低温对大鼠骨骼肌能量代谢的影响——Ⅰ.高能磷酸化合物含量的变化

本实验选择对低温比较敏感的骨骼肌组织作为实验对象。将19只大鼠随机分成3组,其右后肢经冷冻处理使组织温度分别达 5℃、0℃及-5℃,于复温后不同时间测定骨骼肌中四种高能磷酸化合物AMP,ADP、ATP及CP的含量。结果表明,大鼠骨骼肌组织中高能磷酸化合物含量随冷冻时组织最低温度的下降而不同程度的减少,并且具有明显的时相过程。复温后即刻至4小时下降迅速,4～12小时三组值较为接近,其后随时间延长而明显分离。 5℃组恢复得早而且明显,0℃组恢复程度次于 5℃组,-5℃组含量下降最明显而且几乎不恢复。提示:低温使骨骼肌组织能量的产生和贮存过程受到影响。     

光合能量代谢对C_3植物光呼吸的调节作用

C_3植物光呼吸与光合作用关系受光合能量代谢状况的调节。在外界无CO_2和照光条件下,贮藏性光合产物经某种转化途径能“回迁”光合与光呼吸碳循环并显著地受到光合能量代谢的影响。在无CO_2或低CO_2浓度、高光强条件下,此碳素“回迁”过程对协调光合能量代谢与光合碳素代谢平衡,可能起重要作用。     

Saponins can cause the agglutination of phospholipid vesicles

The interaction of saponins with phospholipid vesicles was investigated by means of liposomal agglutination or a precipitation assay. Ginsenoside-Rc, which has an α-l-arabinofuranose residue at the non-reducing terminus, exhibited remarkable agglutinability toward egg yolk phosphatidylcholine vesicles, while other saponins lacking this characteristic sugar residue showed less or no agglutinability. The molar ratio of ginsenoside-Rc to egg phosphatidylcholine in the aggregates was estimated to be 0.4–0.5 by a precipitation assay using ¹⁴C-labeled egg phosphatidylcholine vesicles. The agglutination was inhibited by p-nitrophenyl α-l-arabinofuranoside but not by p-nitrophenyl β-d-glucopyranoside or arabinogalactan. The results indicated that the α-l-arabinofuranose residue in ginsenoside-Rc should be important for the expression of the agglutinability. The agglutinability of ginsenoside-Rc toward lipid vesicles depended on both the polar head groups and fatty acyl chains of phospholipids. Egg yolk phosphatidylcholine vesicles were strongly agglutinated by ginsenoside-Rc, although sphingomyelin, phosphatidylethanolamine, phosphatidic acid and phosphatidylserine were less agglutinated. The agglutinability of ginsenoside-Rc was effective for phosphatidylcholines with short or unsaturated fatty acyl chains. The results suggested that the interaction of ginsenoside-Rc with phospholipid membranes should be affected not only by the chemical structure of the phospholipid but also by the membrane fluidity.     

Differential response of Trifolium species to 4-(2,4-dichlorophenoxy)butyric acid treatments

The differential response of white clover ( Trifolium repens L. cv. Regal Ladino) and berseem clover ( Trifolium alexandrinum L. cv. Mississippi ecotype) was investigated by treating greenhouse cultured plants with 4-(2,4-dichlorophenoxy)butyric acid (2,4-DB). Berseem clover plants were significantly injured by a treatment concentration of 0.6 kg ha^-1 of 2,4-DB, whereas white clover plants were not injured by treatment levels below 2.4 kg ha^-1. The metabolism of 2,4-DB in cell suspension cultures of white clover and berseem clover was investigated using [ring-¹⁴C]-2,4-DB and non-labeled 2,4-DB. White clover cell cultures metabolized ca 4-fold more 2,4-DB than berseem cultures over a 44-h treatment period. The decrease in berseem cell population was 4-fold greater than the decrease in white clover cell population in response to the 8 μ M 2,4-DB treatment. The herbicide and its [ring-¹⁴C]-labeled metabolites were isolated from treated cells and medium after 44 h by partition and thin-layer chromatography. White clover cells metabolized 90% of the [¹⁴C]-2,4-DB and berseem clover cells metabolized 22% of the herbicide. The major portion of the radiolabel was in the glycoside fractions from extracts of both species. The differential response of Trifolium species to 2,4-DB is implied to be due to the differential rate of 2,4-DB metabolism to a glycoside by the clover plants.     

Availability of water controls Crassulacean acid metabolism in succulents of the Richtersveld (Namib desert,South Africa)

Features of Crassulacean acid metabolism (CAM) were studied in a variety of different succulents in response to climatic conditions between March 1977 and October 1983 in the southern Namib desert (Richtersveld). A screening in 1977 and 1978 revealed that nearly all investigated succulents performed a CAM, but overnight accumulation of malate declined gradually with decreasing soil water potential, tissue osmotic potential, and leaf water content. This was further substantiated by an extended period of insufficient rainfall in 1979 and 1980 which damaged the evergreen CAM succulents between 80 and 100%. In most of the species still living, neither CO₂-gas exchange nor diurnal acid fluctuation, indicative of CAM, could be detected unless an abundant rainfall restored both CAM features. Plants persisted in a stage of latent life.Water supply is one necessary prerequisite for CAM in the Richtersveld. But even well-watered plants with CAM were sensitive to short-term water stress caused by high water-vapour partialpressure deficit (VPD) in the night, which reduced or prevented CO₂ uptake and resulted in a linear relation between overnight accumulated malate and VPD. The results do not support the opinion that, for the Namib succulents, CAM is an adaptive mechanism to water stress since long-term and short-term water stress stopped nocturnal malate synthesis, but instead lead to the conclusion that nocuturnal CO₂ fixation is only performed when the water status of the plant can be improved simultaneously.Abbreviations CAM Crassulacean acid metabolism - VPD water vapour pressure deficit Dedicated to Professor H. Ziegler on the occasion of his 60th birthday     

The control of bud dormancy in potato tubers. Measurement of the seasonal pattern of changing concentrations of zeatin-cytokinins

A radioimmunoassay, combined with high-performance liquid chromatography, has been used to analyse the zeatin-type cytokinins of potato (Solanum tuberosum L. cv. Majestic) tubers and tuber buds throughout growth and storage. During tuber growth, zeatin riboside was the predominant cytokinin detected in all tissues. Immediately after harvest, the total cytokinin concentration fell dramatically in the storage tissue, largely as a consequence of the disappearance of zeatin riboside. During storage, levels of cytokinins in the storage tissue remained relatively constant, but increased in the tuber buds. In the buds of tubers stored at 2°C there was a 20-to 50-fold increase in total cytokinin over six weeks, coinciding with the natural break of innate dormancy. At 10°C the rise in the level of bud cytokinins was slower, correlating with the longer duration of innate dormancy. Injecting unlabelled cytokinins into tubers in amounts known to induce sprouting gave rise to increases in cytokinin concentrations in the buds of the same order as the increase associated with the natural break of dormancy. Metabolism of injected cytokinins was greater in non-dormant than in dormant tubers. The roles of cytokinin concentration and the sensitivity of the buds to cytokinin in the control of dormancy are discussed.Abbreviations CK cytokinin - FW fresh weight - HPLC high-performance liquid chromatography - RIA radioimmunoassay - tio⁶ade 6-(4-hydroxy-3-methylbut-trans-2-enylamino)-purine=zeatin - tio⁶adeglc⁹ 6-(4-hydroxy-3-methylbut-trans-2-enylamino)-9--D-glucopyranosyl purine=zeatin-9-glucoside - tio⁶ado 6-(4-hydroxy-3-methylbut-trans-2-enylamino)-9--D-ribofuranosyl purine=zeatin riboside - tio⁶ado-[³H]-diol a radioactive derivative of zeatin riboside, synthesised by periodate-oxidation followed by [³H]NaBH₄-reduction - tio⁶AMP 6-(4-hydroxy-3-methylbut-trans-2-enylamino)-9--D-5-phosphoribofuranosyl purine=zeatin riboside 5-monophosphate - t(ioglc⁴)⁶ade 6-(4-O--D-glucopyranosyl-3-methylbut-trans-2-enylamino)-purine=zeatin-O-glucoside     

Tissue distribution of phenylpropanoid metabolism in cotyledons of Raphanus sativus L.

The tissue distributions of sinapic acid esters (1-sinapoylglucose, sinapolyl-l-malate, 6,3-disinapoylsucrose), kaempferol glycosides, free malic acid and of the enzyme involved in the synthesis of sinapoyl-l-malate, 1-sinapoylglucose: l-malate sinapoyltransferase (SMT), have been investigated in cotyledons of Raphanus sativus L. seedlings. The kaempferol glycosides were mainly localized in the upper epidermis. The sinapoyl esters were found in all tissues, but differed markedly in their concentrations. While disinapoylsucrose was localized predominantly in the mesophyll, most sinapoylmalate was found in the epidermal layers, as was most SMT activity. Ultraviolet microscopy and microfluorospectrophotometry of isolated epidermal peels indicated that the epidermal sinapoyl esters were restricted to guard cells, guard mother cells and adjacent epidermal cells. Upon excitation by UV light (365 nm) these exhibited strong blue fluorescence with an emission maximum at about 480 nm. Our results indicate a highly tissue-and cell-specific secondary metabolism in Raphanus cotyledons and indicate that the biosynthesis of sinapoylmalate is intimately related to the malic-acid metabolism of the guard cells.Abbreviations HPLC high-performance liquid chromatography - SMT 1-sinapoylglucose: l-malate sinapoyltransferase     

A light-enhanced metabolism of sulfite in cells of Cucumis sativus L. cotyledons

The effects of light and several photosynthetic inhibitors on the rate of sulfite metabolism in cells obtained from Cucumis sativus L. cotyledons was studied. The cells were treated with 200 M Na₂SO₃ and the disappearance of sulfite was monitored using either dithiobisnitrobenzoic acid or fuchsin. The rate of sulfite disappearance in light was double the dark rate. Disalicylidene propanediamine at 1 mM increased this light-enhanced metabolism approx. 50%; neither 1 M 3,4-dichlorophenyl-N,N-dimethylurea nor 0.1 mM cyanazine, which completely inhibited CO₂-dependent oxygen evolution, affected the rate of sulfite metabolism. Addition of 200 M Na₂SO₃ to the cells partially inhibited ¹⁴CO₂ fixation. The rate of sulfite consumption by the cells did not affect this inhibition. We conclude that light-dependent sulfite metabolism is cucumber cells may utilize reduced ferredoxin generated as a result of photosynthetic electron transport. An injurious interaction between CO₂ fixation and sulfite appears to occur independently of the sulfite-metabolism process.Abbreviations DCMU 3,4-dichlorophenyl-N,N-dimethylurea - DSPD disalicylidene propanediamine - DTNB 5,5-dithiobis-(2-nitrobenzoic acid)     

Lipoxygenase Metabolism of Arachidonic Acid in Brain

When blood-free mouse brain slices were incubated with exogenous radiolabeled arachidonic acid, gas chromatography/mass spectrometry confirmed that the major radioactive lipoxygenase enzyme product of arachidonic acid was 12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE), with lesser amounts of 5-hydroxy-5,6,8,11,14-eicosatetraenoic acid and 15-hydroxy-5,8,11,13-eicosatetraenoic acid. When 12-[2H]HETE was used to measure endogenous 12-HETE in brain tissue frozen with liquid nitrogen, the level of 12-HETE was 41 +/- 6 ng/g of wet weight tissue. This frozen tissue level was not due to the presence of blood. When brain slices were incubated in vitro for 20 min, the 12-HETE level increased to 964 +/- 35 ng/g of wet weight tissue. Elimination of residual intravascular blood before tissue incubation reduced the brain slice 12-HETE concentration by one-half.     

Effects of Systemically Administered Lithium on Phosphoinositide Metabolism in Rat Brain, Kidney, and Testis

A single subcutaneous dose of 10 mEq/kg LiCl gives rise to an increase in the cerebral cortex level of myo-inositol-1-P (I1P) that closely follows cortical lithium levels and, at maximum, is 40-fold above the control value. Kidney and testis show smaller increases in I1P level following LiCl administration. The I1P level is still sixfold greater than that of untreated rat cortex 72 h later. In cortex, parallel increases also occur in myo-inositol-4-P (I4P) and myo-inositol 1,2-cyclic-P (cI1,2P), whereas myo-inositol-5-P (I5P) remains unchanged. The cortical increases in I1P and I4P levels are partially reversed by administering 150 mg/kg of atropine 22 h after the LiCl, treatment that does not affect cI1,2P. When doses of LiCl from 2 to 17 mEq/kg are given, the cerebral cortex levels of I1P and myo-inositol, measured 24 h later, are found to reach a plateau at about 9 mEq/kg of LiCl, whereas cortical lithium levels continued to increase with greater LiCl doses. Levels of all three of the brain phosphoinositides are unchanged by the 10 mEq/kg LiCl dose, as is the uptake of 32Pi into these lipids. Chronic dietary administration of LiCl for 22 days showed that the effects of lithium on I1P and myo-inositol levels persist for that period. Over the course of the chronic administration of the lithium, levels of I1P, myo-inositol, and of lithium in cortex remained significantly correlated. We believe that these increases in inositol phosphates result from endogenous phosphoinositide metabolism in cerebral cortex and that lithium is capable of modulating that metabolism by reducing cellular myo-inositol levels. The size of the effect is a function of both lithium dose and the degree of stimulation of receptor-linked phosphoinositide metabolism. This property of lithium may explain part of its ability to moderate the symptoms of mania. Our chronic study suggests that prolonged administration of LiCl does not result in compensatory changes in myo-inositol-1-P synthase or myo-inositol-1-phosphatase.