0.01),存在剂量-效应关系(R=0.797,P﹤0.01);各剂量组大鼠AST含量逐渐增加,与对照组比较差异有统计学意义(P﹤0.01),存在剂量-效应关系(R=0.889,P﹤0.01);各剂量组大鼠ALT含量逐渐增加,与对照组比较差异有统计学意义(P﹤0.01),存在剂量-效应关系(R=0.729,P﹤0.01);肝细胞光镜结构改变。结论过量氟可导致大鼠肝细胞发生脂质过氧化作用。     

氟对大鼠自由基、氧化应激及超微结构影响

目的 研究不同浓度氟对大鼠肝脏自由基和氧化应激及超微结构的影响.方法 在饮水中加入不同剂量的氟化钠喂饲大鼠1个月后,测定血清氟含量,肝组织中的一氧化氮(NO)、丙二醛(MDA)含量及谷胱甘肽过氧化物酶(GSH-Px)活性,并观察大鼠肝脏超微结构变化.结果 随染氟剂量的增加,1个月后各剂量组大鼠血氟浓度相应增加,存在剂量-效应关系(月=0.884,P<0.01),但各剂量组问血氟浓度差异无统计学意义;NO含量与对照组比较差异无统计学意义(P>0.05),但存在剂量-效应关系(R=0.361,P<0.05);各剂量组大鼠MDA含量升高,与对照组比较差异有统计学意义(P<0.01),存在剂量-效应关系(R=0.797,P<0.01);各剂量组大鼠GSH-Px活性下降,与对照组比较差异有统计学意义(P<0.01),存在剂量-效应关系(R=-0.912,P<0.01),特别是高氟剂量组MDA的含量最高,而GSH-Px活性最低;中、高剂量组大鼠肝细胞超微结构可见线粒体肿胀,有较多脂肪变性.结论 氟中毒可导致大鼠肝脏处于氧化应激状态、肝细胞超微结构改变.     

氟中毒大鼠血清中NO和MDA及GSH-Px的研究

[目的]研究不同浓度氟对大鼠血清自由基和氧化应激的影响。[方法]在饮水中加入含NaF(分析纯)10,20,40mg/kg的去离子水灌胃喂饲大鼠3月后,测定尿氟、血清氟含量、血液中的钙浓度。血清中的一氧化氮(NO)、丙二醛(MDA)及谷胱甘肽过氧化物酶(GSH-Px)的含量。[结果]随染氟剂量的增加,3月后各剂量组大鼠尿氟浓度相应增加,存在剂量-效应关系(R=0.914,P﹤0.01),与对照组相比有统计学差异(P﹤0.01);各剂量组血氟浓度相应增加,存在剂量-效应关系(R=0.930,P﹤0.01),与对照组相比有统计学差异(P﹤0.05);各剂量组大鼠血钙浓度相应下降,存在剂量-效应关系(R=-0.899,P﹤0.01),与对照组相比有统计学差异(P﹤0.01);各剂量组NO的含量相应增加,存在剂量-效应关系(R=0.951,P﹤0.01),与对照组相比有统计学差异(P﹤0.01);各剂量组MDA含量升高,存在剂量-效应关系(R=0.923,P﹤0.01),与对照组相比有统计学差异(P﹤0.05);各剂量组GSH-Px的活性下降,存在剂量-效应关系(R=-0.966,P﹤0.01),与对照组相比有统计学差异(P﹤0.05),特别是高氟剂量组NO及MDA的含量最高而GSH-Px的活性最低。[结论]慢性氟中毒可导致大鼠处于氧化应激状态。     

氟化物对原代培养大鼠肝细胞酶活力及超微结构的影响

目的研究不同剂量的氟化物对原代培养大鼠肝细胞存活率、酶活力及超微结构的影响。方法采用半原位胶原酶消化法分离大鼠肝细胞;MTT法检测细胞存活率;赖氏法检测培养液中谷草转氨酶(AST)和谷丙转氨酶(ALT)活性;透射电镜观察细胞超微结构改变。结果氟化钠染毒24小时后肝细胞存活率下降,且呈现明显的剂量-效应关系;2mmolL和4mmolL染氟组肝细胞培养液中ALT和AST的活性显著升高(P<005);透射电镜下染氟组肝细胞线粒体肿胀,内质网排列紊乱或断裂。结论过量氟化物对原代培养大鼠肝细胞有明显的毒作用,其主要作用方式是引起细胞膜和细胞器质膜损伤。     

核桃低聚肽对急性酒精性肝损伤大鼠保护作用

目的探讨核桃低聚肽(WOPs)对急性酒精性肝损伤大鼠的保护作用及其机制。方法雄性SD大鼠72只,随机分为6组:空白对照组、模型组、乳清蛋白组(220 mg/kg)和低、中、高剂量WOPs组(220、440、880 mg/kg)。灌胃给予WOPs,连续30 d,用体积分数为50%乙醇以7 g/kg剂量灌胃染毒,制备大鼠急性酒精性肝损伤模型。分离大鼠血清及肝组织,分别检测血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)和肝组织氧化应激相关指标还原型谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)和丙二醛(MDA)含量。结果与模型组比较,WOPs各剂量组大鼠精神状态及行为异常情况均有好转;与模型组比较,低、中、高剂量WOPs组大鼠血清转氨酶ALT活力[分别为(62.38±9.36)、(52.57±9.11)、(64.17±10.40)U/L]、AST活力[分别为(200.40±50.87)、(191.80±76.12)、(173.63±41.35)U/L]明显降低(P 0.05),中、高剂量WOPs组大鼠肝组织SOD活力[分别为(149.21±20.28)、(153.45±19.37)ng/L]、GSH-Px活力[分别为(138.82±9.93)、(146.99±15.05)IU/L]和GSH含量[分别为(568.15±67.31)、(571.61±74.98)ng/L]明显升高(P 0.05);与模型组比较,低、中、高剂量WOPs组大鼠肝脏脂质过氧化代谢产物MDA水平[分别为(3.83±0.56)、(3.62±0.47)、(3.94±0.24)nmol/L]明显下降(P 0.05)。结论 WOPs对酒精引起的大鼠急性肝损伤具有保护作用,其机制可能与抑制酒精引起的机体过度氧化应激反应和脂质过氧化水平,提高机体抗氧化能力有关。     

长期低剂量双酚A暴露对高脂喂养大鼠肝脏的影响

目的探讨长期低剂量双酚A(BPA)暴露对雄性大鼠肝脏的影响。方法将50只8周龄雄性Wistar大鼠随机分为普通对照组、高脂对照组、高脂饲料+低剂量BPA[10μg/(kg·d)]组、高脂饲料+中剂量BPA[50μg/(kg·d)]组和高脂饲料+高剂量BPA[250μg/(kg·d)]组,共5组。连续35周通过饮食途径给予大鼠BPA后,测定体质量、肝脏系数、体脂百分数,肝脏中甘油三酯、总胆固醇、丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)以及肝脏丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-Px)指标。结果高脂饲料组与普通饲料组血清中AST水平无差别,但高脂饲料组的血清中ALT水平明显高于普通饲料组(P0.01);此外,高脂饮食+高剂量BPA组大鼠血清中AST和ALT水平均明显高于高脂饲料组(P0.05),不同剂量的BPA对大鼠体质量、体脂百分数、肝脏中脂肪及MDA和GSH-Px均无明显影响(P0.05)。结论长期高剂量BPA暴露对高脂喂养雄性大鼠肝脏功能具有明显的损害作用。     

4种血清酶在三硝基甲苯染毒致大鼠肝损伤中的变化及意义

[目的]观察三硝基甲苯(TNT)染毒致大鼠肝损伤时血清乳酸脱氢酶(LDH)、谷氨酸氨基移换酶(ALT)、天门冬酸氨基移换酶(AST)和碱性磷酸酶(ALP)的活力变化情况,并探讨其意义。[方法]以50、100和200mg/kg体重剂量的TNT对大鼠每天一次经口染毒,分别于染毒2、4、6和8周后处死,测定血和肝组织TNT代谢产物2,6-二硝基-4-氨基甲苯(DNAT)水平、血靛青绿(ICG)10min滞留率(ICG_(R10))和血清LDH、ALT、AST、ALP的变化情况。[结果]TNT染毒大鼠血和肝组织DNAT均比对照组有明显升高,TNT染毒剂量与大鼠血清或肝组织DNAT呈显著性相关(P<0.01),血清与肝组织DNAT呈显著性相关(P<0.01);各TNT染毒组大鼠血清ICG_(R10)明显高于对照组。TNT高剂量染毒组大鼠血清LDH、ALT、AST和ALP活力有所降低,其他剂量组与对照组相比未见显著性变化;血清或肝组织DNAT与血清LDH呈显著性负相关(P<0.05或0.01),与ALT、AST和ALP均负相关,但未见显著性(P>0.05)。[结论]血清LDH、ALT、AST和ALP指标对TNT染毒诱导的大鼠肝损伤的反应并不敏感,似与TNT代谢产物DNAT对血清4种酶活力可能具有的一定抑制作用有关。     

海参岩藻聚糖硫酸酯对长期饮酒小鼠肝脏保护作用的研究

目的研究海参岩藻聚糖硫酸酯(SC-FUC)对长期饮酒导致的小鼠肝脏功能损伤的改善作用。方法从海地瓜(Acaudina molpadioides)中制备SC-FUC。将ICR小鼠随机分为4组:正常组、模型组以及SC-FUC低、高剂量组,每组12只。各组小鼠按0.08 ml/g bw灌胃受试物,1h后再灌胃白酒,每天一次,连续8w。实验结束后分别检测血清丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)活性,肝脏乙醇脱氢酶(ADH)、乙醛脱氢酶(ALDH)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性、丙二醛(MDA)、谷胱甘肽(GSH)含量以及肝脏中CYP2e1mRNA的表达量。结果 SC-FUC能显著降低小鼠血清ALT和AST活力(P<0.05),提高肝脏ADH、ALDH、GSH-Px活力(P<0.05)和GSH含量(P<0.05),降低MDA含量(P<0.05);降低肝脏中CYP2e1mRNA的表达量(P<0.05)。结论 SC-FUC对长期饮酒小鼠肝脏具有显著的保护作用。     

金属硫蛋白对镍铬联合染毒小鼠肝脏损伤的拮抗作用

目的研究硫酸镍+重铬酸钾联合染毒对小鼠肝脏损伤的影响及金属硫蛋白(MT)的拮抗作用。方法将50只健康SPF级昆明小鼠按体重随机分为5组,分别为溶剂对照组(生理盐水)、镍铬(1.0 mg/kg硫酸镍+0.5 mg/kg重铬酸钾)联合染毒组和低、中、高剂量MT保护(1.0 mg/kg硫酸镍+0.5 mg/kg重铬酸+5.0、10.0、20.0 mg/kg MT)组,每组10只,雌雄各半。采取灌胃方式进行染毒,染毒容量为10 ml/kg,每天1次,连续染毒21 d。检测小鼠丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、γ-谷氨酰转肽酶(GGT)活力及肝组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力和丙二醛(MDA)、谷胱甘肽(GSH)含量。结果与溶剂对照组比较,镍铬联合染毒组小鼠血清AST、ALT、GGT的活力均增高,差异均有统计学意义(P0.05)。各剂量MT保护组小鼠血清AST、ALT、GGT的活力均低于镍铬联合染毒组,差异均有统计学意义(P0.05);且随着MT染毒剂量的升高,MT保护组小鼠血清AST、ALT、GGT的活性均呈下降趋势。与溶剂对照组比较,镍铬联合染毒组小鼠肝组织SOD、GSH-Px活力和GSH含量均下降,而MDA含量升高,差异均有统计学意义(P0.05)。与镍铬联合染毒组比较,各剂量MT保护组小鼠肝组织SOD、GSH-Px活力和GSH含量均升高,而MDA含量均降低,差异均有统计学意义(P0.05),且随着MT染毒剂量的升高,MT保护组小鼠肝组织SOD、GSH-Px活力和GSH含量均呈上升趋势,而MDA含量呈下降趋势。结论 MT对镍铬联合染毒所致小鼠肝脏损伤有较好的拮抗作用,其作用机制可能与MT抗氧化作用有关。     

竹节参总皂苷对肢体缺血再灌注大鼠肝的影响

目的 探讨竹节参总皂苷(total rhizome panacis japonica saponins,tRPJS)预处理是否影响肢体缺血再灌注(I/R)大鼠肝脏自由基的变化,及是否对肝脏具有保护作用.方法 40只雄性健康成年SD大鼠,体重260～300 g,随机分为5组,每组8只:假手术组、I/R组、tRPJS不同剂量组(50,100,200 mg/kg).再灌注3h后经心室抽取血液2ml,进行丙氨酸转氨酶(ALT)、门冬氨酸转氨酶(AST)及乳酸脱氢酶(LDH)检测;取右肝叶进行一氧化氮(N0)、丙二醛(MDA)含量及诱导型一氧化氮合酶(iNOS)、超氧化物歧化酶(SOD)活性检测,光镜下观察肝组织形态学的变化.结果 与假手术组比较,I/R组NO、MDA含量和iNOS活力显著性增高,SOD活力则显著下降,血清ALT、AST、LDH明显升高(P＜ 0.05或0.01),光镜下肝细胞严重肿胀,甚至水变性.tRPJS组的NO、MDA含量和iNOS活力则明显下降,SOD活力增加,血清ALT、AST、LDH也明显下降(P＜ 0.05或0.01);肝细胞肿胀明显减轻.结论 肢体I/R能够导致急性肝损伤,竹节参总皂苷预处理可以明显减少肝脏组织中自由基的产生,降低NO、MDA含量,提高SOD活力,减轻再灌注肝损伤.     

氟砷联合作用对大鼠肝脏抗氧化能力的影响

采用亚慢性动物实验方法，研究了氟、砷及其联合作用对大鼠肝脏ＳＯＤ、ＧＳＨ－Ｐｘ活性及ＭＤＡ、－ＳＨ含量的影响。结果显示：各实验组大鼠肝脏ＭＤＡ含量无明显差别，但染氟组（１５０ｍｇ／Ｌ，ＮａＦ）和染砷组（７５ｍｇ／Ｌ，Ａｓ２Ｏ３）ＳＯＤ、ＧＳＨ－Ｐｘ活性和－ＳＨ含量明显地低于对照组和氟砷联合组，后两组之间ＳＯＤ、ＧＳＨ－Ｐｘ活性无明显差异，氟砷联合组的－ＳＨ含量低于对照组。提示：氟和砷均可使肝脏的抗氧化能力降低；氟与砷同时存在时（氟、砷毒物剂量比为２：１），对肝脏ＳＯＤ、ＧＳＨ－Ｐｘ活性和－ＳＨ含量的影响存在拮抗作用，但对－ＳＨ的拮抗影响较弱。由于氟和砷之间的拮抗效应，使其联合作用对肝脏抗氧化能力的影响低于单纯氟和单纯砷。     

The effect of progressive selenium deficiency on anti-glutathione peroxidase antibody reactive protein in rat liver

Liver glutathione peroxidase (GSH-Px, EC 1.11.1.9) activity decreases when weanling rats are fed a Se-deficient diet. To determine the effect of dietary Se deficiency on the concentration of the protein portion of GSH-Px, weanling rats were fed a Se-deficient (less than 0.02 ppm Se) or a Se-supplemented (0.2 ppm Se as Na2SeO3) 30% torula yeast-based diet and killed 0, 3, 7, 14, 21 or 28 d later. GSH-Px activity was assayed using H2O2, so only the Se-dependent GSH-Px was measured. Anti-GSH-Px antibodies, produced in a rabbit by three injections of purified rat liver GSH-Px, were used in an enzyme-linked immunosorbent assay for GSH-Px protein. Immunoblotting showed that the antibodies were highly specific for GSH-Px. In Se-supplemented rats, liver GSH-Px activity increased 66% and GSH-Px protein increased 50% over the 28 d. In Se-deficient rats, liver GSH-Px activity decreased exponentially to zero with a half-life of 2.8 d. Liver GSH-Px protein also decreased exponentially, but with a longer half-life of 5.2 d (P less than 0.001), and the anti-GSH-Px antibody-reactive protein did not decrease to zero. This experiment shows that both GSH-Px activity and GSH-Px protein decrease exponentially during progressive dietary Se deficiency. The longer half-life of GSH-Px protein compared with GSH-Px activity suggests that an inactive GSH-Px polypeptide is present in rat liver during the early stages of Se deficiency.     

山茶籽对去卵巢和非去卵巢雌性大鼠肝组织影响的实验研究

目的:通过观察山茶籽对去卵巢和非去卵巢雌性大鼠肝组织结构和功能的影响,为山茶籽在妇女疾病的防治和保健提供实验依据。方法:选取6月龄健康雌性大鼠80只,分成4组。对照组(Normal)、去卵巢模型组(OVX)、山茶籽+去卵巢组(Ts+OVX)和山茶籽+对照组(Ts+Normal)。Ts+OVX组和Ts+Normal组,用山茶籽醇提物水溶液灌胃,10 ml.kg-1.d-1(5 g生药/g),两个治疗组的连续用药12周。12周后,麻醉大鼠取左心血,处死后取肝脏。肝切片光镜观察肝组织形态结构,并对血清天门冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、白蛋白(A)和球蛋白(G);肝匀浆谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)和超氧阴离子自由基(O2-.)清除率进行测定,数据进行统计学分析。结果:与Normal组比较,两个治疗组肝体质量比、血清AST、ALT和A/G及肝匀浆GSH-Px、MDA和清除率差异无统计学意义(P>0.05),肝组织切片没有肝组织损害病理改变。结论:山茶籽醇提物对去卵巢和非去卵巢雌性大鼠没有肝损害作用。     

硒对氟中毒致大鼠肝脏损伤的干预作用

目的探讨硒对氟中毒致大鼠肝脏损伤的干预作用。方法以不同方式(先分别喂饲0.375、0.75和1.5mg/L亚硒酸钠溶液6个月,再喂饲50mg/L氟化钠溶液6个月或先饲喂50mg/L氟化钠溶液6个月,再分别饲喂0.375、0.75和1.5mg/L亚硒酸钠溶液6个月)喂饲大鼠,对大鼠肝脏进行组织病理学观察,并测定肝组织谷胱甘肽过氧化物酶(GSH-Px)及超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量及核转录因子κB(NF-κB)表达水平。结果 (1)预防组系列:与先水后氟(水—氟)对照组比,先低硒后氟组(低硒—氟)GSH-Px、SOD活力显著升高(P<0.05);先中硒后氟组(中硒—氟)GSH-Px活力显著升高(P<0.05);各先硒后氟组MDA含量均显著降低(P<0.05)。(2)治疗组系列:与先氟后水(氟—水)对照组比,先氟后低硒组(氟—低硒)和先氟后高硒组(氟—高硒)GSH-Px活力显著升高(P<0.05);先氟后中硒组(氟—中硒)SOD活力显著升高(P<0.05);各先氟后硒组MDA含量均显著降低(P<0.05)。结论硒对氟中毒致大鼠肝脏损伤有一定的干预作用,预防效果好于治疗效果,其中0.375mg/L是本实验条件下硒对慢性氟中毒致大鼠肝脏损伤的最佳预防作用浓度。     

Differential effects of konbu and nori seaweed dietary supplementation on liver glutathione status in normo- and hypercholesterolaemic growing rats

The effects of six balanced diets for 3 weeks on dietary intake, growth, liver weight and fat, plasma cholesterol, total antioxidant capacity, liver glutathione status and antioxidant enzymes in growing male Wistar rats were studied. Ten rats per group were fed casein- and soyabean-based diets with or without 2.4 % cholesterol-raising agent. Seven percent of the diet consisted of a cellulose-wheat starch mix (35:65; control diets), freeze-dried nori (nori diets) or konbu (konbu diets). The 7 % dietary supplement of seaweeds was well accepted and induced normal growth rates in rats. Except for food intake, total and reduced glutathione and total antioxidant capacity, dietary cholesterol addition significantly affected (at least P<0.05) all parameters studied. Alga consumption affected total and reduced glutathione, glutathione reductase activity, plasma cholesterol, and total and cholesterol-adjusted total antioxidant capacity (at least P<0.05). A significant cholesterol-alga interaction was found for liver weight, total glutathione peroxidase (GSH-Px) and the Se-dependent GSH-Px:total GSH-Px ratio (at least P<0.05). GSH-Px activity increased in cholesterol-fed nori rats mainly as Se-dependent GSH-Px, while in konbu and control groups the GSH-Px activity was related to increases in both non-Se-dependent and Se-dependent GSH-Px activities. The decrease in the antioxidant status of konbu rats was related to the high As content of this alga, which led to a compensatory increase in glutathione reductase activity in these animals. In conclusion, although some antioxidant compounds are present in algae, other dietary compounds, such as As, induced poor antioxidant status in rats.     

Hepatotoxic activity of toluene inhalation and protective role of melatonin

This study was designed to investigate the harmful effects of toluene inhalation in the liver of rats and possible protective effects of melatonin on these detrimental effects. For this purpose, 21 adult male Wistar-albino rats were randomly divided into three equal groups. Animals in group I were used as control. The rats in group II were exposed to toluene (3000 ppm/1 hour/day) for 4 weeks, while the rats in group III were treated with melatonin (10 mg/kg/day, intraperitoneally [ip]) plus toluene inhalation. At the end of the experimental period, liver and blood samples were taken from the decapitated animals. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin and albumin levels were determined. Liver tissue sections were stained with routine histological methods and examined under the light microscope. In addition, the sections were immunohistochemically stained using avidin-biotin-peroxidase method for determination of apoptosis. The liver tissue activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and malondialdehyde (MDA) levels were also measured. Toluene inhalation significantly increased serum ALT, AST and tissue MDA, and decreased serum albumin, but did not affect serum ALP, total bilirubin levels and tissue SOD, GSH-Px and CAT activity when compared with controls. The increases in tissue MDA and serum ALT and AST levels induced by toluene inhalation were significantly inhibited by melatonin treatment. In light microscopic observations of tissues from toluene-inhaled rats, massive hepatocyte degeneration, ballooning degeneration and mild pericentral fibrosis were observed. Bax immune reactivity was also increased significantly. Melatonin treatment decreased the balloon degeneration, fibrosis and Bax immune reactivity in the liver of toluene-inhaled rats. In view of the present findings, it is suggested that melatonin has hepatoprotective effects against toluene toxicity via primarily antioxidative properties.     

Glutathione peroxidase acitvity in intestinal and liver tissues of rats fed various levels of selenium, sulfur and alpha-tocopherol.

The effects of various levels of selenium, alpha-tocopherol and sulfur on glutathione peroxidase (GSH-Px) activity in intestinal and liver tissues were determined in male rats fed corn-soybean or Torula yeast diets. Rats fed corn-soybean diets had greater GSH-Px activity in the small intestine, colon and liver tissues, catalase activity and selenium in the liver, and body weight gains than those fed Torula yeast diets. GSH-Px activity in the small intestine, colon, and liver tissues as well as concentration of selenium in the liver increased with increasing levels of selenium in Torula yeast diets but not with corn-soybean diets. Tocopherol supplementation had no significant effect on GSH-Px activity in rats fed Torula yeast or corn-soybean diets supplemented with selenium. Supplemental sulfur decreased GSH-Px activity in the small intestine tissues and increased activity in colon tissues.     

氟砷染毒对大鼠子代肝脏氧化性损伤的研究

「目的」揭示氟、砷共存时对工健康的研究。「方法」采用两代一窝繁殖实验的方法，测定Ｗｉｓｔａｒ大鼠暴露于氟、砷后其子代肝脏中氟、砷的蓄积水平、脂质过化水平和抗氧化能力以及病理组织学检查。「结果」随着暴露剂量的增加肝脏中氟、砷含量显著增加，ＳＯＤ和ＧＳＨ－Ｐx活性随之降低，而ＬＰＯ含量地逐渐增加。肝脏的超微结构的出现病理变 化。停止氟、砷暴露８击后，肝脏中氟、砷含量显著降低，酶的生有所恢复，ＬＰＯ含量明     

Melatonin protects rat liver against irradiation-induced oxidative injury

The aim of this study was to investigate the antioxidant roles of different doses of melatonin (5 and 10 mg x kg (-1) ) against gamma-irradiation-caused oxidative damage in liver tissue after total body irradiation (TBI) with a single dose of 6.0 Gy. Fifty adult rats were divided into 5 equal groups, 10 rats each. Groups I and II were injected with 5 and 10 mg x kg (-1) of melatonin, and group III was injected with an isotonic NaCl solution. Group IV was injected with only 5 mg x kg (-1) of melatonin. Group V was reserved as a sham control. Following a 30-min-period, 6.0 Gy TBI was given to groups 1, 2 and 3 in a single fraction. The liver malondialdehyde (MDA) levels, super oxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were measured in all groups. TBI resulted in a significant increase in the liver tissue MDA levels and a decrease of SOD and GSH-Px activities. The results demonstrated that the liver tissue MDA levels in irradiated rats that were pretreated with melatonin (5 or 10 mg x kg (-1) ) were significantly decreased, while the SOD and GSH-Px activities were significantly increased. Decreasing the MDA levels by melatonin was dose dependent, but the liver tissue SOD and GSH activities were not. The data obtained in this study suggest that melatonin administration prior to irradiation may prevent liver damage by irradiation.