饥饿对南方鲇和草鱼的生长及能量代谢的影响

以南方鲇(Silurus meridionalis)和草鱼(Ctenopharyngodon idellus)为对象,在(27.5±0.5)℃条件下,分别饥饿0d,3d,7d,14d,21d和28d,观察各实验处理对鱼体的生长及能量代谢的影响.研究发现:在饥饿28d后,2种鱼的体质量、体长无显著变化,但各自的肥满度和肝器官指数均显著降低(p0.05),南方鲇脂肪含量的降低幅度大于草鱼,其蛋白含量的降低幅度却小于草鱼.各饥饿处理时间点的草鱼静止代谢率(RMR)均显著高于南方鲇(p0.05),且随饥饿时间的延长呈直线下降的趋势;而南方鲇的RMR则呈先上升再下降的趋势.2种鱼的特定体质量生长率(SGR)在饥饿进程中均呈负增长,南方鲇和草鱼的各线粒体状态3呼吸率和细胞色素C氧化酶活性随饥饿时间延长均表现出了不同的变化的趋势.以上结果表明,南方鲇和草鱼应对饥饿胁迫的生理生态学机制存在组织特异性和物种特异性.通过讨论提出,由于南方鲇与草鱼为不同的营养类型,尤其是捕食行为模式各异,因此进化出不同的适应饥饿胁迫的能量生态对策.     

PGC-1 α 与运动能力

长期的耐力训练可诱导成年的骨骼肌发生一系列的生理性适应,其中包括快肌纤维向慢肌纤维转换,线粒体的生物合成等。过氧化物酶体增殖物受体γ共激活因子1α(PGC-1a)可能在运动诱导骨骼肌的适应机制起着重要作用:增强骨骼肌氧化代谢能力,从而增强利用脂肪和碳水化合物的能力。但研究发现PGC-1a基因敲除小鼠进行长期的训练仍能够诱导线粒体蛋白表达增加。长期耐力训练可诱导骨骼肌PGC-1a表达增加和激活确切生理作用仍需要进一步研究。     

肠易激综合征亚型患者具有肠道和躯体高敏感,自主心血管功能紊乱以及肠道低浓度炎症

研究目的：明确腹泻型肠易激综合征患者是否具有肠道和躯体高敏感、自主心血管功能紊乱以及肠道低浓度炎症。创新要点：发现腹泻型肠易激综合征患者具有自主心血管功能紊乱和肠道低浓度炎症（这两方面在之前研究中尚存争议）。此外,发现腹泻型肠易激综合征患者的肠道高敏感和躯体高敏感、肠道高敏感和自主心血管功能紊乱、躯体高敏感和自主心血管紊乱之间存在相关性,为患者的治疗提供参考。研究方法：2013年9月至2014年5月,62名腹泻型肠易激综合征患者和20名健康志愿者参与到了本研究。所有受试者接受并顺利完成了相关检查和问卷填写。利用恒压器（渐至极限法）检查我们发现腹泻型肠易激综合征患者具有肠道高敏感。同时,采用冷水刺激法和缺血刺激法探明腹泻型肠易激综合征患者具有躯体高敏感。重要结论：腹泻型肠易激综合征患者具有肠道和躯体高敏感、自主心血管功能紊乱以及肠道低浓度炎症。肠道高敏感和躯体高敏感、肠道高敏感和自主心血管功能紊乱、躯体高敏感和自主心血管紊乱之间存在相关性。     

Altered K+ movement in liver mitochondria from alloxan diabetic rats

Summary Potassium movements were monitored in liver mitochondria from control and alloxan diabetic rats with a cationic electrode. There was net accumulation of K⁺ after Ca²⁺ addition to the mitochondria with the diabetic but not with the control.     

Regulation of mitochondrial oxidative phosphorylation by second messenger-mediated signal transduction mechanisms

The mitochondrial oxidative phosphorylation system is responsible for providing the bulk of cellular ATP molecules. There is a growing body of information regarding the regulation of this process by a number of second messenger-mediated signal transduction mechanisms, although direct studies aimed at elucidating this regulation are limited. The main second messengers affecting mitochondrial signal transduction are cAMP and calcium. Other second messengers include ceramide and reactive oxygen species as well as nitric oxide and reactive nitrogen species. This review focuses on available data on the regulation of the mitochondrial oxidative phosphorylation system by signal transduction mechanisms and is organised according to the second messengers involved, because of their pivotal role in mitochondrial function. Future perspectives for further investigations regarding these mechanisms in the regulation of the oxidative phosphorylation system are formulated. Received 11 December 2005; received after revision 14 January 2006; accepted 6 February 2006     

Functional and biochemical characteristics of mitochondrial fractions from rat liver in cold-induced oxidative stress

We determined characteristics of rat liver mitochondrial fractions, resolved at 1000 (M₁), 3000 (M₃), and 10,000 g (M₁₀) after 2 and 10 days cold exposure. In all groups, the M₁ fraction exhibited the highest oxidative capacity, oxidative damage, H₂O₂ production rate, and susceptibility to stress conditions, and the lowest antioxidant levels. Cold exposure increased cytochrome oxidase activity in all fractions and succinate-supported O₂ consumption in the M₁ and M₁₀ fractions during state 3 and state 4 respiration, respectively. With succinate, the H₂O₂ release rate increased in all fractions during state 4 and state 3 respiration, whereas with pyruvate/malate, it increased only during state 4 respiration. Increases in tissue mitochondrial proteins caused a faster H₂O₂ flow from the mitochondrial to cytosolic compartment, which was limited by the reduction in the M₁ fraction. Despite increased liposoluble antioxidant levels, cold also caused enhanced oxidative damage and susceptibility to oxidative challenge and Ca²⁺-induced swelling in all fractions. These changes leading to elimination of H₂O₂-overproducing mitochondria avoided excessive tissue damage. We propose that triiodothyronine, whose levels increase in the cold environment, brings about the biochemical changes producing oxidative damage and those limiting its extent.Received 16 July 2004; received after revision 27 September 2004; accepted 18 October 2004     

Role of nitric oxide in the functional response to ischemia-reperfusion of heart mitochondria from hyperthyroid rats

We investigated the role of nitric oxide (NO) in the mitochondrial derangement associated with the functional response to ischemia-reperfusion of hyperthyroid rat hearts. Mitochondria were isolated at 3000 g from hearts subjected to ischemia-reperfusion, with or without N-nitro-L-arginine (L-NNA, an NO synthase inhibitor). During reperfusion, hyperthyroid hearts displayed tachycardia and low functional recovery. Their mitochondria exhibited O₂ consumption similar to euthyroid controls, while H₂O₂ production, hydroperoxide, protein-bound carbonyl and nitrotyrosine levels, and susceptibility to swelling were higher. L-NNA blocked the reperfusion tachycardic response and increased inotropic recovery in hyperthyroid hearts. L-NNA decreased mitochondrial H₂O₂ production and oxidative damage, and increased respiration and tolerance to swelling. Such effects were higher in hyperthyroid preparations. These results confirm the role of mitochondria in ischemia-reperfusion damage, and strongly suggest that NO overproduction is involved in the high mitochondrial dysfunction and the low recovery of hyperthyroid hearts from ischemia-reperfusion. L-NNA also decreased protein content and cytochrome oxidase activity of a mitochondrial fraction isolated at 8000 g. This and previous results suggest that the above fraction contains, together with light mitochondria, damaged mitochondria coming from the heaviest fraction, which has the highest cytochrome oxidase activity and capacity to produce H₂O₂. Therefore, we propose that the high mitochondrial susceptibility to swelling, favoring mitochondrial population purification from H₂O₂-overproducing mitochondria, limits hyperthyroid heart oxidative stress.Received 24 March 2004; received after revision 9 June 2004; accepted 5 July 2004     

Morphofunctional changes in the mitochondrial subpopulations of conceptus tissues during the placentation process

To establish the role of mitochondrial subpopulations in the mitochondrial maturation process, we studied morphological and functional changes in the mitochondria of different mammalian conceptus tissues during the organogenic and the placentation processes. Mitochondrial subpopulations of three different conceptus tissues, embryo and visceral yolk sac placenta on gestational days 11, 12 and 13 and placenta on days 12 and 13, were examined morphologically by transmission electron microscopy. Cytochrome oxidase activity and protein levels were also measured in each mitochondrial subpopulation. The results indicate two different mitochondrial subpopulation profiles: a homogeneous one, which corresponds to immature mitochondria, and a heterogeneous one, which represents the mature mitochondria. The three tissues studied show different morphologic and metabolic patterns of mitochondrial maturation during the placentation process, rendering them suitable as experimental models to establish the p ossible relationship between mitochondrial maturation and the mitochondrial subpopulations. Received 5 August 2002; received after revision 23 September 2002; accepted 8 October 2002 RID="*" ID="*"Corresponding author.     

糖尿病大鼠尿道功能损害以及病程对其的影响

利用大鼠模型研究糖尿病对尿道功能的损害,以及病程长短对其的影响.雌性SD大鼠(250～275 g),链脲霉素(STZ)65mg/kg腹腔注射得到糖尿病大鼠模型,5周或10周后在乌拉坦麻醉下利用三导管系统,隔离地测定STZ-糖尿病大鼠和正常对照大鼠膀胱等容收缩状态下的膀胱内压,尿道充盈压和括约肌肌电图(EUSEMG).静脉注射横纹肌阻断剂α-bungarotoxin(BGT)后再次测定.与正常对照大鼠对比,5周和10周糖尿病大鼠膀胱内压峰值及平滑肌收缩幅度明显降低,并且尿道括约肌的高频振动收缩(HFOs)出现不规则变化.有3只(27%)5周的糖尿病大鼠和3只(33%)10周的糖尿病大鼠出现逼尿肌-括约肌失协调(detrusor-sphincter dyssynergia,DSD).BGT阻断尿道外括约肌后,糖尿病大鼠的尿道充盈压(UPP)有更明显的下降.提示了糖尿病损伤尿道括约肌功能,引起排尿时尿道阻力增加,导致排尿功能的损伤.早期干预有助于防止糖尿病引起的排尿功能的进一步恶化.     

墨吉对虾Penaeus merguiensis 线粒体16SrRNA 基因序列分析

比较墨吉对虾6个群体的线粒体16SrRNA基因约457个碱基对的DNA序列。结果表明这6个群体间的遗传距离（D）在0-0.0085之间，未发现广东的3个群体与澳洲或新加坡群体间存在地理群体以上的遗传差异。