耐力训练和急性力竭运动对大鼠组织金属硫蛋白含量的不同影响

为探讨金属硫蛋白（ＭＴ）在运动提高机体自我保护能力方面的作用,本实验观察了游泳运动对大鼠心、肝、肺、脑、血管、血浆和骨骼肌等７种组织金属硫蛋白含量的影响。结果表明耐力训练组大鼠心、肝、肺和骨骼肌组织金属硫蛋白含量较正常对照组明显降低１３－３４％（Ｐ＜０．０５）;急性力竭运动组大鼠心、肝、脑、肺和骨骼肌组织其含量较正常对照组则明显升高２１－７５％（Ｐ＜０．０５）;但两组大鼠血管和血浆ＭＴ含量变化与对照组大鼠相比无统计学意义（Ｐ＜０．０５）。推测各组织金属硫蛋白在不同运动形式下的不同变化可能在运动提高机体自我保护能力方面具有积极意义。     

力竭性游泳对大鼠睾丸金属结合蛋白的诱导及其与睾酮和锌…

本研究通过观察大鼠力竭性游泳后睾丸金属结合蛋白（ＴＭＢＰ）、睾酮和锌含量的动态变化,探讨ＴＭＢＰ的被诱导性、诱导特点以及与睾酮合成和锌代谢的关系。结果显示：大鼠力竭性游泳后,ＴＭＢＰ呈一过性升高,峰值在游泳后６ｈ处,达安静时４ １６倍;游后１２ｈ已降回原有水平。这表明ＴＭＢＰ可被力竭性游泳所诱导,并减期不至６ｈ。ＴＭＢＰ诱导性的发现对认识ＴＭＢＰ的功能具有重要的意义。大鼠睾丸酮在力竭性游泳后即刻急     

金属诱导条件下刺猬各组织器官金属硫蛋白含量的比较分析

本文采用Ａｇ－Ｈｂ（血红蛋白）饱和法,Ｃｄ－Ｈｂ饱和法、Ｃｕ－Ｈｂ饱和法及酶联吸附免疫法定量分析刺猬各组织器官中金属硫蛋白含量。结果表明,肌肉注射三种金属盐均有明显的诱导金属硫蛋白合成的作用,诱导强度为Ｃｄ＾２＋＞Ｚｎ＾２＋＞Ｃｕ＾２＋,诱导后金属硫蛋白含量分布规律一致,即肝＞肾＞睾丸＞脾＞心、肺、胃、膀胱、胆汁、大肠、小肠、肌肉、血液,其中镉诱导肝的金属硫蛋白含量每克湿组织约１．８４ｍｇ,为肾的     

金属硫蛋白与肿瘤

近年来的研究发现,一些肿瘤组织的金属硫蛋白含量增加。致癌过程中ＭＴ的写表达与致癌素作用,癌基因激活和肿瘤迅速生长有关。ＭＴ的加旺表达也是细胞产生耐药的机制之一天肿瘤预防和治疗中,ＭＴ可保护细胞低抗重金属和烷化剂的致癌,致突变作用,ＭＴ还可用于肿瘤临床辅助治疗和用作肿瘤标志物。     

小鼠耐力训练后再力竭运动对体内某些生化指标的影响

目的 :通过分析耐力训练后再力竭运动小鼠部分生化指标的变化来探讨耐力训练提高机体抗疲劳能力可能机制及血液再分配的机制。方法 :建立耐力训练后再力竭运动模型 ,测定血清中超氧化物歧化酶 (SOD)活性、过氧化物酶 (POD)活性、过氧化氢酶 (CAT)活性与丙二醛 (MDA )含量及肝、骨骼肌、心肌与血清中一氧化氮 (NO )含量。结果 :运动后即刻 ,非耐力组血清SOD活性及肝NO含量较安静组显著下降 (P <0 .0 5～ 0 .0 1) ,而血清POD与CAT活性及骨骼肌与血清NO含量则显著升高 (P <0 .0 5～ 0 .0 1) ,其余指标无显著变化 (P >0 .0 5)。耐力组CAT活性显著高于非耐力组 (P <0 .0 5) ,血清NO含量显著低于非耐力组 (P <0 .0 1) ,其余指标两组间无显著差异 (P >0 .0 5)。 2 4h恢复后 ,非耐力组血清CAT活性与MDA含量及肝NO较运动后即刻显著升高 (P <0 .0 5～ 0 .0 1) ,血清与骨骼肌NO含量显著下降 (P <0 .0 5) ,而其余指标则无显著变化 (P >0 .0 5)。耐力组血清SOD活性及肝、血清与心肌NO含量较运动后即刻显著升高 (P <0 .0 5) ,而血清CAT活性显著下降 (P <0 .0 5) ,其余指标无显著变化(P >0 .0 5)。耐力组血清CAT活性与MDA含量显著低于非耐力组 (P <0 .0 5) ,而心肌NO含量显著高于非耐力组 (P <0 .0 5) ,其余指标两组间     

锌诱导金属硫蛋白在文蛤不同组织中的表达

采用体外暴露法对文蛤Meretrixmeretrix进行锌(0、1.5mg/L、3mg/L、6mg/L)染毒,研究不同染毒浓度的锌离子在不同染毒时间下,诱导金属硫蛋白(metallothionein,MT)在文蛤足、肝胰腺、鳃、外套膜组织中的表达差异。取经不同浓度的锌溶液在染毒2d及4d后的不同组织匀浆、离心后经Bio-GelP-10凝胶柱层析纯化,用TU-1810紫外可见分光光度计测定每个样品中金属硫蛋白的吸光值。实验结果显示:同一浓度锌离子染毒后,MT在文蛤4个不同组织中的表达量差异较显著,一般为足>肝胰腺>外套膜>鳃;不同染毒浓度的锌离子在不同染毒时间下诱导MT在不同组织中的表达也不同,具有一定的组织差异性和规律性。     

金属硫蛋白

金属硫蛋白为一类广泛地存在于生物界的低分子量、富含半胱氨酸的金属结合蛋白,尤其对Cd,Zn,Cu和Au,Ag等有较强的亲和力。它是一种诱导合成的蛋白质,在体内能被金属和糖皮质激素等所诱导。它具有广泛的生物学功能,主要是参与微量元素的储存、运输和代谢,拮抗电离辐射,清除羟基自由基和重金属解毒等多种作用。某些微量元素缺乏症等疾病也与它有一定关系。今后在某些疾病的治疗、环保中清除有毒金属以及采矿、富集贵重金属等方面有着广泛的应用前景。     

孕酮对家猫肝金属硫蛋白的诱导

胰高血糖素、血管紧张素、糖皮质激素均可诱导鼠、兔肝肾等器官金属硫蛋白（ｍｅｔａｌｏｔｈｉｏｎｅｉｎ,ＭＴ）的合成。兔在怀孕早期ＭＴ对从母体转移Ｚｎ至兔胎儿起调节作用。孕酮是家猫妊娠过程中的主要激素,它是否对肝ＭＴ有诱导作用,研究这一课题有助于阐明孕激...     

Effects of endurance training and acute exhaustive exercise on antioxidant defense mechanisms in rat heart

We investigated whether 8-week treadmill training strengthens antioxidant enzymes and decreases lipid peroxidation in rat heart. The effects of acute exhaustive exercise were also investigated. Male rats (Rattus norvegicus, Sprague-Dawley strain) were divided into trained and untrained groups. Both groups were further divided equally into two groups where the rats were studied at rest and immediately after exhaustive exercise. Endurance training consisted of treadmill running 1.5 h day(-1), 5 days week(-1) for 8 weeks. For acute exhaustive exercise, graded treadmill running was conducted. Malondialdehyde level in heart tissue was not affected by acute exhaustive exercise in untrained and trained rats. The activities of glutathione peroxidase and glutathione reductase enzymes decreased by both acute exercise and training. Glutathione S-transferase and catalase activities were not affected. Total and non-enzymatic superoxide scavenger activities were not affected either. Superoxide dismutase activity decreased by acute exercise in untrained rats; however, this decrease was not observed in trained rats. Our results suggested that rat heart has sufficient antioxidant enzyme capacity to cope with exercise-induced oxidative stress, and adaptive changes in antioxidant enzymes due to endurance training are limited.     

The effects of endurance training and exhaustive exercise on mitochondrial enzymes in tissues of the rat (Rattus norvegicus)

The aim of the present study was to ascertain the effects of training and exhaustive exercise on mitochondrial capacities to oxidize pyruvate, 2-oxoglutarate, palmitoylcarnitine, succinate and ferrocytochrome c in various tissues of the rat. Endurance capacity was significantly increased (P<0.01) by an endurance training program over a period of 5-6 weeks. The average run time to exhaustion was 214.2+/-23.8 min for trained rats in comparison with 54.5+/-11.7 min for their untrained counterparts. Oxidative capacities were reduced in liver (P<0.05) and brown adipose tissue (P<0.05) as a result of endurance training. On the contrary, the oxidative capacity of skeletal muscle was slightly increased and that of heart almost unaffected except for the oxidation of palmitoylcarnitine, which was significantly reduced (P<0.05) as a result of training.     

Effect of endurance exercise training on muscle glycogen supercompensation in rats

Nakatani, Akira, Dong-Ho Han, Polly A. Hansen, Lorraine A. Nolte, Helen H. Host, Robert C. Hickner, and John O. Holloszy. Effect of endurance exercise training on muscle glycogensupercompensation in rats. J. Appl.Physiol. 82(2): 711-715, 1997.The purpose of this study was to test the hypothesis that the rate and extent ofglycogen supercompensation in skeletal muscle are increased byendurance exercise training. Rats were trained by using a 5-wk-long swimming program in which the duration of swimming was gradually increased to 6 h/day over 3 wk and then maintained at 6 h/day for anadditional 2 wk. Glycogen repletion was measured in trained anduntrained rats after a glycogen-depleting bout of exercise. The ratswere given a rodent chow diet plus 5% sucrose in their drinking waterad libitum during the recovery period. There were remarkabledifferences in both the rates of glycogen accumulation and the glycogenconcentrations attained in the two groups. The concentration ofglycogen in epitrochlearis muscle averaged 13.1 ± 0.9 mg/g wet wtin the untrained group and 31.7 ± 2.7 mg/g in the trained group(P < 0.001) 24 h after the exercise.This difference could not be explained by a training effect on glycogensynthase. The training induced ~50% increases in muscle GLUT-4glucose transporter protein and in hexokinase activity inepitrochlearis muscles. We conclude that endurance exercise trainingresults in increases in both the rate and magnitude of muscle glycogensupercompensation in rats.

     

Expression of metallothionein in renal tubules of rats exposed to acute and endurance exercise

The induction of exercise-induced apoptosis in not actively involved in exercise organs, such as kidney could be a result of oxidative stress. Metallothionein (MT) exerts a protective effect in the cell against oxidative stress and apoptosis. We have previously demonstrated an increased incidence of apoptosis in distal tubular cells and collecting ducts in rat kidney after acute exercise. The present study was designed to test the hypothesis that MT may play a protective role in rat renal tubules against exercise-induced apoptosis after the acute exercise and regular training. Male Wistar rats were divided into control, acute exercised and 8-wk regularly trained groups. The kidneys were removed after a rest period of 6 h and 96 h. The ultrastructure of renal tubular cells was examined by electron microscopy. Apoptosis was detected in paraffin sections by the TUNEL technique. Expression of MT was examined by immunohistochemistry. The level of lipid peroxidation (thiobarbituric acid reactive substances - TBARS) was assayed in renal tissue homogenates. After acute exercise, the occurrence of apoptosis was restricted to distal tubules and collecting ducts of rat kidney, whereas the proximal tubules remained unaffected. The 8-wk training did not result in increased apoptosis in tubular cell. MT expression was confined exclusively to proximal tubules in all groups. However, it was significantly increased in acutely exercised animals, as compared to control and trained rats. After the 8-wk training, MT expression remained unaltered as compared to the control group. TBARS levels were significantly increased after acute exercise, while after regular training they remained unchanged. A significant correlation between TBARS level and MT expression was demonstrated. The findings could suggest a protective role of MT against oxidative stress and apoptosis in proximal tubular cells.     

Is exhaustive training adequate preparation for endurance performance?

Our purpose was to test the significance of exhaustive training in aerobic or endurance capacity. The extent of adaptations to endurance training was evaluated by assessing the increase in physical performance capability and oxidative markers in the organs of rats trained by various exercise programs. Rats were trained by treadmill running 5 days.week-1 at 30 m.min-1 for 8 weeks by one of three protocols: T1-60 min.day-1; T2-120 min.day-1; and T3-120 min.day-1 (3 days.week-1) and to exhaustion (2 days.week-1). Groups T2 and T3 ran for longer than T1 in an endurance exercise test (P less than 0.05), in which the animals ran at 30 m.min-1 to exhaustion; no difference was observed between groups T2 and T3. All 3 trained groups showed a similar increase (20-27%) in the fast-twitch oxidative-glycolytic (FOG) fibers with a concomitant decrease in the fast-twitch glycolytic (FG) fiber population in gastrocnemius (p less than 0.05). The capillary supply in gastrocnemius increased with the duration of exercise (p less than 0.05): no difference was found between groups T2 and T3. Likewise, no distinction was seen between groups T2 and T3 in the increase in succinate dehydrogenase activity in gastrocnemius and the heart. These results suggest that the maximal adaptive response to endurance training does not require daily exhaustive exercise.     

Influence of endurance training on muscle [PCr] kinetics during high-intensity exercise

We hypothesized that a period of endurance training would result in a speeding of muscle phosphocreatine concentration ([PCr]) kinetics over the fundamental phase of the response and a reduction in the amplitude of the [PCr] slow component during high-intensity exercise. Six male subjects (age 26 +/- 5 yr) completed 5 wk of single-legged knee-extension exercise training with the alternate leg serving as a control. Before and after the intervention period, the subjects completed incremental and high-intensity step exercise tests of 6-min duration with both legs separately inside the bore of a whole-body magnetic resonance spectrometer. The time-to-exhaustion during incremental exercise was not changed in the control leg [preintervention group (PRE): 19.4 +/- 2.3 min vs. postintervention group (POST): 19.4 +/- 1.9 min] but was significantly increased in the trained leg (PRE: 19.6 +/- 1.6 min vs. POST: 22.0 +/- 2.2 min; P < 0.05). During step exercise, there were no significant changes in the control leg, but end-exercise pH and [PCr] were higher after vs. before training. The time constant for the [PCr] kinetics over the fundamental exponential region of the response was not significantly altered in either the control leg (PRE: 40 +/- 13 s vs. POST: 43 +/- 10 s) or the trained leg (PRE: 38 +/- 8 s vs. POST: 40 +/- 12 s). However, the amplitude of the [PCr] slow component was significantly reduced in the trained leg (PRE: 15 +/- 7 vs. POST: 7 +/- 7% change in [PCr]; P < 0.05) with there being no change in the control leg (PRE: 13 +/- 8 vs. POST: 12 +/- 10% change in [PCr]). The attenuation of the [PCr] slow component might be mechanistically linked with enhanced exercise tolerance following endurance training.     

Effects of exhaustive endurance exercise on pulmonary gas exchange and airway function in women.

Seventeen fit women ran to exhaustion (14 +/- 4 min) at a constant speed and grade, reaching 95 +/- 3% of maximal O(2) consumption. Pre- and postexercise lung function, including airway resistance [total respiratory resistance (Rrs)] across a range of oscillation frequencies, was measured, and, on a separate day, airway reactivity was assessed via methacholine challenge. Arterial O(2) saturation decreased from 97.6 +/- 0.5% at rest to 95.1 +/- 1.9% at 1 min and to 92.5 +/- 2.6% at exhaustion. Alveolar-arterial O(2) difference (A-aDO(2)) widened to 27 +/- 7 Torr after 1 min and was maintained at this level until exhaustion. Arterial PO(2) (Pa(O(2))) fell to 80 +/- 8 Torr at 1 min and then increased to 86 +/- 9 Torr at exhaustion. This increase in Pa(O(2)) over the exercise duration occurred due to a hyperventilation-induced increase in alveolar PO(2) in the presence of a constant A-aDO(2). Arterial O(2) saturation fell with time because of increasing temperature (+2.6 +/- 0.5 degrees C) and progressive metabolic acidosis (arterial pH: 7.39 +/- 0.04 at 1 min to 7.26 +/- 0.07 at exhaustion). Plasma histamine increased throughout exercise but was inversely correlated with the fall in Pa(O(2)) at end exercise. Neither pre- nor postexercise Rrs, frequency dependence of Rrs, nor diffusing capacity for CO correlated with the exercise A-aDO(2) or Pa(O(2)). Although several subjects had a positive or borderline hyperresponsiveness to methacholine, this reactivity did not correlate with exercise-induced changes in Rrs or exercise-induced arterial hypoxemia. In conclusion, regardless of the degree of exercise-induced arterial hypoxemia at the onset of high-intensity exercise, prolonging exercise to exhaustion had no further deleterious effects on A-aDO(2), and the degree of gas exchange impairment was not related to individual differences in small or large airway function or reactivity.