Biomedical subjects

P Raymond

Publications and source records attributed to P Raymond.

At least 37 records · Page 2Linked to original sources

PubMed1996

Bradykinin decreases T-kininogen synthesis in a rat hepatoma cell line: evidence of bradykinin B2-type receptors.

Using the rat H4-II-E-C3 hepatoma cell line, we investigated the presence of [125I][Tyr8]BK binding sites and the direct modulation of T-kininogen synthesis, an acute phase protein of inflammation, by bradykinin (BK) analogues. H4-II-E-C3 membrane preparations exhibited [125I][Tyr8]BK binding sites with a Kd of 4 nM and a Bmax of 120 fmol/mg of protein. Des-Arg9-BK showed no affinity (Ki > 10(-4) M) for these sites. The B2 metabolism-resistant and selective agonist [Phe8 psi (CH2-NH)Arg9]BK decreased the T-kininogen concentration in H4-II-E-C3 medium by 23% (p < 0.05). This effect was reversed by coincubation with the B2 antagonist HOE140. The B1 agonist Sar[D-Phe8]des-Arg9-BK and the B1 antagonist Lys[Leu8]des-Arg9-BK did not modify T-kininogen concentrations. The interaction between cytokines and kinins in the modulation of T-kininogen synthesis was also studied. Preincubation of hepatoma cells for 1 h with interleukin-1 alpha (IL-1 alpha) alone reduced T-kininogen concentrations by 37%, and this effect was blocked by co-addition of HOE140. Preincubation with interleukin-6 (IL-6) increased T-kininogen levels by threefold. Coincubation in the presence of the B2 agonist decreased this augmentation by 24%. The latter effect was reversed by co-addition of HOE140. None of the cytokines tested induced a response to the B1 agonist or antagonist under the experimental conditions studied. Overall, these results support the presence of a functional B2 receptor on H4-II-E-C3 cells that modulates T-kininogen synthesis. We suggest that the receptor is involved in vivo in a retroaction loop between kinins and T-kininogen production during inflammation. We speculate that BK could be a mediator in the modulation of acute phase protein synthesis by the cytokines IL-1 alpha and IL-6.

Acute-Phase Reaction↗

PubMed1996

Metabolic regulation of asparagine synthetase gene expression in maize (Zea mays L.) root tips.

Differential hybridization of a cDNA library constructed with poly(A)+ mRNA from 24 h starved maize (Zea mays L.) root tips, resulted in the isolation of a cDNA (called pZSS1) that was highly induced during glucose deprivation. The nucleotide sequence analysis of the full-length cDNA allowed its identification by comparison with sequence data bases. The 586 amino acid sequence encoded by pZSS1 was shown to be about 60% identical to sequences of asparagine synthetases (EC 6.3.5.4) from Asparagus officinalis, Pisum sativum, Arabidopsis thaliana and Brassica oleracea. Southern blot analysis of maize genomic DNA showed that asparagine synthetase may be encoded by at least two genes. The use of a specific probe for the 3' untranslated region of pZSS1 in Northern blot experiments, revealed that the isolated AS gene was essentially expressed in roots of maize seedlings. Time course analysis revealed that maximal expression of the gene corresponding to pZSS1 occurs between 18 and 24 h after the onset of the starvation treatment. The steady-state levels of transcripts in maize root tips were found to change under various incubation conditions. Exogenous supply of metabolizable sugars downregulated the gene expression, while carbohydrate deprivation or feeding with non-metabolizable sugars resulted in the induction of gene expression. In addition to carbohydrate deprivation, the effects of nitrogen metabolite supply and stress conditions indicate that gene expression might be under metabolic control in maize root tips. The intracellular nitrogen to carbon ratio might be an important factor for the regulation of asparagine synthetase gene expression.

Amino Acid Sequence↗

PubMed1996

Selective kallikrein-kinin system activation in inbred rats differentially susceptible to granulomatous enterocolitis.

BACKGROUND & AIMS: Crohn's disease is characterized by unrestrained inflammation with a genetic component. Genetic susceptibility and activation of the kalli-krein-kinin (contact) system were investigated in experimental enterocolitis and extraintestinal inflammation induced by bacterial polymers. METHODS: Kinetics of inflammation in inbred Lewis and Buffalo rats injected subserosally with peptidoglycan-polysaccharide polymers were correlated with in vivo and in vitro activation of the contact system. RESULTS: Lewis rats had a biphasic course of enterocolitis. Acute inflammation peaked 1 day after injection, gradually decreasing until day 14 when intestinal inflammation spontaneously reactivated and persisted for 16 weeks, accompanied by arthritis, granulomatous hepatitis, anemia, and leukocytosis. Self-limited acute enterocolitis in Buffalo rats resolved by 24 days without extraintestinal involvement. Consumption of the precursor proteins prekalli-krein and high-molecular-weight kininogen indicated activation of the plasma contact system in Lewis rats and closely correlated with chronic intestinal inflammation. Contact system activation did not occur in Buffalo rats, even during acute inflammation. In vitro studies showed a decreased rate of kininogen cleavage in Buffalo plasma. CONCLUSIONS: Selective in vivo and in vitro activation of the contact system in susceptible Lewis rats suggests that this pathway is one determinant of genetic susceptibility to granulomatous enterocolitis and systemic complications.

Acute-Phase Proteins↗

PubMed1996

Serum interspecies differences in metabolic pathways of bradykinin and [des-Arg9]BK: influence of enalaprilat.

Among the different enzymes responsible for the metabolism of bradykinin (BK), three peptidases look relevant in vivo: kininase I (KI), which transforms BK into its active metabolite, [des-Arg9]BK; kininase II (KII); and neutral endopeptidase, which inactivate BK and [des-Arg9]BK. The in vitro incubation of BK and [des-Arg9]BK in the serum of four species with or without enalaprilat and the quantification of the immunoreactivity of both peptides at different time intervals allowed the measurement of the kinetic parameters characterizing their metabolic pathways. Highly sensitive chemiluminescent enzyme immunoassays were used to measure the residual concentrations of BK and [des-Arg9]BK. Half-life (t1/2) of BK showed significant difference among species: rats (10 +/- 1 s) = dogs (13 +/- 1 s) < rabbits (31 +/- 1 s) < humans (49 +/- 2 s). t1/2 values of [des-Arg9]BK were also species dependent: rats (96 +/- 6 s) < < rabbits (314 +/- 6 s) = dogs (323 +/- 11 s) = humans (325 +/- 12 s). Enalaprilat significantly prevented the rapid BK and [des-Arg9]BK degradation in all species except that of [des-Arg9]BK in rat serum. Relative amount of BK hydrolyzed by serum KII was given as follows: rabbits (93.7 +/- 14.8%) = rats (83.6 +/- 6.7%) = humans (76.0 +/- 7.5%) > dogs (50.0 +/- 3.9%). Its importance in the hydrolysis of [des-Arg9]BK was 5.2 +/- 0.5% in rats < < 33.9 +/- 1.5% in humans < 52.0 +/- 1.1% in rabbits < 65.1 +/- 3.4% in dogs. The participation of serum KI in the transformation of BK into [des-Arg9]BK was dogs (67.2 +/- 5.3%) > > humans (3.4 +/- 1.2%) = rabbits (1.8 +/- 0.2%) = rats (1.4 +/- 0.3%). Finally, no significant difference on t1/2 values for BK and [des-Arg9]BK could be demonstrated between serum and plasma treated with either sodium citrate or a thrombin inhibitor. These results revealed striking species differences in the serum metabolism of kinins that could address at least partially some of the controversial data related to the cardioprotective role of kinins.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1996

Chloramphenicol and the inflammatory response in the rat. Upregulation of the gene for T2-kininogen in liver.

Recent observations have indicated that cytokine and glucocorticoid mediators of the inflammatory response in mammals interfere with mitochondrial respiratory capacity of cultured cells. Here, we report studies on the effect of the antibiotic chloramphenicol (CAP), a potent mitochondrial protein synthesis and respiratory inhibitor, on the inflammatory response in the rat. CAP was injected daily (i.p.) at doses of 30, 100 and 300 mg kg-1 during a period of 10 days. Acute inflammation was induced on day 10 by s.c. injection of carrageenan into the hindpaws. Paw edema reaction and liver and serum expression of the acute phase protein T-kininogen were used as markers of the local and systemic inflammatory response, respectively. Albumin was selected as a liver protein whose expression is little or not affected in inflamed rats. We found that the swelling process induced locally by carrageenan injection was significantly altered in rats treated with CAP at the dose level of 300 mg kg-1. The inhibitory effect of CAP was transient, extending up to 3 hr after carrageenan injection. CAP was observed also to alter the mitochondrial respiratory capacity of liver cells, reducing cytochrome C oxidase activity up to 50%. In contrast, liver immunoreactive T-kininogen content and the T2-kininogen mRNA steady-state level were found to increase in a dose-related manner in CAP-treated animals. These values were slightly different from those recorded in control rats inflamed with carrageenan. No significant increase of T-kininogen serum content was seen at all dose levels of CAP injected. Among inflamed animals, those exposed long-term to CAP had elevated liver and serum T-kininogen content and t2-kininogen mRNA steady-state levels. Expression of the gene for albumin was not affected in rats treated or not with CAP. The present observations indicate that CAP influences both local and systemic inflammatory responses in the rat.

Animals↗

PubMed1995

Quantification of compartmented metabolic fluxes in maize root tips using isotope distribution from 13C- or 14C-labeled glucose.

Metabolic pathways of the intermediate metabolism of maize root tips were identified and quantified after labeling to isotopic and metabolic steady state using glucose labeled on carbon-1, -2, or -6 with 14C or 13C. The specific radioactivity of amino acids and the 13C-specific enrichment of specific carbons of free glucose, sucrose, alanine and glutamate were measured and used to calculate metabolic fluxes. The non-triose pathways, including synthesis of polysaccharides, accumulation of free hexoses, and to a lesser extent starch synthesis, were found to consume 75% of the glucose entering the root tips. The cycle of synthesis and hydrolysis of sucrose was found to consume about 70% of the ATP produced by respiration. The comparison of the specific radioactivities of amino acids and phospholipid glycerol phosphate after labeling with [1-(14)C] or [6-(14)C]glucose revealed the operation of the pentose phosphate pathway. The transfer of label from [2-(14)C]glucose to carbon-1 of starch glucosyl units confirmed the operation of this pathway and indicated that it is located in plastids. It was found to consume 32% of the hexose phosphates entering the triose pathways. The remaining 68% were consumed by glycolysis. The determination of the specific enrichment of carbohydrate carbons -1 and -6 after labeling with [1-(13)C]glucose indicated that both the conversion of triose phosphates back to hexose phosphates and the transaldolase exchange contributed to this randomization. Of the triose phosphates produced by glycolysis and the pentose phosphate pathway, about 60% were found to be recycled to hexose phosphates, and 28% were directed to the tricarboxylic acid cycle. Of this 28%, two-thirds were found to be directed through the pyruvate kinase branch and one-third through the phosphoenolpyruvate branch. The latter essentially has an anaplerotic function since little malate was found to be converted to pyruvate (malic enzyme reaction).

Biological Transport↗

PubMed1995

Quantification of des-Arg9-bradykinin using a chemiluminescence enzyme immunoassay: application to its kinetic profile during plasma activation.

There is a renewed interest in the kininase I pathway of kinin metabolism, because des-Arg9-bradykinin (des-Arg9-BK) and des-Arg10-Lys-BK are selective and potent agonists of the B1 receptors, that are apparently upregulated by tissue injury. We have developed a polyclonal rabbit antiserum against des-Arg10-Lys-BK. In a radioimmunoassay for des-Arg10-Lys-BK, this antiserum exhibited high specificity. Notably, native kinins with the C-terminal Arg residue, bradykinin (BK) and Lys-BK, did not cross-react to a significant extent, whereas des-Arg9-BK and digoxigenin (DIG)-des-Arg9-BK exhibited a complete cross-reactivity. The antibodies were used to set up a sensitive chemiluminescence enzyme immunoassay (CLEIA) using the DIG-anti-DIG system as intermediate for the revelation of the immune complexes. The detection limit and the half-maximal saturation concentration for des-Arg9-BK were 27 and 1530 fmol/ml respectively. This assay, as well as another for BK quantification, have been applied in vitro to rabbit plasma activated by kaolin. The conversion of BK into des-Arg9-BK was generally efficient, and the persistence and concentration of both peptides were increased in the presence of enalaprilat an inhibitor of the angiotensin converting enzyme (ACEI). Rabbits treated with bacterial lipopolysaccharide exhibited an increase of plasma immunoreactive des-Arg9-BK that was potentiated in animals also treated with ACEI. This CLEIA for des-Arg9-BK is a new analytical tool applicable to analyze of the kininase I metabolites of kinins in vitro and in vivo. Measurements of des-Arg9-BK may be useful indicators of the kallikrein-kinin system activation.

Amino Acid Sequence↗

PubMed1995

Molecular cloning and characterization of six cDNAs expressed during glucose starvation in excised maize (Zea mays L.) root tips.

In order to isolate glucose-starvation-related cDNAs in maize (Zea mays L.) root tips, a cDNA library was constructed with poly(A)+ mRNA from 24 h starved root tips. After differential screening of the library, we isolated six different cDNAs (named pZSS2 and pZSS7) which were expressed during glucose starvation. Time course analysis revealed that maximum expression of five of these genes occurs 30 h after the onset of the starvation treatment. On the contrary, the expression of mRNAs corresponding to pZSS4 was maximal at an early stage of starvation and then dramatically decreased. The expression of this gene did not seem to be specific for glucose starvation. The pattern of induction of the genes corresponding to pZSS2, pZSS3, pZSS5, pZSS6 and pZSS7 revealed that non-metabolizable sugars such as L-glucose and mannitol induce mRNA transcription similarly to glucose starvation. When D-glucose or any other metabolizable sugar was supplied, the level of transcripts was reduced. Nucleotide sequence analyses of the six cDNAs allowed identification of five of them by comparison with sequence data bases. The protein encoded by clone pZSS2 is analogous to a wound-induced protein from barley. Clones pZSS4 to pZSS7 encode, respectively, a transmembrane protein, a cysteine protease, a metallothionein-like protein and a chymotrypsin/subtilisin-like protease inhibitor. Clone pZSS3 shares no significant homology with any known sequence.

Amino Acid Sequence↗

PubMed1995

Attractiveness of the underling: an automatic power --> sex association and its consequences for sexual harassment and aggression.

One characteristic of men who sexually harass is that they are not aware that their actions are inappropriate or a misuse of their power (L. F. Fitzgerald, 1993a). We investigated the existence and automaticity of a mental association between the concepts of power and sex, and its consequences for sexual harassment tendencies. Using a subliminal priming paradigm, Experiment 1 demonstrated an automatic link between power and sex, and only for men high in the likelihood to sexually harass or aggress. In Experiment 2, male participants were unobtrusively primed with either power-related or neutral stimuli. For men likely to sexually aggress, but not other participants, attraction ratings of a female confederate were significantly higher in the power priming than the neutral priming condition.

Aggression↗

PubMed1995

Ketone potentiation of haloalkane-induced hepato- and nephrotoxicity. I. Dose-response relationships.

Carbon tetrachloride (CCl4) induced hepatotoxicity and chloroform (CHCl3) induced nephrotoxicity were evaluated in male Sprague-Dawley rats pretreated with acetone (A), methyl ethyl ketone (MEK), and methyl isobutyl ketone (MiBK). Dose-response relationships for A, MEK, and MiBK potentiation of CCl4-induced hepatotoxicity and CHCl3-induced nephrotoxicity were compared. A, MEK, and MiBK pretreatment at a dosage of 6.8 mmol/kg, given daily for 3 d, markedly potentiated CCl4-induced liver toxicity as indicated by a decrease in the CCl4 ED50 to 3.4, 4.6, and 1.8 mmol/kg, respectively, compared to vehicle-pretreated rats (17.1 mmol/kg). Similarly, pretreatment with these ketones (13.6 mmol/kg) potentiated CHCl3 kidney toxicity but to a lesser degree; CHCl3 ED50 values for vehicle-, A-, MEK-, and MiBK-pretreated rats were 3.4, 1.6, 2.1, and 2.2 mmol/kg, respectively. Our results indicate a potency ranking profile for the potentiation of CCl4 hepatotoxicity of MiBK > A > MEK and of A > MEK > or = MiBK for CHCl3 nephrotoxicity. These dissimilar ranking profiles could be due to differences in mechanisms of action for the two target sites.

Acetone↗

PubMed1995

Ketone potentiation of haloalkane-induced hepato- and nephrotoxicity. II. Implication of monooxygenases.

Previous results in Sprague-Dawley rats indicate that acetone (A), methyl ethyl ketone (MEK), and methyl isobutyl ketone (MiBK) pretreatment (3 d, po) at dosages of 6.8 and 13.6 mmol/kg potentiate CCl4 hepatotoxicity and CHCl3 nephrotoxicity, respectively. The potentiation potency profile observed was MiBK > A > MEK for liver and A > MEK > or = MiBK for kidney toxicity (Raymond & Plaa, 1995). In the present study, hepatic and renal microsomes from A-, MEK-, and MiBK-pretreated rats (6.8 or 13.6 mmol/kg) were examined for cytochrome P-450 content, substrate-specific monooxygenase activity (aminopyrine and benzphetamine N-demethylase, aniline hydroxylase) and in vitro covalent binding of 14CHCl3 and 14CCl4. Of the three ketones, only MiBK significantly increased P-450 content of liver and renal cortical microsomes. Similarly, 14CCl4 covalent binding under aerobic and anaerobic conditions was significantly increased by MiBK pretreatment only. 14CHCl3 covalent binding by renal cortical microsomes was significantly increased only under aerobic conditions by MiBK pretreatment. MiBK (13.6 mmol/kg) increased (threefold) aminopyrine N-demethylation in both liver and kidney, but only benzphetamine N-demethylation (two-fold, at 6.8 and 13.6 mmol/kg) in liver; A and MEK had no effect on either monooxygenase. All ketones at dosages of 6.8 and 13.6 mmol/kg increased aniline hydroxylation in liver (two-fold) and kidney (fivefold). Comparable profiles for P-450 induction, haloalkane covalent binding, and aminopyrine or benzphetamine N-demethylase activity were observed in liver and kidney microsomes. This profile was consistent with the ketone potentiation potency ranking profile observed in vivo for liver but not kidney injury. These findings affirm the importance of ketone-enhanced bioactivation for potentiation of CCl4 hepatotoxicity but suggest an alternative mechanism for CHCl3 nephrotoxicity.

Acetone↗

PubMed1993

Effects of glucose starvation on the oxidation of fatty acids by maize root tip mitochondria and peroxisomes: evidence for mitochondrial fatty acid beta-oxidation and acyl-CoA dehydrogenase activity in a higher plant.

Fatty acid beta-oxidation was studied in organellar fractions from maize root tips by h.p.l.c. and radiometric analysis of the products of incubations with [1-14C]octanoate and [1-14C]palmitate. In crude organellar fractions containing both mitochondria and peroxisomes, octanoate and palmitate beta-oxidation, as determined by the production of acetyl-CoA, was functional and, for palmitate, was activated 4-12-fold after subjecting the root tips to 48 h of glucose starvation. The sensitivity to a 'cocktail' of respiratory-chain inhibitors containing cyanide, azide and salicylhydroxamate depended on the conditions of incubation, with no inhibition in a medium facilitating peroxisomal beta-oxidation and a significant inhibition in a medium potentially facilitating mitochondrial beta-oxidation. Indeed, preparations of highly purified mitochondria from glucose-starved root tips were able to oxidize octanoate and palmitate to give organic acids of the tricarboxylic acid cycle. This activity was inhibited 5-10-fold by the above cocktail of respiratory-chain inhibitors, with no parallel accumulation of acetyl-CoA, thus showing that the inhibition affected beta-oxidation rather than the pathway from acetyl-CoA to the organic acids. This provides the first evidence that the complete beta-oxidation pathway from fatty acids to citrate was functional in mitochondria from a higher plant. Moreover, an acyl-CoA dehydrogenase activity was shown to be present in the purified mitochondria. In contrast with the peroxisomal activity, mitochondrial beta-oxidation showed the same efficiency with octanoate and palmitate and was strictly dependent on glucose starvation.

Acetyl Coenzyme A↗

PubMed1993

Hepatic lidocaine metabolism and complications of cirrhosis. Implications for assessing patient priority for hepatic transplantation.

The number of patients awaiting hepatic transplantation continues to exceed organ donation. As a result, many liver transplant candidates will develop life-threatening complications of their liver disease and not survive the pretransplant waiting period. Recent studies have demonstrated that hepatic lidocaine metabolism into monoethylglycinexylidide (MEG-X) can predict pretransplant survival. The present study was performed to determine if MEG-X could also predict pretransplant complications and thereby be useful in stratifying persons being evaluated for hepatic transplantation. A total of 57 patients with biopsy-proven cirrhosis underwent MEG-X testing. Of 57 patients, 30 (53%) developed life-threatening complications of their liver disease--i.e., variceal bleeding, grade II hepatic encephalopathy or worse, and spontaneous bacterial peritonitis. MEG-X values were greater in persons without complications of liver disease than in persons with complications (25.7 +/- 2.9 versus 14.7 +/- 1.4 ng/ml, respectively). No patients with MEG-X greater than 30 ng/ml developed a major complication. No significant difference in any of the standard liver function tests existed between persons who developed complications and patients who did not. In this group of 57 patients, 4 (7%) died from complications of cirrhosis. Mean MEG-X for patients who died (5.5 +/- 1.6 ng/ml) was significantly less (P < 0.05) than observed for other patient groups. All patients who died had MEG-X values below 10 ng/ml. This suggests that MEG-X testing could be an extremely useful test in the evaluation of patients for hepatic transplantation by identifying persons at increased risk for developing complications of chronic liver disease.

Adult↗

PubMed1992

Tight junction permeability and liver plasma membrane fluidity in lithocholate-induced cholestasis.

The present study correlated the reversibility of bile flow (BF) impairment with biochemical and morphological changes in the liver after injection of a cholestatic dose (12 mumole/100 g body weight) of lithocholic acid (LCA). BF declined maximally at 60 min but recovered totally at 210 min after LCA treatment. During the cholestatic period, there was an increase in tight junction permeability as measured by the bile to plasma (B/P) ratio of inulin and using lanthanum as a tracer. Cholesterol content and the cholesterol/phospholipid ratio in liver plasma membranes (LPM) were augmented while the fluidity of bile canalicular membranes (BCM) was decreased at 30 and 60 min after LCA injection. These changes in cholesterol content and membrane fluidity seemed to be correlated with LCA incorporation in LPM; their reversal at 120 min preceded the recovery of BF (210 min). Some biochemical disorders were evident after LCA injection, but they did not correlate with the variation in BF. These data suggest that increased tight junction permeability and decreased BCM fluidity are important pathogenic steps in LCA-induced cholestasis.

Animals↗

PubMed1992

Effects of glucose starvation on mitochondrial subpopulations in the meristematic and submeristematic regions of maize root.

Mitochondria isolated from 3-mm long maize (Zea mays L. var Dea) root tips were found to be heterogeneous on Percoll density gradients. The ultrastructure of these isolated mitochondria correlated well with that of mitochondria observed in situ and was consistent with the existence of mitochondria at different stages of maturation during cell development. The mitochondria of higher density presented an ultrastructure with many cristae and a dense matrix. These mitochondria showed classic respiratory properties, although with low ADP/O ratios. In contrast, the mitochondria of lower density showed few cristae and a clear matrix and did not seem to be fully functional because their rate of respiration was low and showed weak respiratory control. Lower- and higher- density mitochondria were shown to be differentially affected during the first stages of glucose starvation. The higher-density mitochondria from glucose-starved maize root tips retained the ultrastructure and most of the respiratory properties of nonstarved mitochondria, whereas lower- and intermediate-density mitochondria were absent in the mitochondrial preparations from glucose-starved maize root tips and were not observed in situ. Quantitatively, there was a decrease of the total mitochondrial pool when expressed as the amount of mitochondrial protein per root tip. However, this decrease affected low- and intermediate-density mitochondria, but not higher-density mitochondria. Thus, it was shown that a significant pool of functional mitochondria is maintained in maize root tips during the first stages of glucose starvation. The reasons for these apparently selective effects of glucose starvation on mitochondria are discussed in relation to effects on mitotic and differentiation processes.

Journal Article↗

PubMed1992

Increased Fatty Acid beta-Oxidation after Glucose Starvation in Maize Root Tips.

The effects of glucose starvation on the oxidation of fatty acids were studied in excised maize (Zea mays L.) root tips. After 24 hours of glucose starvation, the rate of oxidation of palmitic acid to CO(2) by the root tips was increased 2.5-fold. Different enzyme activities were tested in a crude particulate fraction from nonstarved root tips and those starved for 24 hours. The activities of the beta-oxidation enzymes crotonase, hydroxyacyl-coenzyme A (CoA) dehydrogenase, and thiolase and those of catalase, malate synthase, and peroxisomal citrate synthase were higher after starvation. However, no isocitrate lyase activity was detected, thus suggesting that the glyoxylate cycle does not operate. The overall beta-oxidation activity was assayed as the formation of [(14)C]acetyl-CoA from [(14)C]palmitic acid after high-performance liquid chromatography analysis of the CoA derivatives. An activity was detected in sugar-fed root tips, and it was increased by two-to fivefold in starved roots. Because the recovery of enzyme activities is only marginally better in starved roots compared with nonstarved roots, these results indicate that the beta-oxidation activity in the tissues is increased during sugar starvation. This increase is probably an essential part of the response to a situation in which lipids and proteins replace carbohydrates as the major respiratory substrates. These results are discussed in relation to the metabolic changes observed in senescing plant tissues.

Journal Article↗

PubMed1991

Transactive memory in close relationships.

Memory performance of 118 individuals who had been in close dating relationships for at least 3 months was studied. For a memory task ostensibly to be performed by pairs, some Ss were paired with their partners and some were paired with an opposite-sex partner from another couple. For some pairs a memory structure was assigned (e.g., 1 partner should remember food items, another should remember history items, etc.), whereas for others no structure was mentioned. Pairs studied together without communication, and recall was tested in individuals. Memory performance of the natural pairs was better than that of impromptu pairs without assigned structure, whereas the performance of natural pairs was inferior to that of impromptu pairs when structure was assigned.

Adult↗

PubMed1991

Oxidative phosphorylation by mitochondria extracted from dry sunflower seeds.

The role of mitochondria in the phosphorylation of ADP to ATP in the early steps of seed germination has been studied. Mitochondria were extracted from dry sunflower (Helianthus annuus) seeds. Adenylate kinase-dependent ATP synthesis was inhibited by p(1),p(5)-di(adenosine-5')pentaphosphate. Synthesis of ATP was observed with the different substrates: citrate, alpha-ketoglutarate, succinate, malate, pyruvate or NADH. This synthesis was activated by cytochrome c, and inhibited by cyanide, oligomycin, carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone, and carboxyatractyloside. The ATP/O values with succinate were 0.85 and 1.2 in the absence or presence, respectively, of cytochrome c. Electron micrographs showed that mitochondria of dry tissues have different structures when observed in situ or in vitro after aqueous extraction, suggesting that profound changes occurred after the contact with the aqueous medium. These results confirm previous data obtained in vivo showing that mitochondria present in dry seeds are able to synthesize ATP as soon as the seeds are rehydrated.

Journal Article↗