硒对高碘小鼠肝脏两种含硒酶的影响

目的:研究硒对高碘小鼠肝脏含硒酶的影响,探讨硒干预高碘危害的机制。方法:40只雌性Balb/c小鼠按体重随机分为4组:正常对照组(NC);高碘对照组(HI),饮用3.0mg/LI的高碘水;高碘+硒I组(HI+Se1),高碘水中补充0.5mg/LSe;高碘+硒II组(HI+Se2),高碘水中补充1.0mg/LSe。5个月后,观察甲状腺病理变化,测定血清总T4(TT4)、总T3(TT3)、反式T3(rT3)水平以及肝脏硒含量、谷胱甘肽过氧化物酶(GSH-Px)活性、1型脱碘酶(DI-1)活性及mRNA表达。结果:高碘组小鼠出现了弥漫胶质性甲状腺肿;与正常对照组相比,高碘组的血清TT4水平显著升高,TT3水平显著降低;而补硒可显著抑制TT4的升高和TT3的降低;高碘组肝脏硒含量降低,MDA含量显著升高,GSH-Px和DI-1活性分别降低了47%和33%,DI-1mRNA的表达也下调。而两个补硒组能显著升高肝硒含量,增强GSH-Px活性以及DI-1活性和表达,其中以0.5mg/L的硒剂量作用最为明显。结论:适当剂量的硒可通过影响含硒酶的活性和mRNA的表达来发挥对高碘危害的干预作用。     

硒与人体健康

本文着重综述了微量元素硒的功能及对人体健康的影响、硒相关疾病与临床应用现状，并介绍了硒缺乏与硒中毒研究进展。     

陕南安康地区大竹园镇砷中毒患者血清PICP、PINP与COL1α1序列检测

目的 研究陕南安康地区大竹园镇高砷高氟高硒地区的砷皮肤损伤患者体内Ⅰ型胶原代谢状况.方法 采用病例对照研究,选取安康大竹园镇燃高砷高氟高硒石煤区29例砷皮肤损伤患者为病例组,西安市非砷中毒区30例为对照组.用石墨炉原子吸收光谱法测定砷和硒含量.氟离子选择性电极法测定氟含量,ELISA检测血清中Ⅰ型前胶原羧基前肽(PICP)和Ⅰ型前胶原氨基前肽(PINP)的含量,高保真PCR扩增-美国ABI3100测序仪作正反向直接测序检测Ⅰ型胶原α1多肽链(COL1α1)碱基突变.结果 在偏相关分析中控制其他影响因素后,PICP与血清氟呈弱负相关r=-0.4,P≤0.05),PINP与发氟呈中度负相关(r=-0.5,P<0.05),与发硒呈中度正相关(r=0.5,P<0.05).但血清PICP、PINP与COL1α1序列在病例组和对照组间无统计学显著性差异(P>0.05).结论 发氟和发硒是影响PINP代谢的主要影响因素,且发氟升高可使PINP降低而发硒升高町使PINP增高.但在陕南安康地区大竹园镇砷、氟和硒三元素联合性增高地区的砷皮肤损伤患者体内的PICP、PINP含量和Ⅰ型胶原α1基因序列却无显著性改变.提示在该地区,发硒增高引起PINP的升高可能抑制了由发氟升高引起PINP的降低.     

锌、硒对砷诱导金属硫蛋白合成影响的研究

目的:探讨锌、硒对砷诱导金属硫蛋白合成的影响。方法:采用亚慢性毒性实验方法,分别测定小鼠肝脏中金属硫蛋白(MT)、丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活力。结果:砷低剂量组、单纯锌组和单纯硒组肝脏MT含量升高,高于对照组和砷高剂量组(P<0.05)。随着砷染毒剂量的增加,小鼠肝脏组织中MDA含量增加,SOD、GSH-Px活性降低,且呈剂量-效应关系。结论:亚砷酸钠能够诱导小鼠产生金属硫蛋白,金属硫蛋白含量与抗氧化能力存在相关性,锌、硒能抑制MDA生成量,提高SOD、GSH-Px活性,增加抗氧化能力,从而拮抗砷毒性。     

硒和砷对HepG2细胞氧化应激和DNA氧化损伤及修复的作用

目的研究硒和砷单独及联合作用对HepG2细胞氧化应激和DNA氧化损伤及修复的影响。方法采用不同浓度的硒(2.5、5.0和10.0μmol/L亚硒酸钠)和砷(1.56、3.13、6.25、12.5和25.0μmol/L亚砷酸)为受试物单独或联合处理HepG2细胞。荧光法测定丙二醛(MDA)作为氧化应激的指标,高效液相色谱-电化学检测法(HPLC-EC)测定8-羟基鸟苷(8-OHdG)作为DNA氧化损伤的指标,Western Blot检测hOGG1表达作为DNA氧化损伤修复的指标。结果在硒和砷单独作用的条件下,可观察到:(1)5.0、10.0μmol/L的亚硒酸钠和6.25、12.5、25.0μmol/L的亚砷酸均引起HepG2细胞MDA含量增加、8-OHdG生成增多、hOGG1表达明显下降(P<0.05,P<0.01);(2)较低浓度的亚硒酸钠(2.5μmol/L)具有有限的抑制8-OHdG生成的作用(P>0.05)。在硒和砷联合作用的条件下,可观察到:(1)2.5μmol/L的亚硒酸钠和6.25μmol/L的亚砷酸同时染毒使MDA含量和8-OHdG的生成均较相应砷剂量组下降(P<0.05);(2)2.5μmol/L的亚硒酸钠与6.25、12.5和25.0μmol/L的亚砷酸同时染毒,hOGG1表达与相应砷剂量组比较没有明显差异(P>0.05)。结论5.0、10.0μmol/L的亚硒酸钠和6.25、12.5、25.0μmol/L的亚砷酸均可引起HepG2细胞氧化应激增强、8-OHdG生成增多、hOGG1表达明显下降;一定剂量的硒(2.5μmol/L的亚硒酸钠)对砷诱导的HepG2细胞氧化应激和DNA氧化损伤具有抑制作用,但对砷所致的DNA氧化损伤修复不产生明显影响。     

硒酸酯多糖辅助癌症化疗的临床观察

 对64例Ⅱ－Ⅳ癌症患者，采用随机对照分组(化疗＋硒组，单化组)，观察硒酸酯多糖在化疗期间的辅助效应。结果：化疗加硒组，骨髓毒性低于单纯化疗组，化疗期间感染率低于单化组，但无统计学意义，免疫球蛋白、食欲均优于单化组(P<0.01，P<0.05)有统计学意义，说明硒酸酯多糖在化疗中对机体正常组织有保护作用。     

硒酵母中硒的化学形态分析与评价

 利用Ｔｒｉｓ－缓冲液－甘油提取法对硒酵母的化学形态进行了分析，并与透析法进行比较。结果表明，经过特殊工艺生产的硒酵母虽然总硒含量达到４０００μｇ／ｇ以上，但其中５０％以上的硒为硒蛋氨酸形态的蛋白质或其它大分子态硒，无机态硒仅占３％左右，而游离态硒只占０．０１％。说明硒酵母有广阔的开发前景，同时也为硒制剂提供了适宜的质量监测方法。     

Hypothesis: Iodine, selenium and the development of breast cancer

Background: In this paper we examine some of the evidence linking iodine and selenium to breast cancer development. Seaweed is a popular dietary component in Japan and a rich source of both of these essential elements. We hypothesize that this dietary preference may be associated with the low incidence of benign and malignant breast disease in Japanese women. In animal and human studies, iodine administration has been shown to cause regression of both iodine-deficient goiter and benign pathological breast tissue. Iodine, in addition to its incorporation into thyroid hormones, is organified into anti-proliferative iodolipids in the thyroid; such compounds may also play a role in the proliferative control of extrathyroidal tissues. Selenium acts synergistically with iodine. All three mono-deiodinase enzymes are selenium-dependent and are involved in thyroid hormone regulation. In this way selenium status may affect both thyroid hormone homeostasis and iodine availability. Conclusion: Although there is suggestive evidence for a preventive role for iodine and selenium in breast cancer, rigorous retrospective and prospective studies are needed to confirm this hypothesis.     

Serum tocopherols, selenium and lung cancer risk among tin miners in China

Objective: To evaluate the association of prediagnostic serum antioxidants and lung cancer risk we conducted a case–control study nested in an occupational cohort of tin miners. Methods: Male workers free of cancer enrolled in the cohort. During up to 6 years of follow-up, 339 lung cancer cases were diagnosed and, among these cases, those who donated blood prospectively (n = 108) were eligible for this study. For each case, two controls alive and free of cancer at the time of case diagnosis were matched on age and date of blood collection. Results: Overall, we observed no association between serum alpha-tocopherol, gamma-tocopherol or selenium levels and lung cancer risk. However, a significant gradient of decreasing lung cancer risk with increasing serum alpha-tocopherol was apparent for men less than 60years old (odds ratio by tertile: 1.0, 0.9, 0.2; trend p = 0.002). Alpha-tocopherol was also protective in men who reported no alcohol drinking (OR by tertile: 1.0, 0.6, 0.3; trend p = 0.008). Conclusion: Although there were no significant overall associations between prospectively collected serum alpha-tocopherol, gamma-tocopherol or selenium and incidence of lung cancer, results from this study suggest that higher alpha-tocopherol levels may be protective in men less than 60 years old and in those who do not drink alcohol.