维生素E和去铁敏对三硝基甲苯(TNT)急性染毒大鼠红细胞毒性的影响

分别给摄食普通饲料和维生素E缺乏饲料的两组雄性Wistar大鼠用1000mg/kgTNT灌胃染毒,8小时和16小时后处死动物,取血观察红细胞高铁血红蛋白(MetHb)、还原形谷胱甘肽(GSH)及低渗溶血率的变化。结果表明,两组动物MetHb均在染后出现明显的升高,与饲料中的维生素E含量无明显关系。然而,仅在维生素E缺乏组动物观察红细胞GSH 的显著下降和低渗溶血率的明显升高。给该组动物补充维生素E或在染毒前注射去铁敏(desferrioxamine),虽未能减少MetHb的形成,却可保护大鼠红细胞对抗TNT的损害,如防止GSH的耗竭和溶血倾向的出现。     

黄磷对大鼠肝微粒体和线粒体Ca^2＋泵的影响

在体外实验中,用不同浓度黄磷(0.026μg/ml,0.26μg/ml,2.60μg/ml)与大鼠肝微粒体和线粒体共同孵育,发现黄磷对肝微粒体和线粒体Ca~(2 )-ATP酶呈现抑制作用,且随剂量增大,抑制作用加重;在孵育的早期,对微粒体Ca~(2 )ATP酶的抑制更明显。在整体动物实验中,黄磷染毒后6小时,对肝微粒体和线粒体Ca~(2 )-ATP酶发生抑制。染毒后3小时,对肝微粒体~(45)Ca摄取发生抑制;染毒后6小时,对肝线粒体~(45)Ca摄取发生抑制。实验结果表明,黄磷对微粒体和线粒体Ca~(2 )泵机制的损害可能是引起中毒性肝损害的一个重要因素。     

克山病病区饲料对大白鼠组织中脂质过氧化物的积蓄和线粒体膨胀收缩的影响

1.用克山病病区粮食,非病区粮食,病区粮食补硒及常备用的四种饲料饲养大白鼠三个月后,观察到常备组动物生长最好,其余三组之间无差别。心脏和肝脏的脏体比值以病区组为最大,常备组显著小于其他三组。2.测定了全血,心和肝线粒体及其上清液中的硒水平和GSH—Px活力,二者均与饲料硒水平呈正相关。无论是心或是肝上清液中的硒含量和GSH—Px活力均较线粒体高。肝线粒体中的GSH—Px活力低于心线粒体。缺硒时,其变化最大。3.自发膨胀时心线粒体以常备组膨胀最小,肝线粒体则病区组最小。用GSH—Px诱发后,心线粒体的膨胀四组无差别;而肝线粒体膨胀时,病区组显著小于常备组与补硒组。除病区组的肝线粒体外,GSH诱发膨胀时,膨胀速度随GSH浓度增加而增加。无论是心或肝的线粒体膨胀后,加ATP收缩程度各组之间均无统计学的差别。4.全血、心匀浆、心线粒体和肝线粒体的TBA值经t测验无显著差别,而喂养160天以后的动物肝匀浆的TBA值似乎有差异,并与GSH—Px活力呈相反的变化。在膨胀时,线粒体的TBA值较膨胀前高,GSH诱发膨胀后,其膨胀速度较自发膨胀快,其TBA也较自发膨胀高。心线粒体在4mMGSH诱发膨胀后,病区组与非病区组的TBA值显著高于常备组与补硒组。     

维生素E对大鼠肝线粒体酶活性的影响

目的观察维生素E（VE）补充对大鼠肝线粒体ATP酶和抗氧化酶活性的影响。方法Wistar大鼠随机分成4组，对照组、VE1、VE2和VE3干预组；对照组给予普通饲料，3个干预组均喂饲添加维生素E的饲料，剂量分别为335，1340，5025mg／kg饲料，喂养10周后，摘取肝脏提取线粒体，测定Na^＋-K^＋-ATP酶、Ca2^＋-Mg^＋-ATP酶、谷胱甘肽过氧化物酶（GSH—Px）、超氧化物歧化酶（SOD）的活性及丙二醛（MDA）的含量。结果VE1组与对照组相比，SOD、GSH—Px、Na^＋-K^＋-ATP酶、Ca2^＋-Mg2^＋-ATP酶活性显著升高（P〈0．05），MDA水平显著降低（P〈0．05）。VE2、VE3组与对照组相比未见改善。VE2、VE3和VE1组相比，SOD、GSH—Px、Na^＋-K^＋-ATP酶、Ca2^＋-Mg^＋-ATP酶活性显著降低（P〈0．05），MDA水平显著升高（P〈0．05）。结论补充适量VE（335mg／kg）能显著增强大鼠肝线粒体ATP酶活性及氧化能力；较高剂量VE；（1340，5025mg／kg）组未能改善大鼠肝线粒体ATP酶活性及抗氧化能力。     

不同维生素E水平对四氯化碳肝损害的影响

方法：大鼠经２９天喂养造成不同ＶＥ水平的模型。一次腹腔注射０．６５ｍｌ／ｋｇ四氯化碳（ＣＣｌ４）。结果：２４小时后，肝匀浆中丙二醛（ＭＤＡ）水平明显增高，ＶＥ缺乏组升高更明显，ＶＥ添加组ＭＤＡ明显下降。肝匀浆中总巯基、非蛋白巯基、蛋白巯基在染毒后未发生明显改变，也未发现不同水平ＶＥ对其有影响。ＣＣｌ４染毒后，血清丙氨酸转氨酶（ＡＬＴ）明显升高：随着饲料ＶＥ水平增高，ＡＬＴ上升幅度增大，病理检查变性坏死面积稍有增加，提示ＶＥ似有促进肝细胞坏死作用，脂质过氧化可能不是ＣＣｌ４致肝细胞坏死的唯一机理。肝匀浆甘油三酯（ＴＧ）在染毒后明显升高，说明ＴＧ在肝脏中蓄积。饲料ＶＥ增高，其蓄积程度减轻，但对血清中ＴＧ影响不大。ＶＥ也可降低血清中胆固醇的含量。结论：ＶＥ有预防ＣＣｌ４所致ＴＧ在肝中蓄积和脂肪肝形成的作用。     

维生素E对氯化镍染毒大鼠肺组织p15基因甲基化过程的影响

为探讨维生素E对氯化镍染毒大鼠肺组织p15基因甲基化过程的影响,研究人员以0.1、0.2、0.4和0.8mg/mL氯化镍灌胃染毒大鼠,并设立对照组(生理盐水)和拮抗组(0.8mg/mL氯化镍+5mg/mL维生素E组),持续6周。染毒结束后处死大鼠,制备肺组织匀浆,采用分光光度法,测定谷胱甘肽(GSH)和丙二醛(MDA)水平的变化;以荧光定量聚合酶链反应(PCR)     

DEHP对大鼠脂质过氧化反应的影响

目的：探讨DEHP对大鼠脂质过氧化反应的影响。方法：通过对不同剂量DEHP染毒大鼠的血液,肝组织匀浆,线粒体匀浆中GSH－Px,GST,SOD,MDA指标的测定,结果：随着DEHP染毒剂量的增加,大鼠血中,组织中的GSH－Px,GST,SOD活性降低,MAD含量增加,尤其是大剂量组,差异均有显著性（P＜0．05,P＜0．01）,结论：DEHP可明显增加大鼠体内的脂质过氧化反应。     

镉对大鼠十二指肠吸收钙的抑制作用

为了阐明镉中毒时出现的缺钙问题,作者将Wistar系雄性大鼠(6周龄)分成两组,每组8只,对照组喂以无镉饲料,实验组喂以含镉100ppm(CdCl_2)饲料,共实验33天。实验期间记录体重;于实验第7、10、16、19、25和28天,记录饲料消耗量,并收集粪、尿样,测定钙和磷的浓度;实验至第8、17、26天,采取心血,测定血清钙和磷的浓度;至第29或30天时,经口给予~(45)Ca和Ca,1和2小时后,取心血测定血清~(45)Ca的放射性;实验末,处死动物,测定十二指肠粘膜、肾脏皮质和髓质匀浆     

三硝基甲苯(TNT)对大鼠肝脏混合功能氧化酶(MFO)的影响

用离体(肝微粒体细胞色素P-450含量、氨基比林脱甲基酶活性)和活体(摄入~(14)C-氨基比林后的~(14)CO_2呼吸分析)指标观察TNT对雄性Wistar大鼠肝脏MFO的影响,同时进行PB诱导和非诱导两种处理的比较。急性腹腔内注射3天后,高剂量TNT(100mg/kg/天)显著抑制MFO;PB诱导后,抑制程度加强;而且低剂量TNT(20mg/kg/天)也显示出明显的抑制作用。当动物亚急性(30天)经口摄入含0.15%TNT的混合饲料时,MFO活性变化的形式与动物是否事先经PB诱导有关。在非诱导组,MFO活性随染毒时间的延长而逐渐增加;但是在PB诱导组,MFO活性的变化呈典型的双期效应,染毒早期增高,中期逐渐下降,晚期则出现MFO活性的明显抑制。根据上述结果,对TNT影响MFO的规律进行扼要讨论。     

维生素E对低温暴露大鼠肝线粒体功能的影响

1.本实验对动物在低温环境中补充维生素E的摄取量,对肝线粒体功能的影响进行了观察。 2.在-2°±1℃的环境用基础饲料补充30mg维生素E/100g饲养大鼠,14天后,离休肝线粒体ADP/○比值下降显著减少,RCR降低显著改善,说明在低温环境中增加维生素E的摄取量对肝线粒体的功能有保护作用。 3.本丈对低温环境中补充维生素E对机体耐寒能力的影响作了讨论。     

Dermal penetration and systemic distribution of 14C-labeled vitamin E in human skin grafted athymic nude mice

In vivo percutaneous penetration and tissue distribution of 14C-labeled vitamin E applied to human skin grafted onto athymic nude mice were determined. At 1 hr, mouse skin contained the highest level of radioactivity, followed by the muscle, blood, liver, lung, adipose tissue, spleen, kidney, brain, heart, and eyes. A linear increase with time in tissue radioactivity was observed throughout the 24 hr experimental period. At 4 and 24 hrs skin grafts were highly radioactive. At 4 hrs the epidermis and the upper portion of the dermis contained more radioactivity than the remaining portion of the dermis. In contrast, at 24 hrs the highest level of radioactivity was detected in the lower dermis. No radioactivity was detected in expired air while 0.2% of the dose was found in the urine. The data show that vitamin E does penetrate skin and that the dermis acts as a barrier or reservoir for this highly lipophilic compound.     

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。     

三硝基甲苯作业工人和HBsAg阳性者血清铜蓝蛋白和谷胱甘肽过氧化物酶活性的变化

对河南省某化工厂职业接触ＴＮＴ作业工人现场劳动卫生学调查和健康监护结果表明，车间空气中ＴＮＴ浓度绝大多数超过ＭＡＣ（１ｍｇ／ｍ３），作业工人皮肤污染严重。ＴＮＴ接触组与对照组血清ＧＰＴ活性升高和ＨＢｓＡｇ阳性检出率两组间无显著性差异，表明这两组人群肝功能属于正常范围。同时发现，ＴＮＴ接触组和ＨＢｓＡｇ阳性组血清铜蓝蛋白和谷胱甘肽过氧化物酶活性均极显著低于对照组（Ｐ＜０．０２，Ｐ＜０．００１）；ＨＢｓＡｇ阳性组这两项指标极显著低于ＴＮＴ接触组（Ｐ＜０．０５，Ｐ＜０．０２）。表明ＴＮＴ和ＨＢＶ诱发的肝损伤机理可能部分归因与活性氧生成有关。     

恒河猴三硝基甲苯染毒后咖啡因清除率的变化

应用恒河猴做成亚慢性三硝基甲苯染毒（ＴＮＴ）模型，在染毒前，染毒中期和试验表明咖啡因在动物体内的清除呈一级动力学，半衰期为８。８８小时，这一结果说明咖啡因符合肝脏代射模型药物的要求。ＴＮＴ染毒后咖啡因清除率（ＣＬｃａ）下降，而同期血清甘胆酸（ＣＡ）浓度无变化。这一结果说明ＣＬｃａ可能比ＣＡ能列早地反映接触ＴＮＴ后的机体反应。染毒三个月后处死动物直接测定肝混合功能氧化酶（ＭＦＯ）活性，发现咖啡因清除     

Whole-body and body-part-specific bioconcentration of explosive compounds in sheepshead minnows

Sheepshead minnows (Cyprinodon variegatus) were exposed to radiolabeled isotopes of the explosives 2,4,6-trinitrotoluene (TNT), exahydro-1,3,5-trinitro-1,3,5-triazine (commonly known as RDX), and octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine (commonly known as HMX), yielding the bioconcentration factors (BCF) of 3.3, 0.7, and 0.1 L kg⁻¹, respectively. For TNT, the body residue of transformation product exceeded that of the parent compound by factors of 1, 8, and 16 for total aminonitrotoluenes, total extractable compounds, and total transformation products, respectively, with substantial bioaccumulation of both non-identified extractable and unextractable (i.e., tissue-bound), compounds. In comparison, the sum body residues of RDX and HMX transformation products were <4 times higher than for parent compounds. The concentrations of RDX and HMX and their transformation products were similar among liver, viscera (excluding liver), gills, and body remains (integument and muscles), while 46% of the TNT transformation products resided in the liver, and 64% of the parent compound was in the viscera.     

Circadian and circannual rhythms in sexual activity and plasma hormones (FSH,LH, Testosterone) of five human males

Sexual activity (SA), both sexual intercourse and masturbation, was recorded every day, during the course of 14 months, in five males (26–32 years), synchronized with lights-on at 0700 ± 1 hr and lights-off at 2300 ± 1.5 hr. Circadian rhythms of plasma testosterone (pT), LH, and FSH (among other hormonal variables) were documented every other month during the same time span (sampling at 4-hr intervals, for 28 hr, on test days). Both conventional and cosinor methods were used for statistical analysis to validate ultradian (~ 8 hr), circadian (~ 24 hr), and circannual (~ 1 year) rhythms. The detected rhythms were quantified in terms of acrophase ø (location of the peak on the time scale), amplitude A (half the total variability), and rhythm-adjusted mean M. Circadian rhythms are detected for both SA and pT. The circadian chronograms for SA computed on a monthly basis, during the year, show two prominent peaks located in the late evening and early morning (and a minor peak in the early afternoon). The circadian pT ø shows an annual phase shift (pT ø is found in May at ~ 0800 and in November at ~ 1400 with p <0.05). Circannual rhythms are detected as well with ø located on September 10 for SA (from July 16 to December 10, with 95% confidence limits); pT ø on October 6 (from July 16 to December 26); FSH ø on February 6 (from December 1 to April 10); and LH ø on March 8 (from January 18 to April 26). The autumnal peak in plasma testosterone 24-hr mean level is presumably one factor which favored the autumnal rise in sexual activity of the subjects.     

Effect of the chelating agent sodium tripolyphosphate on cadmium toxicity in mice

The mechanism by which Sodium tripolyphosphate (STPP) increases cadmium toxicity after sc administration was investigated in mice after a dose of Cd (30 μmole/kg), alone or with STPP (90 μmole/kg). The effects of STPP on acute Cd toxicity, development of Cd-induced liver necrosis, rate of Cd transport, distribution of Cd among organs, and Cd binding to metallothionein (MT) was followed. Histological liver changes were not observed during the first 12 hr after injection of Cd, but already 6–8 hr after injection of Cd + STPP early centrilobular necroses and blood stasis appeared. At 12 hr more advanced necroses were present. STPP administered alone was nontoxic and did not change the liver morphology, when compared to animals killed immediately after injection. During the first 12 hr after administration of Cd with STPP there was a much faster transport of Cd giving rise to higher liver and kidney concentrations of Cd and partial inhibition of Cd-MT binding, compared with animals receiving the same dose of Cd without STPP.     

Mode of action of a new non-steroidal post-coital antifertility agent (centchroman: 67/20 CDRI) in rats

The estrogenicity and antiestrogenicity of the compound Centchroman, 67/20 CDRI, trans-2-2-dimethyl 1-3 phenyl-4-p(beta-pyrrolidinoithoxy phenyl) 7-methoxy chroman hydrochloride, a synthetic nonsteroidal compound, was studied using uterine and liver glycogen and uterine sialic acid as biochemical parameters. Estradiol caused significant increases in uterine and liver glycogen 6 and 18 hours after administration; Centchroman 67/20 caused a marked increase in uterine glycogen at 6 hrs which plateaued at this level for 48 hrs after the administration. Liver glycogen showed a steady increase even 48 hrs after the administration of 67/20. Uterine sialic acid in estrogen-treated rats reached a peak level at 6 hrs, decreased significantly by 18 hrs, and plateaued at this level up to 48 hrs. Compound 67/20, on the other hand, caused an increase in uterine sialic acid 18 hrs after the administration of the drug. Pretreatment with the compound for either 6 or 48 hrs before administration of 17-beta-estradiol inhibited the estradiol-induced increase in uterine and liver glycogen and also uterine sialic acid. However, simultaneous administration of the compound with 17-beta-estradiol was effective only in inhibiting the estradiol-induced increase in uterine sialic acid. In light of the present data, it is concluded that the antiimplantation/antifertility action of the compound 67/20 may be due to its inherent estrogenic and antiestrogenic properties.     

Effects of high doses of leucine and ketoleucine on glycogen and protein metabolism in acute uremia

Binephrectomized rats treated with high doses of ketoleucine (0.5 g/rat per 20 hr) expired after about 45 hr. In contrast, survival time was 100% 60 hr after ureteral ligation. In comparison to animals receiving low-protein diets, addition of leucine to the diet almost doubled muscle and liver protein content whereas ketoleucine increased liver protein during the first 40 hr after operation about 1.5-fold. Skeletal muscle protein content was enhanced in the ureter-ligated rats with administration of ketoleucine. There was also about a 10-fold elevation in liver glycogen and total carbohydrate content between the 20th and 60th hr in binephrectomized rats fed leucine at 5-hr intervals. In skeletal muscle glycogen, there were no significant differences among the acutely uremic rats fed at 10-hr intervals low-protein diets alone or supplemented with leucine or ketoleucine. Leucine inhibits glycogenolysis by lowering phosphorylase alpha activity in muscle and liver, whereas ketoleucine enhances glycogenolysis in acute uremia. In rats supplemented with letoleucine, there is a progressive inactivation of glycogen synthetase I which occurs in parallel with increasing phosphorylase alpha activity. In binephrectomized rats receiving leucine supplements at 5-hr feeding intervals, the activity of liver glycogen synthetase I increases up to a maximum of 90% of total enzyme activity.