复印作业对人体氧化和过氧化的影响

目的探讨复印作业对人体氧化和过氧化的影响。方法检测１０４例复印作业者和１００例健康成人血浆ＶｉｔＣ、ＶｉｔＥ、β－胡萝卜素（β－ＣＡＲ）、过氧化脂质（ＬＰＯ）含量及红细胞超氧化物歧化酶（ＳＯＤ）、过氧化氢酶（ＣＡＴ）、谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活力和ＬＰＯ含量。结果与健康成人组比较，复印作业组的血浆ＶｉｔＣ、ＶｉｔＥ、β－ＣＡＲ和红细胞ＳＯＤ、ＣＡＴ、ＧＳＨ－Ｐｘ平均值皆显著降低（Ｐ＜０．０１），而血浆及红细胞ＬＰＯ平均值明显升高（Ｐ＜０．０１），３种不同机型复印作业组各指标平均值间皆差异无显著性（Ｐ＞０．０５），配备通风装置组与未配备通风装置组各指标平均值间差异皆有显著性（Ｐ＜０．０１），复印作业工龄与各指标间均呈一定程度的直线相关（Ｐ＜０．０２～０．０００１）。结论复印从业人员体内氧化和过氧化反应加剧     

硒酸酯多糖对化疗致癌症患者脂质过氧化的拮抗作用

为了解硒酸酯多糖对肿瘤患者体内过氧化脂质（ＬＰＯ）及谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性的影响，对６０例肿瘤病人随机分成三组：不服硒组、服硒４００μｇ／ｄ组及８００μｇ／ｄ组，并与１５名正常人对照比较。结果为癌患者血清ＬＰＯ明显高于正常人（Ｐ＜０．０１），血清Ｓｅ明显低于正常人（Ｐ＜０．０１），而全血ＧＳＨ含量及ＧＳＨ－Ｐｘ活性明显低于正常人（Ｐ＜０．０５）。服硒酸酯多糖者化疗后血清Ｓｅ较不服者明显升高（Ｐ＜０．０５），ＧＳＨ及ＧＳＨ－Ｐｘ活性明显升高（Ｐ＜０．０１，Ｐ＜０．０５），而ＬＰＯ含量显著下降（Ｐ＜０．０５）。服硒酸酯多糖４００μｇ／ｄ组与８００μｇ／ｄ组之间上述各指标均无明显差异。提示肿瘤病人摄入适量（４００μｇ／ｄ）硒酸酯多糖可增加体内ＧＳＨ－Ｐｘ活性，减轻化疗药物对正常细胞的过氧化损伤。     

补硒对低硒居民血小板活化状态的影响

应用１２５Ｉ标记放免法测定血浆血栓素（ＴＸＡ２）、前列环素（ＰＧＩ２）和血小板ＴＸＡ２生成，以比浊法和ＥＬＩＳＡ分别测定血小板聚集性和β－血小板球蛋白（βＴＧ），电镜观察血小板形态，对比研究补硒（２００μｇＳｅ／ｄ，亚硒酸钠，１２周）和未补硒低硒居民上述参数的变化。用２，３－二氨基萘荧光法和谷胱甘肽还原酶偶联法测定硒含量和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性。结果表明，补硒使红细胞硒和ＧＳＨ－Ｐｘ活性显著增高（Ｐ＜０．０１）；血浆ＴＸＡ２、ＴＸＡ２／ＰＧＩ２比值及血小板ＴＸＡ２生成和聚集性均显著低于未补硒组（Ｐ＜０．０１或０．０５），但血浆ＰＧＩ２和βＴＧ含量以及血小板βＴＧ含量和释放率无显著改变（Ｐ＞０．０５）；补硒可明显减轻病区低硒居民血小板的形态变化，使α－颗粒数显著高于未补硒组（Ｐ＜０．０１）；红细胞硒或ＧＳＨ－Ｐｘ活性分别与血浆ＴＸＡ２和血小板ＴＸＡ２生成呈显著负相关（ｒ＝－０．６９６，－０．７８０；－０．６７６和－０．７９６，Ｐ＜０．０１），与ＡＤＰ诱导的血小板聚集性显著负相关（ｒ＝－０．３９０，－０．３７２，Ｐ＜０．０５）；与凝血酶诱导的聚集性呈不显著的负相关（ｒ＝－０．２７９，－０．３０９?     

析因设计在Cu和VE对CCl4所致肝损伤的联合保护作用中的应用

利用两因素多水平析因试验设计，按Ｃｕ（０，０．０５，０．１，０．２，０．４ｍｇ／ｋｇ）和ＶＥ（０，１５０ｍｇ／ｋｇ）将６０只大鼠随机分成１０组，按组合条件饲养，７天后腹腔注射ＣＣｌ４，从血清酶学和组织酶学方面，探讨微量元素Ｃｕ和ＶＥ对ＣＣｌ４所致肝损伤的保护作用。结果表明：对ＳＯＤ、ＧＰＴ、ＧＯＴ３项指标单独Ｃｕ组和单独ＶＥ组与ＣＣｌ４组比较均有显著性差异（Ｐ＜０．０１），说明Ｃｕ和ＶＥ都对ＣＣｌ４所致肝损伤有保护作用。但对Ｃｕ来说，保护效果并不随剂量的增加而增强。同时，Ｃｕ和ＶＥ具有联合保护作用（Ｐ＜０．０１），当ＶＥ用量为１５０ｍｇ／ｋｇ时，Ｃｕ的用量为０．１ｍｇ／ｋｇ，取得最优保护效果     

硒的化学形态对大鼠肝T45‘—脱单碘酶活力的影响

用低硒地区施硒肥（Ｎａ２ＳｅＯ３）粮饲料（Ｓｅ０．１００ｍｇ／ｋｇ）和硒含量相近的补硒（Ｎａ２ＳｅＯ３）粮饲料（Ｓｅ０．０９９ｍｇ／ｋｇ）分别喂养大鼠８周，观察不同化学形态硒对动物肝Ｔ４５＇－脱单碘酶（ＩＤ－Ｉ）活力、肝含量及血谷胱甘肽地氧化物酶（ＧＳＨ－Ｐｘ）活力的影响。结果表明，硒肥粮组与补硒粮组相比较，肝ＩＤ－Ｄ活性明显高（Ｐ＜０．０１），肝硒含量亦主同，但没有显著意义，而血ＧＳＨ－Ｐｘ活力     

大豆磷脂合剂对大鼠血清、组织脂质水平和脂质过氧化及脂肪肝的影响

大豆磷脂合剂（大豆磷脂和ＶＥ按一定比例混合）５０ｍｇ·Ｃａｐｉｔａ（－１）·ｄ（－１）饲喂实验性高脂血症和脂肪肝大鼠四周。可使大鼠血清总胆固醇（ＴＣ）、血清脂质过氧化物（ＬＰＯ）、肝脏脂质过氧化物（肝ＬＰＯ）、肝脏和主动脉壁胆固醇和甘油三酯含量（肝ＣＨ、肝ＴＧ，主动脉ＣＨ，主动脉ＴＧ）明显减少（Ｐ＜０．０１）；血清高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）水平升高（Ｐ＜０．０１）；肝脏脂肪变性程度减轻（Ｐ＜０．０１）。实验结果提示：大豆磷脂合剂具有降低血脂、促进脂肪肝恢复和延缓血清和组织脂质过氧化的生物学作用。     

β-胡萝卜素和核黄素对大鼠脂质过氧化的影响

目的：进一步探讨亚硝胺通过脂质过氧化而致癌的可能途径,以及研究β－胡萝卜素（β－Ｃ）和核黄素（ＶＢ２）通过抑制脂质过氧化反应而影响亚硝胺致癌的可能途径。方法：将５０只二级ＳＤ雄性大鼠随机分成５组。实验组在每日灌胃二甲基亚硝胺（ＮＤＭＮ）１．７５ｍｇ／ｋｇ的基础上,每日分别给予β－Ｃ２５ｍｇ／ｋｇ和／或ＶＢ２１８ｍｇ／ｋｇ补充,实验期为２８天。实验结束时,收集血液,摘取肝脏和肾脏,测红细胞和肝肾匀浆ＳＯＤ活性,全血ＧＳＨ－Ｐｘ活性,血清和肝肾匀浆ＭＤＡ含量,血清ＲＯＯＨ以及全血Ｈｂ含量。结果：１．ＮＤＭＮ可使ＳＯＤ和ＧＳＨ－Ｐｘ活性下降（Ｐ＜０．０５）,ＭＤＡ和ＲＯＯＨ产生增多（Ｐ＜０．０５）。２．添加β－Ｃ后,ＳＯＤ和ＧＳＨ－Ｐｘ活性有明显提高（Ｐ＜０．０５）,ＭＤＡ和ＲＯＯＨ的含量明显降低（Ｐ＜０．０５）。３．添加ＶＢ２后,肝ＳＯＤ和全血ＧＳＨ－Ｐｘ活性均有明显提高（Ｐ＜０．０５）,但ＭＤＡ和ＲＯＯＨ的含量没有差异（Ｐ＞０．０５）。４．同时补充β－Ｃ和ＶＢ２后,各项指标的变化与单纯β－Ｃ组基本一致。结论：脂质过氧化也是亚硝胺致癌的途径之一;一定剂量的β－Ｃ可对抗ＮＤＭＮ引发的脂质过氧化;核黄素对提高抗氧化?     

矽肺与NO、氧化及脂质过氧化关系的探讨

目的探讨矽肺与ＮＯ及氧化和脂质过氧化的关系。方法检测７３例矽肺患者和６０例健康对照者的血浆ＮＯ、ＶｉｔＣ、ＶｉｔＥ、β胡萝卜素（βＣＡＲ）、过氧化脂质（ＬＰＯ）含量及红细胞超氧化物歧化酶（ＳＯＤ）、过氧化氢酶（ＣＡＴ）、谷胱甘肽过氧化物酶（ＧＳＨＰｘ）活力和ＬＰＯ含量。结果与对照组比较,矽肺组的血浆ＶｉｔＣ、ＶｉｔＥ、βＣＡＲ含量及红细胞ＳＯＤ、ＣＡＴ、ＧＳＨＰｘ活力显著降低,血浆ＮＯ、ＬＰＯ含量及红细胞ＬＰＯ含量显著升高（Ｐ＜０．０５或Ｐ＜０．０１）;各检测值与病程均有相关;血浆ＮＯ、ＶｉｔＥ含量及红细胞ＳＯＤ活力、ＬＰＯ含量与病程相关最密切。结论矽肺患者体内的ＮＯ代谢异常,氧化和脂质过氧化反应病理性加剧。     

硒多糖、亚硒酸钠对大鼠血硒浓度和肝细胞色素P_(450)单加氧酶系的影响

研究了一次和连续７天腹腔注射硒多糖、亚硒酸钠对大鼠血硒浓度及肝细胞色素Ｐ４５０、ｂ５、ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶、谷胱甘肽硫转移酶（ＧＳＴ）和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）的影响；并比较了硒多糖与亚硒酸钠的作用。结果表明：一次腹腔注射Ｓｅ０．６ｍｇ／ｋｇ体重的硒多糖和亚硒酸钠后，血硒浓度迅速增加，在注射后２小时血硒浓度达到高峰，随后血硒浓度逐渐下降。亚硒酸钠在大鼠体内的吸收和排出均较硒多糖快。连续７天腹腔注射０．２ｍｇ／ｋｇ体重剂量硒多糖和亚硒酸钠后，硒多糖和亚硒酸钠组大鼠血硒浓度分别为对照组的２．６倍和２．１倍，其中硒多糖组的血硒含量显著高于亚硒酸钠组（Ｐ＜０．０５）；硒多糖和亚硒酸钠在体内、外均降低肝细胞色素Ｐ４５０、ｂ５的含量，抑制ＧＳＴ的活性，硒多糖的作用尤为显著，分别为对照组的５７％、７０％和６２％（Ｐ＜０．０５）。两种硒化合物对ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶无明显影响。硒多糖和亚硒酸钠均能显著增强ＧＳＨ－Ｐｘ的活性（Ｐ＜０．０５）。     

尘肺患者血清β－胡萝卜素与抗氧化功能的研究

本研究测定了尘肺病人、慢性支气管炎（慢支）病人及健康成人的血清β－胡萝卜素（ＢＣ）和ＶｉｔＡ含量以及血清脂质过氧化酶（ＬＰＯ）含量，超氧化物歧化酶（ＳＯＤ）和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ活性。结果发现，尘肺组血清ＢＣ含量明显低于健康组和慢支组（Ｐ＜０．０１）。而血清ＶｉｔＡ含量３个组相近（Ｐ＞０．０５）。与健康组和慢支组比较，尘肺组血ＬＰＯ含量明显升高，ＳＯＤ和ＧＳＨ－Ｐｘ活性则明显降低（Ｐ均＜０．０ｌ）。上述结果提示，尘肺病人抗氧化功能明显减弱可能与血清ＢＣ含量较低有关。     

硒和维生素E对喂克山病病区粮大鼠胰岛素、C肽水平的影响及其发生机制

饲以克山病病区粮对大鼠胰岛B细胞分泌功能的影响及补充硒和维生素E(VE)的保护作用研究结果表明,病区粮组大鼠血清胰岛索、C肽水平显著下降,胰岛B细胞C肽分泌贮备减少,胰腺谷胱甘肽过氧化物酶(GSH-Px)活力明显降低,脂质过氧化物(LPO)含量升高。在病区粮内分别加入0.44mg/kg亚硒酸钠和500mg/kg VE及联合补充上述剂量硒和VE可明显提高血清胰岛素、C硒水平,增加C肽分泌贮备,升高胰腺GSH-Px活力及降低LPO含量。此结果提示,克山病病区粮可引起大鼠胰岛B细胞功能受损,胰岛素分泌不足,此改变在克山病时可能成为加重心肌损害的原因之一。     

硒和维生素E对大鼠糖尿病易感性的影响

目的 :　观察硒 ( Se)和维生素 E( VE)对糖尿病 ( DM)易感性的影响。方法 :　应用膳食低 Se复加注射链脲佐菌素 ( STZ)法制成大鼠 DM模型 ,补充一定剂量的 Se和 (或 ) VE,观察对大鼠 DM易感性的影响。结果 :　膳食低 Se、低 VE可明显增加大鼠 DM易感性 ,表现为血清 C肽水平和胰岛 C肽分泌贮备显著降低 ,血糖明显升高 ,并可显著增加 DM大鼠死亡率。在膳食中联合补充 0 .2 mg Se、50 0 mg VE/ kg,明显增加了 DM大鼠血清和胰岛 C肽含量、降低 DM大鼠血糖水平 ,亦使 DM大鼠死亡率显著降低。结论 :　在 DM亚临床状态下 ,联合补充适量 Se和 VE可改善胰岛内分泌细胞代谢偏移及功能紊乱 ,拮抗致病因素的胰岛损伤效应 ,降低 DM易感性。     

硒和维生素E对胰岛细胞保护作用的研究

目的　观察膳食硒 ( Se)、维生素 E( VE)水平对糖尿病中间性状——胰岛β细胞合成及分泌胰岛素功能的影响 ,探讨其对糖尿病 ( DM)易感性的作用。方法　用低 Se膳食造成大鼠低 Se模型 ,再应用链脲佐菌素 ( streptozotocin,STZ)诱导成 DM模型 ,结合放免技术观察胰岛功能的变化。结果　低 Se、低 VE大鼠对 DM易感性明显增强 ,表现为血清胰岛素水平明显降低 ,胰岛素分泌贮备显著减少 ,血清果糖胺水平明显升高。分别或联合补充 0 .2 mg Se及 50 0 mg VE/kg饲料可程度不同地提高血清胰岛素水平及其分泌贮备 ,降低血清果糖胺含量 ,其中联合补充 Se和VE的生物学效应最佳。结论　DM发作前 ,Se和 VE的联合生物学效应 ,可拮抗 DM致病因素引起的胰岛损害 ,具有重要的胰岛细胞保护作用     

Antioxidant effect of vitamin E and selenium on hepatotoxicity induced by dimethoate in female adult rats

Acute exposure to pesticides can cause hepatotoxicity. Our study pertains to the potential ability of selenium and/or vitamin E, used as nutritional supplements, to alleviate oxidative stress induced by dimethoate. Female Wistar rats were randomly divided into seven groups of six each: group I served as controls; group II received in their drinking water dimethoate (2 g L⁻¹); group III received both dimethoate and selenium (0.5 mg/kg of diet); group IV was treated with dimethoate and vitamin E (100 mg/kg of diet); group V received dimethoate+selenium+vitamin E and groups VI and VII received either selenium or vitamin E. The exposure of rats to dimethoate for 30 days promoted oxidative stress with an increase in malondialdehyde and a decrease in glutathione and non-protein thiol levels. A decrease in glutathione peroxidase, superoxide dismutase and catalase activities was also observed. While, plasma transaminases, lactate dehydrogenase activities and bilirubin levels increased. Co-administration of selenium and/or vitamin E through diet improved the biochemical parameters cited above. Liver histological studies confirmed biochemical parameters and the beneficial roles of selenium and vitamin E.     

硒和维生素E缺乏对大鼠胰腺腺泡功能的影响

饲予大鼠克山病病区粮引起血清淀粉酶与脂肋酶活性阵低，胰腺腺泡合成淀粉酶与脂肪酶的能力减弱，并伴有胰腺ＧＳＨ－Ｐｘ活力明显下降，ＬＰＯ合量升高，硒含量明显减少。在病区粮中补一定剂量晒或ＶＥ可明显提高血清淀粉酶与脂肪酶活性，增加肽腺腺泡淀粉酶与脂肪酶的合成，同时使ＧＳＨ－Ｐｘ活力升高，ＬＰＯ含量降低。此结果提示，克山病病区粮中的致病因素可引起胰腺外分泌功能的原发性损害，其机制可能与晒和ＶＥ缺乏有关。     

Inhibition of 7,12‐dimethylbenz[a] anthracene‐induced lipid peroxidation and mammary tumor development in rats by vitamin e in conjunction with selenium

The effects of combined dietary vitamin E supplementation and a relatively low increase in selenium levels on 7,12‐dimethylbenz[a]anthracene (DMBA) induction of lipid peroxidation in the short term and development of mammary tumors in the long term were investigated in female Sprague‐Dawley rats. Control animals were fed the basal diet (20 mg/kg vitamin E and 0.6 mg/kg selenium) throughout the experiment. Three other groups received a high vitamin E diet (235 mg/kg vitamin E and 0.6 mg/kg selenium) at different times, the first two from three weeks after DMBA treatment and the other throughout the experiment. When the vitamin E diet with selenium supplementation was applied until three weeks after DMBA or until the termination of the experiment, tumor yields (tumors per rat) were significantly inhibited compared with the control group. On the other hand, delaying the supplementation of vitamin E until three weeks postcarcinogen produced no prophylactic effect. The elevation of lipid peroxidation levels observed immediately after DMBA administration was also significantly inhibited in both mammary fat pads and livers of animals in the high vitamin E group. It was therefore concluded that the inhibitory effect of vitamin E in combination with selenium on tumorigenesis might be causally related to reduction of carcinogen treatment associated with lipid peroxidation, the latter presumably playing an important role in DMBA‐induced mammary carcinogenesis.     

Inhibition of 7,12-dimethylbenz[a]anthracene-induced lipid peroxidation and mammary tumor development in rats by vitamin E in conjunction with selenium.

The effects of combined dietary vitamin E supplementation and a relatively low increase in selenium levels on 7,12-dimethylbenz[a]anthracene (DMBA) induction of lipid peroxidation in the short term and development of mammary tumors in the long term were investigated in female Sprague-Dawley rats. Control animals were fed the basal diet (20 mg/kg vitamin E and 0.6 mg/kg selenium) throughout the experiment. Three other groups received a high vitamin E diet (235 mg/kg vitamin E and 0.6 mg/kg selenium) at different times, the first two from three weeks after DMBA treatment and the other throughout the experiment. When the vitamin E diet with selenium supplementation was applied until three weeks after DMBA or until the termination of the experiment, tumor yields (tumors per rat) were significantly inhibited compared with the control group. On the other hand, delaying the supplementation of vitamin E until three weeks postcarcinogen produced no prophylactic effect. The elevation of lipid peroxidation levels observed immediately after DMBA administration was also significantly inhibited in both mammary fat pads and livers of animals in the high vitamin E group. It was therefore concluded that the inhibitory effect of vitamin E in combination with selenium on tumorigenesis might be causally related to reduction of carcinogen treatment associated with lipid peroxidation, the latter presumably playing an important role in DMBA-induced mammary carcinogenesis.     

Low-protein diets reduce PKAalpha expression in islets from pregnant rats

We investigated the effect of protein restriction on insulin secretion and the expression of protein kinase (PK)Aalpha and PKCalpha in islets from control and pregnant rats. Adult control nonpregnant (CN) and control pregnant (CP) rats were fed a normal-protein diet (17%), whereas low-protein nonpregnant (LPN) and low-protein pregnant (LPP) rats were fed a low-protein diet (6%) for 15 d. In the presence of 2.8 and 8.3 mmol glucose/L, insulin secretion by islets of CP rats was higher than that by islets of CN rats. Compared with the CN groups, insulin secretion by islets of LPN rats was lower with 8.3 but not with 2.8 mmol glucose/L. The insulin secretion by islets of LPP rats was higher than by LPN rats at both glucose concentrations. IBMX (1 mmol/L), a phosphodiesterase inhibitor, increased insulin secretion by islets from pregnant rats, and this effect was greater in islets of CP rats than in LPP rats. Forskolin (0.01-100 micromol/L), a stimulator of adenylyl cyclase, increased insulin secretion only in islets of CN and CP rats, with a higher 50% effective concentration in islets of CP rats compared with CN rats. The insulin secretion induced by phorbol 12-myristate 13-acetate (a stimulator of PKC) was higher in islets of LPN and LPP rats than in the respective controls, especially at 8.3 mmol glucose/L. PKAalpha, but not PKCalpha, expression was lower in islets of rats fed low protein than in the controls, regardless of the physiological status of the rats. All endocrine cells of the islets, including beta-cells, expressed the PKAalpha isoform. The cytoplasmic distribution of this enzyme in beta-cells was not modified by pregnancy and/or protein restriction. In conclusion, our results indicate that the response of islets from rats fed low protein during pregnancy is similar to that of control rats, at least for physiologic glucose concentration. However, the decreased response to IBMX and forskolin indicates decreased production and/or sensitivity to cAMP; this was associated with a decrease in PKA expression, which may result in lower PKA activity.     

Insufficient dietary vitamin e increases the concentration of 7beta-hydroxycholesterol in tissues of rats fed salmon oil

This study was conducted to determine the interaction between the type of dietary fat (coconut oil or salmon oil) and the vitamin E concentration of the diet [10, 20, 40 or 240 mg alpha-tocopherol equivalents (alpha-toc)/kg] in relation to the concentration of 7beta-hydroxycholesterol (7beta-OH) in liver, plasma, LDL and erythrocytes of rats. In the rats whose diet contained salmon oil, the concentration of 7beta-OH was dependent on the dietary vitamin E concentration. Rats whose diet contained 10 mg alpha-toc/kg had significantly higher concentrations of 7beta-OH in all samples studied than those whose diet contained 20, 40 or 240 mg alpha-toc/kg. Increasing the dietary vitamin E concentration from 40 to 240 mg alpha-toc/kg did not reduce the concentration of 7beta-OH in any samples. In the rats whose diet contained coconut oil, the concentration of 7beta-OH was independent of the dietary vitamin E concentration in all samples. The study shows that insufficient vitamin E in the diet increases the formation of 7beta-OH in rats fed salmon oil, whereas a dietary vitamin E supply in excess of the requirement does not lower 7beta-OH concentrations compared with an adequate vitamin E supply.     

硒和维生素E对饲予克山病病区粮大鼠肝脏自由基代谢的影响

饲予克山病病区粮对大鼠肝脏自由基代谢的影响及补充硒和维生素E的预防作用研究结果显示:病区粮组动物肝脏谷胱甘肽过氧化物酶活性明显下降,脂质过氧化物含量和自由基水平显著升高。在病区粮饲料中分别加入100ppmDL-α-生育酚和0.22ppm亚硒酸钠,均可明显降低脂质过氧化物含量和自由基水平。病区粮组动物肝脏α-生育酚和还原型谷胱甘肽含量均明显增加,提示硒缺乏可增加其对维生素E的需要量和使还原型谷胱甘肽生成增多。结果表明,克山病病区粮食中的致病因素能引起动物肝脏自由基代谢的紊乱,硒和维生素E对其都有很好的预防作用,提示维生素E的相对不足也有可能在克山病发病机制中起重要作用。