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PubMed1997

Safety of slow pathway ablation in patients with long PR interval: further evidence of fast and slow pathway interaction.

Whether the presence of abnormal PR before selective slow pathway ablation for AV node reentrant tachycardia increased the risk of complete heart block remains controversial. We report our experience in seven patients with prolonged PR intervals undergoing catheter ablation for AV reentry tachycardia. Their mean age was 66 +/- 12 years; four patients were female and three were male. RF ablation was performed using an anatomically guided stepwise approach. In six patients, common type AV node reentry was induced and uncommon type was observed in the remaining patient. In all seven patients, successful selective slow pathway ablation was associated with no occurrence of complete heart block and was followed by shortening of the AH interval in five patients. In all seven patients, successful ablation was achieved at anterior sites (M1 in two patients and M2 in five patients). Despite AH shortening after ablation, the 1:1 AV conduction was prolonged after elimination of the slow pathway, excluding either sympathetic tone activation or parasympathetic denervation. In conclusion, selective slow pathway ablation can be performed safely in the majority of patients with prolonged PR interval before the procedure. Because successful ablation is achieved at anterior sites in most patients, careful selection and monitoring of catheter position is required.

Aged↗

PubMed1990

Sites of conduction block in accessory atrioventricular pathways. Basis for concealed accessory pathways.

Catheter recordings of accessory pathway (AP) activation were used to identify the site of antegrade and retrograde AP conduction block in 126 consecutive patients undergoing electrophysiological testing. Activation was recorded from 89 of 121 left free-wall and posteroseptal pathways (left APs) and from 12 of 24 right free-wall, midseptal, and anteroseptal pathways (right APs). The recorded APs were further subdivided into those exhibiting consistent antegrade conduction during sinus rhythm (overt APs: 50 left APs, eight right APs), those exhibiting intermittent antegrade conduction (intermittent APs: six left APs, two right APs), and those exhibiting only retrograde conduction (concealed APs: 33 left APs, two right APs). The sites of block were recorded during decremental atrial and ventricular stimulation. The sites of both antegrade and retrograde block were determined in 40 of 50 overt left APs and six of eight overt right APs. Antegrade and retrograde block occurred at or near the AP-ventricular (AP-V) interface in 37 of 40 overt left APs and two of six overt right APs and at the atrial-AP (A-AP) interface in one of 40 overt left APs and four of six overt right APs. In three of three overt left APs with no retrograde conduction, retrograde block occurred at or near the AP-V interface. The site of antegrade and retrograde block differed in only two of 58 overt pathways. There was no difference between overt APs limited at the A-AP or the AP-V interface in the shortest atrial or ventricular pacing cycle length maintaining 1:1 antegrade or retrograde AP conduction, respectively. Both antegrade and retrograde block occurred near the AP-V interface in four of six intermittent left APs and zero of two intermittent right APs and near the A-AP interface in two of six intermittent left APs and one of two intermittent right APs. The sites of both antegrade and retrograde block were determined in 28 of 33 concealed left APs, and both occurred at or near the AP-V interface in 26 and A-AP interface in two APs. In two of two concealed right APs, antegrade block occurred at the AP-V interface. These findings suggest that both antegrade and retrograde conduction are limited by factors operating near the AP-V interface in overt left APs and at the A-AP or AP-V interface in overt right APs. Factors limiting antegrade conduction in concealed APs appear to be located almost always near the AP-V interface.

Atrioventricular Node↗

PubMed1977

Phosphatidylcholine-lysophosphatidylcholine cycle pathway enzymes in rabbit lung. II. Marked differences in the effect of gestational age on activity compared to the CDP-choline pathway.

Lysophosphatidylcholine (lysoPC), a breakdown product of phosphatidylcholine (PC), might be important in pulmonary PC synthesis through fatty acid exchange reactions. This study defines the levels of three of the enzymes of the PC-lysoPC cycle pathway (lysophospholipase (LPL) (EC. 3.1.1.5), lysophosphatidylcholine-lysophosphatidylcholine acyltransferase (LAT), and acyl-CoA lysophosphatidylcholine acyltransferase (acryl-CoA LAT) (EC. 2.3.1.23)) in developing fetal rabbit lung and compared them with the enzymes of the CPD-choline synthetic pathway (choline kinase (CK) (EC. 2.7.1.32), phosphorylcholine cytidyl transferase (CyT) (EC. 2.7.7.15), and phosphorylcholine glyceride transferase (PCGT) (EC. 2.7.8.2). Lung homogenates of fetal rabbits of known gestation, newborn, and adult rabbits were used for the enzyme, protein, and phospholipid analyses. Total lung phospholipid, PC, and protein increased with gestational age. Thirty days' gestation, newborn, and maternal lung activities of CK, CyT, and PCGT had decreased to only 50% of their activities at 22-26 days' gestation. In contrast, LPL and LAT activities increased 4-5-fold from 22-26 days to 30 days' gestation, and increased further in the newborn lung, finally to a level matching maternal lung (about 8-10-fold higher than the 22-26 days' gestation activities). The microsomal acyl-CoA LAT also showed a similar increasing activity with gestational age. In fetal lung, enzymic activities for the apparent major PC synthetic pathway decreased. In contrast, the marked increases in LPL, LAT, and acyl-CoA LAT activities with increasing gestational age and at birth suggests importance of the PC lysoPC cycle pathway in regulating synthesis and turnover with maturation.

1-Acylglycerophosphocholine O-Acyltransferase↗

PubMed1993

The interleukin-6 (IL-6)/IL-6-receptor system induces human chorionic gonadotropin production by activating tyrosine kinase-dependent signal transduction pathway different from pathways triggered by protein kinase activators including gonadotropin releasing hormone.

Interleukin-6 (IL-6) may play an important role in human CG (hCG) production by activating the IL-6-receptor (-R) system on human trophoblasts. Trophoblasts produced hCG in response to rIL-6 as well as to 8-bromo cAMP (8-Br-cAMP), 12-O-tetradecanoyl phorbol-13-acetate (TPA), and calcium ionophore A23187. To determine whether the signal transduction pathway activated by the IL-6-R system depends on protein kinases such as protein kinase A, protein kinase C, and Ca2+/calmodulin-dependent kinase, trophoblasts were stimulated with recombinant (r-) IL-6 in the presence or absence of protein kinase inhibitors such as N(2-methyl-aminoethyl)-5-isoquinoline sulfonamide dihydrochloride (H8), and 1-(5-isoquinolinesulfomyl)-2-methylpiperazine (H7) and a calmodulin antagonist, N-(6-aminohexyl)-5-chloro-1- napthalenesulfonamide (W7), H8, H7, and W7 failed to suppress rIL-6-induced hCG production but completely inhibited hCG production induced by 8-Br-cAMP, TPA, and the GnRH agonist (GnRHa), respectively. In contrast, genistein, a tyrosine kinase inhibitor, completely suppressed rIL-6-induced hCG production but failed to inhibit hCG production induced by 8-Br-cAMP, TPA, and A23187. Genistein also did not suppress GnRH-induced hCG production. The addition of genistein to rIL-1- and rTNF-alpha-stimulated trophoblasts inhibited rIL-1-induced and rTNF-alpha induced hCG production but maintained rIL-1- and rTNF-alpha-induced IL-6 production. These results show that the IL-6/IL-6-R system-induced signal transduction pathway in the placenta probably stimulates hCG production by activating a tyrosine kinase pathway. The experiment with genistein shows that the GnRH/GnRH-R system activates a signal transduction pathway distinct from that activated by the IL-6/IL-6-R system.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1990

"CD3low" human thymocyte populations can readily be triggered via the CD2 and/or CD28 activation pathways whereas the CD3 pathway remains nonfunctional.

We have investigated the role of the CD2 and the CD28 Ag-independent pathways of activation on CD3low thymocytes. We previously showed that anti-CD28 mAb synergized with anti-CD2 mAb directed against epitopes T11.1 and T11.2, in the activation of purified resting T cells or unseparated thymocytes. Proliferation induced via CD2 plus CD28 was mediated via an IL-2-dependent pathway and was not affected by prior modulation of the CD3-TCR complex. Here, we show that a subset of CD3low thymocytes, although unresponsive to CD3 activation, can be activated to proliferate through the CD2 or the CD28 pathways, in the presence of exogenous IL-2. The mitogenic combination of mAb to CD2 and CD28 induces a proliferation of thymocytes which, in absence of exogenous lymphokines, is restricted to the more mature intrathymic subpopulation, CD1a-. However, CD3low thymocytes can also be triggered through the CD2 plus CD28 activation pathways but require at least addition of exogenous IL-2 to proliferate. This study demonstrates that a fraction of immature CD3low thymocytes possesses functional CD2 and CD28 surface molecules at a time when CD3 is not yet functional.

Age Factors↗

PubMed1978

Kinetic assessment of alternative complement pathway activity in a hemolytic system. II. Influence of antibody on alternative pathway activation.

By using a kinetic assay, we have examined the role of antibody in the lysis of rabbit erythrocytes (RaRBC) through the alternative complement (C) pathway. Sera from some hypogammaglobulinemic (Hgamma) humans and all agammaglobulinemic chickens tested had subnormal activity in the assay. Heated normal human or chicken sera, but not heated Hgamma sera, restored activity to deficient Hgamma serum and initiated hemolysis in the presence of rabbit serum as C source. Absorption of heated normal human serum with RaRBC, but not with sheep erythrocytes or zymosan, removed its ability to reconstitute deficient Hgamma serum. Normal hemolytic activity could be resotred to Hgamma serum with human IgM, IgG, or colostral IgA, with goat anti-RaRBC IgG, or with an eluate from serum-sensitized RaRBC, but not with myeloma IgA. Restoration of hemolytic activity to Hgamma serum could be achieved in a dose-dependent fashion with the F(ab')2 fragment of IgG. These results suggest that antibody exerts a significant rate-limiting effect on alternative pathway activity in the RaRBC lytic system. This raises the possibility that antibody may be required for efficient alternative pathway activity in vivo and that the pyogenic infections that occur in Hgamma individuals are due to inefficient activation and fixation of C3 through either the classical or alternative pathway.

Agammaglobulinemia↗

PubMed1995

An epitope-selective, transporter associated with antigen presentation (TAP)-1/2-independent pathway and a more general TAP-1/2-dependent antigen-processing pathway allow recognition of the HIV-1 envelope glycoprotein by CD8+ CTL.

The lysis of virally infected cells by CTLs requires the recognition of processed fragments of viral proteins presented in association with class I MHC molecules on the surfaces of infected cells. Processing begins in the cytosol with the degradation of viral proteins into peptides that are then transported into the endoplasmic reticulum (ER) for association with newly synthesized class I molecules. Transport is mediated by a heterodimer of the MHC-encoded proteins, transporter associated with Ag presentation (TAP)-1 and TAP-2. Uncertainty exists over the site of processing of viral envelope (env) proteins. The extracellular domains of env proteins are not present in the cytosol, the site in which the class I-restricted Ag-processing pathway begins. Rather, the ecto-domains of env proteins are cotranslationally translocated into the ER during biosynthesis. We have analyzed the processing of the HIV-1 env protein by using a large series of env-specific human CD8+ CTL clones. These studies have led to the delineation of two distinct processing pathways. The first pathway permits a subset of class I-restricted epitopes in the ecto-domain of the env protein to be generated efficiently by a TAP-1/2-independent mechanism localized to the ER or a premedial Golgi compartment. A second, more general pathway that is capable of generating all env epitopes uses as a substrate env protein mislocalized to the cytosol and produces peptides that are transported from the cytoplasm to the ER in a TAP-1/2-dependent fashion.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1995

[Supraventricular tachycardia due to simultaneous conduction in the rapid and slow nodal pathways. Treatment by ablation of the slow pathway].

The authors report the case of a 70 year old woman with frequent attacks of supraventricular tachycardia resistant to antiarrhythmic therapy. The tachycardia was irregular with predominantly normal QRS complexes. Electrophysiological investigation showed dual conduction in the atrioventricular node and tachycardia was induced by atrial extrastimulus. However, reentrant tachycardia could not be induced, the refractory period of the slow pathway being much longer than that of the rapid pathway. The mechanism of the tachycardia was simultaneous conduction of the sinus rhythm through the two nodal conduction pathways. This was successfully treated by radiofrequency ablation of the slow pathway.

Aged↗

PubMed1996

Characterization of crystallization pathways during cholesterol precipitation from human gallbladder biles: identical pathways to corresponding model biles with three predominating sequences.

In model biles, five crystallization sequences are present as functions of bile salt/lecithin (egg yolk) ratio and their positions on phase diagrams are influenced by bile salt hydrophobicity, temperature, and total lipid concentration (D. Q-H. Wang and M.C. Carey. J. Lipid Res. 1996.37: 606-630). To determine whether the same pathways occur ex vivo during cholesterol precipitation from human gallbladder biles, we examined 22 cholesterol gallstone (CSI = 1.56 +/- 0.26), 4 pigment gallstone (0.69 +/- 0.06), and 4 control biles (0.85 +/- 0.22) by microscopy and lipid analytic techniques for 30 days. Temperature was varied (4-45 degrees C) to move relative compositions into adjacent pathways or supersaturated zones to test whether the same bile could be forced to crystallize in different sequences. Sequences in native bile were identical to those in model systems composed of mixed bile salts-lecithin-cholesterol mixtures, and three corresponding pathways (B, C, D; op. cit.) were observed at 37 degrees C. With increasing lecithin content, we found i) B: plate-like cholesterol monohydrate crystals appeared before arc-shaped (putatively anhydrous cholesterol) crystals which transformed via helices and tubules into plate-like crystals and no liquid crystals formed; ii) C: lamellar liquid crystals, typified by birefringent multilamellar vesicles, were detected before cholesterol monohydrate crystals, and subsequently arc, helical and tubular crystals appeared; and iii) D: precipitation of lamellar liquid crystals was followed by cholesterol monohydrate crystals and no arc crystals were detected. Added EDTA prevented calcium bilirubinate formation, but crystallization sequences in these biles were identical to those without EDTA. We conclude that i) cholesterol crystallization pathways and sequences in human gallbladder biles are identical to model biles matched for appropriate physical-chemical conditions; ii) three of the five sequences observed in model biles were found in native bile; and iii) calcium bilirubinates neither promote biliary cholesterol crystallization nor influence crystal growth.

Bile Acids and Salts↗

PubMed1985

Inhibition of cleavage of the third component of human complement (C3) by its small cleavage fragment, C3a: inhibition occurs with the classical-pathway, but not the alternative-pathway, C3 convertase.

Activation of the third component of complement (C), C3, is central to the functioning of the C system in inflammation. Cleavage of C3 by the C3 convertases of both the classical and alternative pathways results in the formation of two split products, C3b and C3a. C3a inhibited cleavage of C3 by the classical-pathway C3 convertase. The inhibition varied in a concn-dependent relationship, with a concn of approximately 40 micrograms/ml yielding 50% inhibition. Removal of the carboxy terminal arginine from the C3a did not alter the inhibition. C3a did not inhibit cleavage of C3 by the alternative C pathway C3 convertase, or cleavage of C5 by C5 convertase. The C3-cleaving capacity of EAC142oxy that had been previously incubated with C3a could be recovered completely by washing the cells, indicating that the C3a binding to the EAC42oxy cell must have been reversed without having had an effect on the amount of C2 bound. Ribonuclease, a molecule of similar size and charge to C3a, did not affect C3 cleavage and C3a inhibition was not reduced by providing a surface for non-specific adsorption of the C3a, suggesting that the effect of C3a on C3 cleavage was not mediated by non-specific interaction with cell surfaces. C3a inhibited the C3-cleaving capacity of the fluid-phase enzyme, C42oxy, to the same degree as it inhibited the cell-bound enzyme, EAC42oxy, indicating that the C3a must interact with the C42 complex directly. Inhibition of C3 cleavage by C3a is the first demonstration of product inhibition of a complement enzyme. It may provide another control of C3 activation.

Arginine↗

PubMed1979

Activation of the classical complement pathway by nephritic factor bound to the alternative pathway C3/C5 convertase.

Nephritic Factor (NF), the potent alternative pathway activator, which is occasionally found in association with certain types of nephritis has recently been identified as an IgG class autoantibody specific for the C3 convertase (C3bB) of the alternative pathway. In these studies we have examined the possibility that the cell-bound NF-stabilized C3 convertase (EC3 bBNF) binds and activates the first component of the classical pathway of complement. EC3bBNF bound C1q, and the extent of binding was dependent upon the number of NF molecules bound per cell and decreased parallel to the dissociation and release of NF from the cells. Interaction of C1 with bound NF resulted in its activation as shown by the proteolytic conversion of proenzyme C1s to its activated form C1s. As was the case with C1q binding, C1 activation was dependent on the number of NF molecules bound per cell. Thus the NF-stabilized C3 convertase binds and activates C1.

Binding Sites↗

PubMed1978

Intra- and extrahypothalamic vasopressin and oxytocin pathways in the rat. Pathways to the limbic system, medulla oblongata and spinal cord.

Vasopressin and oxytocin pathways were specifically localized in glutaraldehyde-paraformaldehyde fixed rat brains, with the use of the unlabelled antibody enzyme method and purification of the first antiserum. Vasopressin and oxytocin containing pathways were traced from the paraventricular nucleus towards the dorsal and ventral hippocampus, the nuclei of the amygdala, substantia nigra and substantia grisea, nucleus tractus solitarius, nucleus ambiguus and to the substantia gelatinosa of the spinal cord. In addition, a vasopressin containing pathway between the suprachiasmatic nucleus and the lateral habenular nucleus was demonstrated. The possible nature (axons or dendrites) and role of these extrahypothalamic fibres is discussed in relation to water balance, milk ejection and avoidance behaviour.

Animals↗

PubMed1996

The nitric oxide-cyclic GMP pathway is required for nociceptive signalling at specific loci within the somatosensory pathway.

The involvement of nitric oxide in nociceptive processing was examined at the main loci of synaptic transmission within the rat somatosensory pathway from the caudal sural cutaneous nerve. Intrathecal (lumbar 1-3) administration of the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (30 micrograms), inhibited nitric oxide synthase in this region of the spinal cord by greater than 80% but had no significant effect on nitric oxide synthase in parietal cerebral cortex, thalamus or medulla/pons. In a rat model of peripheral neuropathy (one to two week ligation of the caudal sural cutaneous nerve), intrathecal administration of the same dose of N omega-nitro-L-arginine methyl ester prevented the hyperalgesic response to thermal stimuli. Administration of 30 micrograms N omega-nitro-L-arginine methyl ester into the lateral ventricle had no effect on nitric oxide synthase in the lumbar 1-3 region of the spinal cord but gave substantial inhibition in higher areas of the somatosensory pathway (parietal cerebral cortex, thalamus and medulla/pons). Nitric oxide synthase in the parietal cerebral cortex (but not thalamus) was inhibited to a greater extent in the hemisphere ipsilateral to the site of administration. Administration of 30 micrograms N omega-nitro-L-arginine methyl ester into the lateral ventricle decreased thermal hyperalgesia, but only when N omega-nitro-L-arginine methyl ester was administered contralateral to the ligated caudal sural cutaneous nerve and therefore ipsilateral to the cortical nociceptive processing from this nerve. Intrathecal and intracerebroventricular administration of the selective inhibitor of nitric oxide-sensitive guanylyl cyclase, 1-H-[1,2,4]oxadiazalo[4,3-a]quinoxalin-1-one, also decreased the hyperalgesic response to thermal stimuli. These data demonstrate that, in a model of neuropathic pain, nitric oxide is involved in nociceptive processing at spinal and cerebrocortical synaptic loci of the somatosensory pathway and that its actions appear to be mediated through guanylyl cyclase.

Animals↗

PubMed1991

Multiple signal transduction pathways lead to extracellular ATP-stimulated mitogenesis in mammalian cells: I. Involvement of protein kinase C-dependent and -independent pathways.

We recently reported that extracellular ATP was mitogenic for Swiss 3T3, 3T6, and A431 cells (Huang et al.: Proc. Natl. Acad. Sci. USA, 86:7904-7908, 1989). Here we examined the possible involvement of activation of the protein kinase C (PKC) signal transduction pathway in the mechanism of action of extracellular ATP. A potent synergistic stimulation of DNA synthesis in quiescent cultures of 3T3 and 3T6 cells was observed when ATP was presented in combination with growth factors that activate PKC, such as bombesin, vasopressin, or tumor-promoting phorbol esters. This finding suggests that ATP and these mitogens do not act through a common mechanism. In contrast, ATP was unable to show synergism with phorbol esters in A431 cells. We discovered striking differences when we examined the kinetics of formation of diacylglycerol (DAG) stimulated by ATP among these cell lines. Thus, ATP stimulated a sustained biphasic increase of DAG in A431 cells, but only a rapid transient increase of DAG formation was observed in 3T3 and 3T6 cells. The breakdown of phosphatidylcholine was stimulated by ATP in A431 cells; however, a significantly reduced effect was displayed in 3T6 cells. Furthermore, we found that the diacylglycerol-kinase inhibitor, 1-monooleoylglycerol, greatly potentiated ATP-stimulated DNA synthesis in A431 cells. Finally, down-regulation of PKC by long-term exposure to phorbol dibutyrate (PDBu) prevented stimulation of DNA synthesis induced by bombesin, vasopressin, or phorbol esters in 3T3 or 3T6 cells, while it had no such effect on ATP-stimulated mitogenesis in the presence of insulin or epidermal growth factor. On the other hand, PDBu-mediated down-regulation of PKC partially inhibited [3H [thymidine incorporation stimulated by ATP in A431 cells. Taken together, we conclude that a protein kinase C-dependent pathway is partially involved in ATP-stimulated DNA synthesis in A431 cells, but a protein kinase C-independent pathway exists in 3T3 and 3T6 cells. Pertussis toxin (PTX) inhibited the sustained phase of DAG formation and the breakdown of phosphatidylcholine stimulated by ATP in A431 cells. This suggests involvement of a PTX-sensitive G protein.

Adenosine Triphosphate↗

PubMed1990

Common biochemical pathway of dysmorphogenesis in murine embryos: use of the glucocorticoid pathway by phenytoin.

Phenytoin (5,5-diphenylhydantoin), a common anticonvulsant drug, is known to produce anomalies in the craniofacial region of animals and humans. Furthermore, recent evidence suggests that phenytoin disrupts craniofacial and neural tube morphogenesis by inhibiting the arachidonic acid cascade, a pathogenesis already implicated for glucocorticoids and hyperglycemia in the palate. This study tested the hypothesis that phenytoin interferes with the arachidonic acid cascade via the same biochemical pathway demonstrated for glucocorticoids. The proposed pathway was tested at two levels. First, indomethacin, an inhibitor of the enzyme cyclooxygenase, was used in culture to block the correction of phenytoin-induced defects by arachidonic acid. Second, cortexolone, an anti-glucocorticoid that binds at the glucocorticoid receptor binding site, was tested for its ability to prevent phenytoin-induced teratogenicity. Eighty-four percent of the embryos cultured in phenytoin and 93% of those cultured in phenytoin plus arachidonic acid and indomethacin had neural tube and/or craniofacial deformities. In contrast, only 14% of the embryos cultured in phenytoin plus cortexolone were affected. Indomethacin itself produced anomalies in 83% of the exposed embryos. These data are consistent with the hypothesis that the teratogenic action of phenytoin in murine embryo cultures occurs via the glucocorticoid anti-inflammatory pathway. Thus, the glucocorticoid receptor appears to be responsible for mediating phenytoin-induced teratogenicity.

Animals↗

PubMed1994

In situ behavior of the pyrimidine pathway enzymes in Saccharomyces cerevisiae. 4. The channeling of carbamylphosphate to aspartate transcarbamylase and its partition in the pyrimidine and arginine pathways.

In Saccharomyces cerevisiae the two first reactions of the pyrimidine pathway are catalyzed by a multifunctional protein bearing carbamylphosphate synthetase and aspartate transcarbamylase activities. The present study shows that this complex exhibits channeling of the intermediary metabolite carbamylphosphate, although this channeling is not absolute. Transient time to attain steady state and concentration of this intermediary metabolite were determined under different conditions. It is shown that the process of channeling does not significantly affect the concentration of the intermediary product. This result is in agreement with the theoretical modeling made by Cornish Bowden et al. The lack of channeling increases the transient time necessary to reach the steady rate of reaction by only a factor of three. In addition, channeling has only a small effect on the partition of carbamylphosphate between the pyrimidine and arginine biosynthetic pathway in a mutant strain devoid of the carbamylphosphate synthetase specific to the arginine pathway. The use of a mutant form of the complex suggests that it is between the carbamylphosphate synthetase and aspartate transcarbamylase catalytic sites belonging to the same polypeptide chain that channeling occurs.

Arginine↗

PubMed1998

Involvement of the mevalonic acid pathway and the glyceraldehyde-pyruvate pathway in terpenoid biosynthesis of the liverworts Ricciocarpos natans and Conocephalum conicum.

The incorporation of 13C-labeled glucose into borneol, bornyl acetate, the sesquiterpenes cubebanol and ricciocarpin A, phytol, and stigmasterol has been studied in axenic cultures of the liverworts Ricciocarpos natans and Conocephalum conicum. Quantitative 13C NMR spectroscopic analysis of the resulting labeling patterns showed that the isoprene building blocks of the sesquiterpenes and stigmasterol are built up via the mevalonic acid pathway, whereas the isoprene units of the monoterpenes and the diterpene phytol are exclusively derived from the glyceraldehyde-pyruvate pathway. These results indicate the involvement of both isopentenyl diphosphate biosynthetic pathways in different cellular compartments.

Camphanes↗

PubMed1982

Regulation of pathways of glucose metabolism in kidney. Specific linking of pentose phosphate pathway activity with kidney growth in experimental diabetes and unilateral nephrectomy.

The pentose phosphate pathway operates at an elevated level in rat kidney following induction of diabetes and in the compensatory hypertrophy following unilateral nephrectomy in control and alloxan-diabetic rats, as shown by the yields of 14CO2 from [1-14C]glucose, [6-14C]glucose and 3H2O yields from [2-3H]glucose. The elevated flux through the pentose phosphate pathway is correlated with the increased RNA content and weight of the kidney. The direct utilization of NADPH for reductive synthetic reactions and the potential for indirect utilization via the sorbitol route and the linked transhydrogenase reactions of the glucuronate-xylulose pathway, for NADH and ATP generation, are also discussed.

Animals↗