ISSN:0892-6638    

DOI:10.1096/fasebj.7.8.8500685

出版商:Wiley    

年代:1993

数据来源: WILEY

ISSN:0892-6638    

DOI:10.1096/fasebj.7.8.8500686

出版商:Wiley    

年代:1993

数据来源: WILEY

摘要:

The reductive pentose phosphate cycle (Benson‐Calvin cycle) is the main biochemical pathway for the conversion of atmospheric CO2to organic compounds. Two unique systems that link light‐triggered events in thylakoid membranes with enzyme regulation are located in the soluble portion of chloroplasts (stroma): the ferredoxin‐thioredoxin system and ribulose 1,5‐bisphosphate carboxylase/oxygenase‐Activase (Rubisco‐Activase). The ferredoxin‐thioredoxin system (ferre‐doxin, ferredoxin‐thioredoxin reductase, and thioredoxin) transforms native (inactive) glyceraldehyde‐3‐P dehydrogenase, fructose‐1,6‐bisphosphatase, sedoheptulose‐1,7‐bisphosphatase, and phosphoribulokinase to catalytically competent forms. However, the comparison of enzymes reveals the absence of common amino acid sequences for the action of reduced thioredoxin. Thiol/disulfide exchanges appear as the underlying mechanism, but chloroplast metabolites and target domains make the activation process peculiar for each enzyme. On the other hand, Rubisco‐Activase facilitates the combination of CO2with a specific ϵ‐amino group of ribulose 1,5‐bisphosphate carboxylase/oxygenase and the subsequent stabilization of the carbamylated enzyme by Mg2+, in a reaction that depends on ATP and ribulose 1,5‐bisphosphate. Most of these studies were carried out in homogenous solutions; nevertheless, a growing body of evidence indicates that several enzymes of the cycle associate either with thylakoid membranes or with other proteins yielding supra‐molecular complexes in the chloroplast.—Wolosiuk, R. A.; Ballicora, M. A.; Hagelin, K. The reductive pentose phosphate cycle for photosynthetic CO2assimilation: enzyme modulation.FASEB J. 7:622‐637; 1993.

ISSN:0892-6638    

DOI:10.1096/fasebj.7.8.8500687

出版商:Wiley    

年代:1993

数据来源: WILEY

摘要:

General anesthesia markedly impairs normal control of body temperature, reducing the threshold (triggering core temperature) for thermoregulatory vasoconstriction from ≍37 to ≍34.5°C. Sweating and active vasodilation thresholds similarly are increased, widening the range of temperaturesnottriggering regulatory compensations from ≍0.2 to ≌ 4°C. However, once initiated, the gains (slopes of response intensity vs. core temperature curves) and maximum intensities of thermoregulatory responses are nearly normal. Intraoperative core temperature initially decreases rapidly because anesthetic‐induced inhibition of tonic thermoregulatory vasoconstriction causes a core‐to‐peripheral redistribution of body heat. The subsequent slower, linear decrease in body temperature results from heat loss exceeding metabolic heat production. And finally, after 3‐4 h of anesthesia, core temperature stabilizes at an abnormally low value. In patients experiencing minimal heat loss, and therefore not becoming sufficiently hypothermic to trigger vasoconstriction, this plateau can be passive steady state in which heat loss equals production. Conversely, patients becoming sufficiently hypothermic will trigger thermoregulatory vasoconstriction that both decreases cutaneous heat loss and sequesters some metabolic heat in the core. Epidural and spinal anesthesia also cause core hypothermia by inhibiting tonic thermoregulatory vasoconstriction, producing an internal redistribution of heat from the warm core to cooler peripheral tissues. Core hypothermia provokes thermoregulatory responses including vasoconstriction (above the block level) and shivering. Nonetheless, many patients feel warmer after induction of regional anesthesia, apparently because perceived skin temperature is elevated. The following review will focus on anesthetic‐induced impairment of normal thermoregulatory control and the resulting alterations in heat balance.—Sessler, D. I. Perianesthetic thermoregulation and heat balance in humans.FASEB J. 7:638‐644; 1993.

ISSN:0892-6638    

DOI:10.1096/fasebj.7.8.8500688

出版商:Wiley    

年代:1993

数据来源: WILEY

摘要:

Growth hormone‐releasing hormone (GHRH) and interleukin‐1 (IL‐1) are putative endogenous sleep‐promoting substances. Evidence is reviewed showing that,1) GHRH and IL‐1 promote non‐rapid eye movement sleep (NREMS);2) if their production is enhanced, sleep is enhanced; and3) if they are inhibited using either specific antibodies or peptide antagonists, sleep is reduced. Both are in the brain and both are also indirectly linked to sleep/wake cycles by various other evidence, e.g., growth hormone release and IL‐1 plasma levels vary in phase with sleep/wake cycles, Finally, their actions are directly linked to each other; e.g., IL‐1‐induced growth hormone release is mediated via GHRH. The evidence reviewed strongly implicates both GHRH and IL‐1 as key components in humoral sleep regulation. Humoral theories of sleep regulation are complementary to neural theories; both mechanisms affect each other and undoubtedly continuously interact to regulate sleep/wakc cycles.—Krueger, J. M., Obál, F., Jr. Growth hor mone‐releasing hormone and interleukin‐1 in sleep regulation.FASEB J. 7:645‐652; 1993.

ISSN:0892-6638    

DOI:10.1096/fasebj.7.8.8500689

出版商:Wiley    

年代:1993

数据来源: WILEY

摘要:

Polyamines are thought to have several vital roles in cell growth and differentiation. The highly regulated polyamine metabolic pathway provides cells with the ability to finely control the intracellular concentration of these ubiquitous polycations. Although earlier studies of regulation of polyamine content were concentrated on the biosynthetic reactions, recently the importance of the catabolic processes, particularly the highly regulated acetylation step in polyamine degradation, has become apparent. This work has led to an understanding of how a cell may, in a tightly controlled manner, facilitate the breakdown, excretion, cycling, and/or intracellular shuttling of the polyamines. This myriad of possibilities appears to be regulated initially at a single rate‐limiting enzymatic step, the N1‐acetylation of spermidine or spermine, by spermidine/spermine N1‐acetyltransferase (SSAT). Recent cloning of the human SSAT gene has facilitated a more detailed study of this enzyme. SSAT appears to have a role in the determination of tumor sensitivity to a new class of antineoplastic agents. The further study of SSAT and the associated polyamine metabolism should provide a better understanding of the regulation and function of these cations.—Casero, R. A., Jr., Pegg, A. E. Spermidine/spermine N1‐acetyltransferase—the turning point in polyamine metabolism.FASEB J. 7:653‐661; 1993.

ISSN:0892-6638    

DOI:10.1096/fasebj.7.8.8500690

出版商:Wiley    

年代:1993

数据来源: WILEY

摘要:

The interconversion of lysine and β‐lysine, which is catalyzed by lysine 2,3‐aminomutase, is formally similar to the isomerization reactions catalyzed by adenosylcobalamin‐dependent aminomutases. However, lysine 2,3‐aminomutase is activated by 5‐adensoylmethi‐onine and not by adenosylcobalamin. Lysine 2,3‐aminomutase also contains [FeS] clusters, Co(II), and pyridoxal 5′‐phosphate, all of which are required for maximum activity. Lysine 2,3‐aminomutase acts through a mechanism akin to that of the adenosylcobalamin‐dependent enzymes in which substrate radicals are intermediates. However, the 5‐deoxyadenosyl moiety ofS‐adenosylmethionine mediates hydrogen transfer in place of the 5′‐deoxyadenosyl moiety of adenosylcobalamin. 5′‐Deoxyadenosine is an intermediate in adenosylcobalamindependent reactions and in the reaction of lysine 2,3‐aminomutase. The 5′‐deoxyadenosyl radical, derived either from adenosylcobalamin orS‐adenosylmethionine, appears to participate in these reactions. Similarly, the ribonucleotide reductase fromLactobacillus leichmaniiis activated by adenosylcobalamin, whereas the ribonucleotide reductase from anaerobically grownEscherichia coliis activated byS‐adenosylmethionine and an activating enzyme. The 5′‐deoxyadenosyl radical seems to participate in the activation of both reductases. Therefore, both adenosylcobalamin and 5‐adenosylmethionine appear to serve as sources of 5′‐deoxyadenosyl radicals in nature.S‐Adenosylmethionine is not as chemically elegant a molecule as adenosylcobalamin, so it may be regarded as “a poor man's adenosylcobalamin.”—Frey, P. A. Lysine 2,3‐aminomutase: is adenosylmethionine a poor man's adenosylcobalamin?FASEB J. 7:662‐670; 1993.

ISSN:0892-6638    

DOI:10.1096/fasebj.7.8.8500691

出版商:Wiley    

年代:1993

数据来源: WILEY

摘要:

Atomic structures of thymidylate synthase (TS) reveal key steps in a multi‐step reaction and show quantitatively how conformation change is involved in mediating the methyl transfer reaction catalyzed by TS. Numerous alterations in TS produced by mutation, screened by complementation, and further characterized can be understood in terms of the structure and profound structure change required during the TS reaction.—Stroud, R. M., Finer‐Moore, J. S. Stereochemistry of a multistep‐bipartite methyl transfer reaction: thymidylate synthase.FASEB J. 7:671‐677; 1993.

ISSN:0892-6638    

DOI:10.1096/fasebj.7.8.8500692

出版商:Wiley    

年代:1993

数据来源: WILEY

摘要:

Circumventricular organs (CVOs), small structures bordering the ventricular spaces in the midline of the brain, have common morphological and endocrine‐like characteristics that distinguish them from the rest of the nervous system. Among their unique features are cellular contacts with two fluid phases — blood and cerebrospinal fluid — and neural connections with strategic nuclei establishing circuitry for communications throughout the neuraxis. A variety of additional morphological and functional characteristics of the CVOs implicates this group of structures in a wide array of homeostatic processes. For three of the circumventricular organs — the subfornical organ (SFO), the organum vasculosum of the lamina terminalis (OVLT), and the area postrema (AP) — recent findings demonstrate these structures as targets for blood‐borne information reaching the brain. We propose that these three sensory CVOs interact with other nuclei in the maintenance of several homeostatic processes by way of neural and humoral links. We emphasize the collective role of brain CVOs in the maintenance of body fluid homeostasis as a model for the functional integration of these fascinating “windows of the brain” within central neurohumoral systems.—Johnson, A. K., Gross, P. M. Sensory circumventricular organs and brain homeostatic pathways.FASEB J. 7:678‐686; 1993.

ISSN:0892-6638    

DOI:10.1096/fasebj.7.8.8500693

出版商:Wiley    

年代:1993

数据来源: WILEY

摘要:

Although several tyrosine kinases are present in human neutrophils, little is known regarding the biochemical basis for their activation. We have identified two tyrosine kinase activities in 0.1 and 1% Triton cell extracts of human neutrophils using a non‐denaturing gel assay. The first protein tyrosine kinase activity of a faster mobility was associated exclusively with the 0.1% Triton cell extract. The second activity, of slower mobility, was mainly associated with the 0.1% Triton cell extract and to a lesser extent with the 1% Triton cell extract. A modulation of the activities and the distribution of these two tyrosine kinase activities was observed upon stimulation of neutrophils with PDBu (phorbol 12,13‐dibutyrate), a direct PKC (protein kinase C) activator. The addition of 1 μM PDBu induced a time‐dependent decrease of both tyrosine kinases in the 0.1% Triton cell extract. Although the fast mobility tyrosine kinase activity disappeared completely, the slow mobility tyrosine activity decreased only partially. Concomitantly, an increase in the latter activity was detected in the 1% Triton cell extract. The pattern of tyrosine phosphorylation upon PDBu stimulation was also examined and the results showed that the phorbol ester induced time‐dependent increases in the level of phosphotyrosine‐containing proteins in at least 10 distinct bands. Two lines of evidence indicated that the effects of PDBu were mediated by PKC:1) The stereo‐isomer of PDBu, 4α‐PDBu, did not affect the activities and distribution of the tyrosine kinases, and2) The PKC inhibitor, RO 318220, prevented the redistribution of the tyrosine kinase activities and inhibited the stimulation of tyrosine phosphorylation induced by PDBu. These results show that the activity and distribution of at least two human neutrophil tyrosine kinases are modulated after the activation of PKC and that the low mobility tyrosine kinase activity is the most sensitive to PDBu. Based on previous studies, the fast mobility tyrosine kinase activity was likely to be a member of the pp60srctyrosine kinase family and the slower one may be related to the pp93fes. Furthermore, these results begin to define the nature of the relationships among the PKC‐ and the tyrosine kinase‐signaling pathways.—Gaudry, M., Caon, A. C., Naccache, P. H. Modulation of the activity and subcellular distribution of protein tyrosine kinases in human neutrophils by phorbol esters,FASEB J. 7:687‐693; 1993.

ISSN:0892-6638    

DOI:10.1096/fasebj.7.8.7684713

出版商:Wiley    

年代:1993

数据来源: WILEY