Effect of dietary sulfur amino acids on the taurine content of rat tissues

Summary.  The effect of dietary sulfur amino acids on the taurine content of rat blood and tissues was investigated. Three types of diet were prepared for this study: a low-taurine diet (LTD), normal taurine diet (NTD; LTD + 0.5% Met), and high-taurine diet (HTD; LTD + 0.5% Met + 3% taurine). These diets had no differing effect on the growth of the rats. The concentration of taurine in the blood from the HTD- and NTD-fed rats was respectively 1,200% and 200% more than that from LTD-. In such rat tissues as the liver, the taurine content was significantly affected by dietary sulfur amino acids, resulting in a higher content with HTD and lower content with LTD. However, little or no effect on taurine content was apparent in the heart or eye. The activity for taurine uptake by the small intestine was not affected by dietary sulfur amino acids. The expression level of taurine transporter mRNA was altered only in the kidney under these dietary conditions: a higher expression level with LTD and lower expression level with HTD. Received January 8, 2002 Accepted January 18, 2002 Published online August 20, 2002 Authors' address: Dr. Hideo Satsu, Laboratory of Food Chemistry, Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan, Fax: +81-3-5841-8026 E-mail: asatsu@mail.ecc.u-tokyo.ac.jp Abbreviations: HTD, high-taurine diet; NTD, normal taurine diet; LTD, low-taurine diet; TAUT, taurine transporter; CSA, cysteine sulfinate; CDO, cysteine dioxygenase; CSAD, cysteine sulfinate decarboxylase; PBS, phosphate-buffered saline; DIDS, 4,4′-diisothiocyanostilbene-2′,2′-disulfonic acid     

Effect of ischemia,calcium depletion and repletion,acidosis and hypoxia on cellular taurine content

Summary.  Occlusion of the left main coronary artery led to a time-dependent release of taurine from the heart. Upon reperfusion, there was a second phase of taurine release, which exceeded the amount of taurine that exited the heart during the 45 min ischemic insult. To obtain information on the mechanism underlying the release of taurine, three variables were examined, acidosis, hypoxia and calcium overload. It was found that large amounts of taurine also leave the cell during the calcium paradox, a condition induced by perfusing the heart with calcium containing buffer following a period of calcium free perfusion. However, little taurine effluxes the hearts exposed to buffer whose pH was lowered to 6.6. Isolated neonatal cardiomyocytes subjected to chemical hypoxia also lost large amounts of taurine. However, the amount of taurine leaving the cells appeared to be correlated with the intracellular sodium concentration, [Na⁺]_i. The data suggest that taurine efflux is regulated by [Na⁺]_i and cellular osmolality, but not by cellular pH. Received November 15, 2001 Accepted January 15, 2002 Published online October 3, 2002 Acknowledgements This study was supported with a grant from the Taisho Pharmaceutical Company. Authors' address: Dr. Stephen W. Schaffer, Department of Pharmacology, University of South Alabama, School of Medicine, Mobile, Alabama, U.S.A., E-mail: sschaffe@jaguarl.usouthal.edu     

Treatment of hypertension with oral taurine: experimental and clinical studies

Summary.  Oral taurine treatment has been studied extensively as a hypotensive agent. Several rat models of hypertension have been used to prove that dietary taurine supplementation can alleviate high blood pressure, among other cardiovascular problems. Experimental models mentioned in this review are the spontaneously hypertensive rat, the DOCA-salt rat, the Dahl-S rat, the renovascular hypertensive rat, the hyperinsulinemic rat and the ethanol-treated rat. The beneficial effects of taurine were also demonstrated in studies involving human subjects suffering essential hypertension. Taurine supplementation of 6 g/day for as little as 7 days resulted in measurable decreases in blood pressure in these patients. In both rat and human studies, the effects of taurine appeared to be dependent on the modulation of an overactive sympathetic system. However, taurine has positive effects on other types of cardiovascular problems and thus may act through more than one mechanism. Received January 8, 2002 Accepted January 18, 2002 Published online August 20, 2002 Acknowledgement The Taisho Pharmaceutical Co. of Tokyo, Japan, is thanked for their financial support to the senior author. Authors' address: Dr. John B. Lombardini, Department of Pharmacology, Texas Tech University Health Sciences Center, Lubbock, U.S.A., E-mail: jbarry. lombardini@ttmc.ttuhsc.edu     

Impaired generation of taurine chloramine by synovial fluid neutrophils of rheumatoid arthritis patients

Summary.  Taurine (Tau), a dominant free amino acid present in neutrophil cytoplasm, serves as a scavenger for hypochlorous acid (HOCl) released during these cells activation. The resulting taurine chloramine (Tau-Cl) exerts potent anti-inflammatory properties. In the present study we tested the hypothesis that the formation of Tau-Cl is impaired in neutrophils isolated from rheumatoid arthritis (RA) patients. The inhibition of zymosan-triggered chemiluminescence in the presence of exogenous Tau was used for indirect measurement of Tau-Cl generation. The chemiluminescence of neutrophils isolated from peripheral blood (PB) of healthy volunteers and RA patients was inhibited by Tau with similar potency. By contrast, synovial fluid (SF) neutrophils of these patients were significantly less sensitive for Tau-mediated inhibition. Therefore, our data indicate impaired generation of Tau-Cl in neutrophils isolated from SF of RA patients. Received November 29, 2001 Accepted January 9, 2002 Published online August 30, 2002 Acknowledgements This work was supported by grants from the State Committee for Scientific Research of Poland (No. P05A 104 19) and the Institute of Rheumatology. The Institute of Rheumatology is supported by a core grant from the State Committee for Scientific Research of Poland. Authors' address: Ewa Kontny, Ph.D, Department of Pathophysiology and Immunology, Institute of Rheumatology, Spartanska 1, 02-637 Warsaw, Poland, E-mail: zpatiir@warman.com.pl Abbreviations: Tau, taurine; Tau-Cl, taurine chloramine; PB, peripheral blood; SF, synovial fluid; RA, rheumatoid arthritis     

Dietary taurine enhances cholesterol degradation and reduces serum and liver cholesterol concentrations in rats fed a high-cholesterol diet

Summary.  The effect of taurine on hypercholesterolemia induced by feeding a high-cholesterol (HC) diet (10 g/kg) to rats was examined. When taurine was supplemented to HC for 2 wk, serum total cholesterol significantly decreased and serum HDL-cholesterol increased compared with the HC diet group. In the hypercholesterolemic rats fed the HC diet, the excretion of fecal bile acids and hepatic cholesterol 7α-hydroxylase (CYP7A1) activity and its mRNA level increased significantly, and the supplementation of taurine further enhanced these indexes, indicating an increase in cholesterol degradation. Agarose gel electrophoresis revealed that, in hypercholesterolemic rats fed the HC diet, the serum level of the heavier VLDL increased significantly, but taurine repressed this increase and normalized this pattern. Significant correlations were observed between the time-dependent increase of CYP7A1 gene expression and the decrease of blood cholesterol concentration in rats fed the HC diet supplemented with taurine. These results suggest that the hypocholesterolemic effects of taurine observed in the hypocholesterolemic rats fed the HC diet were mainly due to the enhancement of cholesterol degradation and the excretion of bile acid. Received December 4, 2001 Accepted January 2, 2002 Published online September 10, 2002 Acknowledgment This work was supported by a grant of Taisho Pharmaceutical Co., Ltd (Japan). We thank J. I. Gordon for their generous gifts of cDNAs. Authors' address: Dr. Hidehiko Yokogoshi, School of Food and Nutritional Sciences, The University of Shizuoka, Shizuoka 4228526, Japan, E-mail: yokogosi@u-shizuoka-ken.ac.jp     

Synthesis and transformations of a pyrazole containing <Emphasis Type="Italic">α</Emphasis>,<Emphasis Type="Italic">β</Emphasis>-didehydro-<Emphasis Type="Italic">α</Emphasis>-amino acid derivatives

Summary.  2H-Pyran-2-ones 1 were transformed with various hydrazines into (E)- or (Z)-α,β-didehydro-α-amino acid (DDAA) derivatives 4 (and 7) containing a highly substituted pyrazolyl moiety attached at the β-position. With heterocyclic hydrazines, the products 4 were accompanied also by decarboxylated enamines E-6. In order to separate (E/Z)-mixtures of acids, they were transformed to the corresponding methyl esters 9 and 10 by the application of diazomethane. Catalytic hydrogenation under high pressures with Pd/C as a catalyst resulted in the formation of racemic alanine derivatives 11. Received January 29, 2002 Accepted May 27, 2002 Published online December 18, 2002 RID="*" ID="*"  Dedicated with deep respect to Professor Waldemar Adam on the occasion of his 65^th birthday. Acknowledgements We thank the Ministry of Education, Science and Sport of the Republic of Slovenia for the financial support (P0-0503-103). Dr. B. Kralj and Dr. D. Žigon (Center for Mass Spectroscopy, “Jožef Stefan” Institute, Ljubljana, Slovenia) are gratefully acknowledged for the mass measurements. Authors' address: Prof. Marijan Kočevar, Faculty of Chemistry and Chemical Technology, University of Ljubljana, Aškerčeva 5, SI-1000 Ljubljana, Slovenia, E-mail: marijan.kocevar@uni-lj.si     

Effects of taurine on polymorphonuclear phagocytosis activity in burned patients

Summary.  This study determines the effects of taurine (Tau) on phagocytosis of polymorphonuclear neutrophils (PMN) isolated from normal subjects (n = 41) and severely burned patients (n = 20). Phagocytosis was measured by nitroblue of tetrazolium (NBT) reduction in samples with and without latex bead stimulation. Taurine was added at doses of 0.2, 0.4, 0.8 and 1.6 mM to stimulated samples. In control cells there were statistically significant increases in phagocytosis after addition of Tau 0.8 mM and 1.6 mM to as compared to samples without Tau addition (295 ± 23% and 330 ± 35% vs. 248 ± 18%; mean ± S.E.; p < 0.05). A statistically significant increase in phagocytosis was observed in cells from the burned population after addition of Tau 1.6 mM (288 ± 38% vs. 198 ± 13%; mean ± S.E.; p < 0.05). No changes in phagocytosis were found in cells from a subgroup of burn patients (n = 13) followed over 7, 15 and 21 days. These results indicate that taurine supplementation in vitro at doses of 0.8 to 1.6 mM improves the phagocytic capacity of neutrophils in healthy subjects and in patients with severe burn injury, mainly when neutrophil function is unaltered. Received December 17, 2001 Accepted January 17, 2002 Published online August 30, 2002 Authors' address: Dr. Mireia Farriol, Centre d'Investigacions Bioquímicas i Biología Molecular (CIBBIM), Hospital General Vall d'Hebron Passeig Vall d'Hebron 119-129, E-08035 Barcelona, Spain, Fax: 34-93-2746831, E-mail: farriol@hg.vhebron.es     

Synthesis of N-quinonyltaurines

Summary.  Both 1,4-benzoquinones and 1,4-naphthoquinones were attached to the non-proteinogenic amino acid taurine to form N-quinonyl taurine derivatives. The products were formed via the direct Michael-like addition or by substitution of a good leaving group. An attempt to bridge the two moieties via an ureido spacer resulted in the formation of a bis-quinonylamino isocyanurate derivative. Preliminary MO calculations provided internal ground-state geometries and orbital coefficients of the HOMO levels in two representing taurine conjugates. Received May 6, 2002 Accepted August 13, 2002 Published online December 18, 2002 Acknowledgments This research was supported by the Israel Science Foundation founded by the Academy of Science and Humanities. We wish to thank Ms. Ethel Solomon for skilled technical help. Authors' address: Prof. Shmuel Bittner, Department of Chemistry, Ben-Gurion University of the Negev, P.O. Box 653, Beer-Sheva 84105, Israel, Fax: (972)-8-6472943, E-mail: bittner@bgumail.bgu.ac.il     

Chronic taurine supplementation ameliorates oxidative stress and Na+ K+ ATPase impairment in the retina of diabetic rats

Summary.  This study evaluates the effect of 4 months supplementation with 2% and 5% taurine (w/w) on the retina of diabetic rats. In non-diabetic rats, taurine does not modify glycemia, body weight, retinal conjugated dienes (CD), lipid hydroperoxide (LP), and Na⁺K⁺ATPase activity. In diabetic rat, at 2, 4, 8, 16 weeks following the onset of diabetes, retinal CD and LP are significantly and progressively increased, while pump activity is gradually and significantly reduced. In taurine supplemented diabetic rats, glycemia is not affected but lipid peroxidation is significantly decreased. Finally, taurine preserves ATPase activity being 5% more effective than 2% taurine. We conclude that taurine supplementation ameliorates biochemical retinal abnormalities caused by diabetes, thereby suggesting that taurine may have a role in the prevention of retinal changes in diabetes. Received November 26, 2001 Accepted January 10, 2002 Published online October 3, 2002 Authors' address: Prof. Flavia Franconi, Department of Pharmacology, University of Sassari, Via Muroni 23a, I-07100 Sassari, Italy, Fax: 39-79228715, E-mail: franconi@ssmain.uniss.it     

Interactions between taurine and ethanol in the central nervous system

Summary.  This purpose of this review will be to summarize the interactions between the endogenous amino acid taurine and ethyl alcohol (ethanol) in the central nervous system (CNS). Taurine is one of the most abundant amino acids in the CNS and plays an integral role in physiological processes such as osmoregulation, neuroprotection and neuromodulation. Both taurine and ethanol exert positive allosteric modulatory effects on neuronal ligand-gated chloride channels (i.e., GABA_A and glycine receptors) as well as inhibitory effects on other ligand- and voltage-gated cation channels (i.e., NMDA and Ca²⁺ channels). Behavioral evidence suggests that taurine can alter the locomotor stimulatory, sedating, and motivational effects of ethanol in a strongly dose-dependent manner. Microdialysis studies have revealed that ethanol elevates extracellular levels of taurine in numerous brain regions, although the functional consequences of this phenomenon are currently unknown. Finally, taurine and several related molecules including the homotaurine derivative acamprosate (calcium acetylhomotaurinate) can reduce ethanol self-administration and relapse to drinking in both animals and humans. Taken together, these data suggest that the endogenous taurine system may be an important modulator of effects of ethanol on the nervous system, and may represent a novel therapeutic avenue for the development of medications to treat alcohol abuse and alcoholism. Received November 21, 2001 Accepted January 4, 2002 Published online August 20, 2002 Acknowledgements This work was supported by funds from the State of California for medical research on alcohol and substance abuse through the University of California at San Francisco. The author wishes to thank Drs. C. W. Hodge and P. H. Janak for their support and helpful discussions. Author's address: Dr. M. Foster Olive, Ernest Gallo Clinic and Research Center, Department of Neurology, University of California at San Francisco, 5858 Horton Street, Suite 200, Emeryville, California, U.S.A., Fax +1/510/985 3101, E-mail: folive@itsa.ucsf.edu     

A study on the estimation of sulfur-containing amino acid metabolism by the determination of urinary sulfate and taurine

Summary.  Sulfate and taurine are major end products of sulfur-containing amino acid metabolism in mammals including humans, and they are excreted in urine. Average excretions (μmol/mg of creatinine) in the morning urine of 58 female college students were: total (free plus ester) sulfate (a), 12.53 ± 3.85; free sulfate, 11.57 ± 3.69; taurine, 0.78 ± 0.53. Ratio of total sulfate and taurine was 10 : 0.6. Regression lines obtained by plotting total sulfate, free sulfate, or total sulfate plus taurine against urea have shown that the former excretions are significantly correlated with urea excretion. Excretion of total sulfate at zero point of urea excretion (b) was 5.30, which corresponded to 42.3% of average excretion (12.53) and was assumed to be derived from dietary sulfate. The difference 7.23 (a − b) seemed to be derived from sulfur-containing amino acids. It was pointed out that the difference of average sulfate excretion and sulfate excretion at zero urea excretion, namely a − b, was appropriate for the metabolic index of sulfur-containing amino acids of the group examined. As free sulfate constituted 92.3% of total sulfate, excretion of ester sulfate was at a constant level, and that of taurine was not significantly correlated with urea excretion, the value of free sulfate corresponding to the value a − b of total sulfate mentioned above seemed to be a reliable and convenient index in the assessment of sulfur-containing amino acid metabolism. Received December 3, 2001 Accepted January 2, 2002 Published online August 30, 2002 Authors' address: Dr. Toshihiko Ubuka, Department of Clinical Nutrition, Kawasaki University of Medical Welfare, Kurashiki Okayama, 701-0193 Japan, E-mail: ubukatos@mw.kawasaki-m.ac.jp     

Co-variation of plasma sodium,taurine and other amino acid levels in critical illness

Summary.  This study investigates the relationship between changes in plasma sodium and changes in amino acid levels in a patient with post-traumatic sepsis and prolonged critical illness. Ninety-two consecutive measurements were performed at regular intervals over a period of many weeks; these consisted in the determination of full amino-acidograms, plasma sodium and complementary variables. A unique, highly significant inverse correlation between taurine and plasma sodium was found (r² = 0.48, p < 0.001). All other amino acids were unrelated, or much more weakly related, to sodium. Taurine was also strongly and directly related to phosphoethanolamine, glutamate and aspartate. Changes in sodium and in levels of these amino acids explained up to 86% of the variability of taurine. Besides, levels of these amino acids maintained a high degree of co-variation, remaining reciprocally related one to each other, directly, with r² ranging between 0.33 and 0.59 (p < 0.001 for all). There were similar findings for β-alanine, which however was measured inconsistently. These data provide gross clinical evidence of a specific link binding plasma sodium and taurine levels, and may be consistent with occurrence of opposite and interdependent shifts of sodium and taurine between intravascular and extravascular space, to maintain osmoregulation. Co-variation of taurine with the other amino acids may be related to the same phenomenon, and/or to similarities in transport systems and chemical structure, or true metabolic interactions. Received April 16, 2002 Accepted June 19, 2002 Published online November 14, 2002 RID="*" ID="*"  Presented at the 7^th International Congress on Amino Acids and Proteins, Vienna (Austria), August 6–10, 2001. Acknowledgements The authors acknowledge the kind assistance of Mr. Maurizio Cianfanelli, from the Catholic University School of Medicine, Rome, Italy. Authors' address: Dr. Carlo Chiarla, Via Augusto Tebaldi, 19, I-00168 Roma, Italy, E-mail: carlo.chiarla@rm.unicatt.it     

3-Carboxy-4-phosphonocyclopentane amino acids: New metabotropic glutamate receptor ligands

Summary.  Two glutamic acid analogs (1SR,3RS,4RS)- and (1SR,3SR,4SR)-1-amino-4-phosphono cyclopentane-1,3-dicarboxylic acids (APCPD) have been synthesized. Pure E-(diethoxy-phosphoryl)-acrylic acid ethyl ester was obtained from ethyl propiolate, phenol and triethylphosphite. It was used as dienophile in a Diels-Alder reaction. Oxidation and cyclization afforded 3-(ethoxy-carbonyl)-4-(diethoxy-phosphoryl)-cyclopentanone. Bucherer-Bergs reaction and hydrolysis yielded APCPD-III and -IV which are inactive on mGlu1a receptor and antagonists on mGlu2 and mGlu8a receptors. Received April 2, 2002 Accepted July 11, 2002 Published online December 18, 2002 Acknowledgments This work was supported by grants from the CNRS, the programs “Physique et Chimie du Vivant” (PCV00–134, CNRS) and “Molécules et Cibles Thérapeutiques” (CNRS/INSERM), RETINA France and the Fondation de France (Comité Parkinson). A.-S. B. was supported by fundings from Parke-Davis Pharmaceutical Research (Ann Arbor, MI) and the Fondation de la Recherche Médicale. Authors' address: Dr Francine C. Acher, Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques, UMR8601-CNRS, Université René Descartes-Paris V, 45 rue des Saints-Pères, 75270 Paris Cedex 06, France, Fax: (33) 1 42 86 83 87, E-mail: acher@biomedicale.univ-paris5.fr     

Effect of taurine chloramine,the product of activated neutrophils,on the development of collagen-induced arthritis in DBA 1/J mice

Summary.  Taurine chloramine (TauCl), a product of neutrophil myeloperoxidase – halide system, formed by a reaction of taurine with HOCl, is known as an anti-microbial and anti-inflammatory long-lived oxidant. We previously reported that TauCl inhibits in vitro the production of proinflammatory cytokines (IL-6, IL-8) by RA synoviocytes. Therefore we performed this study to investigate the effect of TauCl treatment on the development of collagen-induced arthritis (CIA) in DBA1/J mice. Early administration of TauCl (after primary immunization) resulted in the delay of the onset of CIA, but had no effect on severity of arthritis. TauCl, given daily for 21 days after booster immunization, did not reduce the symptoms of arthritis in those mice, which already developed CIA, but significantly diminished incidence of the disease (55% vs. 90% of placebo mice). The mechanism of this effect is unknown. This is the first in vivo study suggesting that TauCl may be used for immune intervention in chronic inflammatory diseases. Received November 30, 2001 Accepted January 25, 2002 Published online August 20, 2002 Acknowledgments We express our gratitude to K. Szewczyk for skillful technical assistance. This work was supported by grants from the Committee of Scientific Research (Warsaw, Poland) Grant No. 4PO5B01018, and partially by Grant No.: PO 5A 10419. Authors' address: Janusz Marcinkiewicz, Ph.D., M.D., Department of Immunology, Jagiellonian University Medical College, 18 Czysta St., 31-121 Kraków, Poland, E-mail: mmmarcin@cyf-kr.edu.pl     

Taurine chloramine modulates cytokine production by human peripheral blood mononuclear cells

Summary.  The effect of taurine (Tau) and taurine chloramine (Tau-Cl) on the production of TNF-α, IL-1β, and IL-6 by peripheral blood mononuclear cells of healthy volunteers was examined. Cells were stimulated with bacterial lipopolysaccharide (LPS) in the presence of either Tau or Tau-Cl. After 24 h culture the cytokine concentrations were measured in both culture supernatants (secreted) and cell lysates (cell-associated) using ELISA. In LPS-stimulated cells Tau-Cl inhibited both the secreted and cell-associated IL-1β and IL-6, while exerted dual effect on TNF-α production: raising it slightly at low and reducing at higher concentration. By contrast, Tau had no significant effect on the cytokine production. These results indicate that Tau-Cl modulates synthesis of pro-inflammatory cytokines, and therefore it may play a role in the initiation and propagation of immune response. Received November 29, 2001 Accepted January 18, 2002 Published online August 30, 2002 Acknowledgments This research was supported by grants from the State Committee for Scientific Research of Poland (No 4 P05B 01018) and the Institute of Rheumatology (No I/14). The Institute of Rheumatology is supported by a core grant from the State Committee for Scientific Research of Poland. Authors' address: Ewa Kontny, Ph.D., Department of Pathophysiology and Immunology, Institute of Rheumatology, Spartanska 1, 02-637 Warsaw, Poland, E-mail: zpatiir@warman.com.pl Abbreviations: Tau, taurine; Tau-Cl, taurine chloramine; LPS, lipopolysaccharide; TNF-α, tumor necrosis factor-α; IL-1β, interleukin 1β; IL-6, interleukin 6; PBMC, peripheral blood mononuclear cells     

Cysteine metabolism in periportal and perivenous hepatocytes: Perivenous cells have greater capacity for glutathione production and taurine synthesis but not for cysteine catabolism

Summary.  Hepatocyte preparations highly enriched in cells from either the periportal or the perivenous zone of the liver acinus were prepared using a digitonin/collagenase perfusion method. Five enzymes of cysteine metabolism were assayed in both periportal and perivenous preparations. The ratios of periportal to perivenous activity were 0.76, 0.60, 0.81, 1.62, and 1.01 for cysteine dioxygenase, cysteinesulfinate decarboxylase, γ-glutamylcysteine synthetase, cystathionase, and asparate (cysteinesulfinate) aminotransferase, respectively. Only cysteinesulfinate decarboxylase activity was significantly different between periportal and perivenous cells. In incubations with 2 mmol/L [³⁵S]cysteine, total cysteine catabolism ([³⁵S]taurine plus [³⁵S]sulfate) between periportal and perivenous cells was not different, which is consistent with the observation of similar cysteine dioxygenase activity across the hepatic acinus. Consistent with the lower cysteinesulfinate decarboxylase activity in periportal cells, 16% of the total catabolism of [³⁵S]cysteine in periportal cells resulted in taurine synthesis compared to 28% in perivenous cells. A lower rate of [³⁵S]glutathione synthesis was observed in periportal cells compared to perivenous cells, but γ-glutamylcysteine synthetase activity was not significantly different between perivenous and periportal cells. Cysteinesulfnate decarboxylase can be added to the list of enzymes whose activities are markedly enriched in perivenous cells. Received January 15, 2002 Accepted February 4, 2002 Published online September 4, 2002 Acknowledgements This work was supported by the National Research Initiative Competitive Grants Program/United States Department of Agriculture Competitive Research Grant 02-37200-7583. Authors' address: Dr. Martha H. Stipanuk, Division of Nutritional Sciences, 227 Savage Hall, Cornell University, Ithaca, NY 14853-6301, U.S.A., E-mail: mhs6@cornell.edu     

Modeling species richness controlled by community-intrinsic and community-extrinsic processes: coastal fish communities as an example

 This article focuses on the analysis of coastal fish communities along the Norwegian Skagerrak coast. Species numbers are estimated based on annual samples of the fish communities within 12 fjords from 1953 to 1994. On this basis, a community dynamics model (incorporating both community-intrinsic and community-extrinsic processes) was developed and analyzed. This model is then discussed on the basis of other community models available through the literature, both phenomenologically oriented and process-oriented models. Received: January 17, 2002 / Accepted: May 13, 2002 Acknowledgments We thank Dr. Masakado Kawata for the invi-tation to present this paper at the 19th Symposium of the Society of Population Ecology held in Yamagata, Japan, October 26–28, 2001: “Evolution of Biodiversity: Theories and Facts.” Valuable input was provided after the presentation at this meeting, which we greatly appreciated. The reformulation of the model in terms of ΔS was kindly suggested to us by Prof. Joan Roughgarden. Thanks to Dr. Hildegunn Viljugrein for advice on the BUGS analyses and to two anonymous reviewers for constructive comments. This work has been supported by grants from the Norwegian Science Council (NFR). Correspondence to:N.C. Stenseth     

Regeneration of lipophilic antioxidants by NAD(P)H:quinone oxidoreductase 1

Summary.  The aim of this work was to study the activity of NAD(P)H:(quinone acceptor) oxidoreductase 1 (EC 1.6.99.2) in the regeneration of lipophilic antioxidants, alpha-tocopherol, and reduced-coenzyme Q analogs. First, we tested whether or not two isoforms of the NAD(P)H:(quinone acceptor) oxidoreductase 1 designated as “hydrophilic” and “hydrophobic” (H. J. Prochaska and P. Talalay, Journal of Biological Chemistry 261: 1372–1378, 1986) show differential enzyme activities towards hydrophilic or hydrophobic ubiquinone homologs. By chromatography on phenyl Sepharose, we purified the two isoforms from pig liver cytosol and measured their reduction of several ubiquinone homologs of different side chain length. We also studied by electron paramagnetic resonance the effect of NAD(P)H:(quinone acceptor) oxidoreductase 1 on steady-state levels of chromanoxyl radicals generated by linoleic acid and lipooxygenase and confirmed the enzyme's ability to protect alpha-tocopherol against oxidation induced with H₂O₂-Fe²⁺. Our results demonstrated that the different hydrophobicities of the isoforms do not reflect different reactivities towards ubiquinones of different side chain length. In addition, electron paramagnetic resonance studies showed that in systems containing the reductase plus NADH, levels of chromanoxyl radicals were dramatically reduced. Morever, in the presence of oxidants, alpha-tocopherol was preserved by NAD(P)H:(quinone acceptor) oxidoreductase 1, supporting our hypothesis that regeneration of alpha-tocopherol may be one of the physiologic functions of this enzyme. Received May 20, 2002; accepted September 20, 2002; published online May 21, 2003 RID="*" ID="*" Correspondence and reprints: Departamento de Biología Celular, Fisiología e Inmunología, Facultad de Ciencias, Edificio Severo Ochoa, Campus de Rabanales, Universidad de Córdoba, 14014 Córdoba, Spain.     

Effect of D-amino acids on some mitochondrial functions in rat liver

Summary.  We studied the role of the D-amino acids (D-aa) D-serine, D-alanine, D-methionine, D-aspartate, D-tyrosine and D-arginine on rat liver mitochondria. The stability of D-amino acids, mitochondrial swelling, transmembrane potential and oxygen consumption were studied under oxidative stress conditions in rat liver mitochondria. In the presence of glutamate-malate all D-aas salts increased mitochondrial swelling, while in the presence of succinate plus rotenone only D-ala, D-arg and D-ser, induced mitochondrial swelling. The transmembrane potential (ΔΨ) was decreased in the presence of 1 μM Ca²⁺. The D-aas inhibited oxygen consumption in state 3. The D-aa studied exerted effects on mitochondria via an increase of free radicals production. Received January 15, 2002 Accepted April 14, 2002 Published online September 4, 2002 Acknowledgements The authors appreciated the partial economical support from Mexican grants of CONACYT (to A.S.-M. during its sabbatical) and CIC-UMSNH (2.5) and critical readings from Rafael álvarez-González. Authors' address: Alfredo Saavedra-Molina, Instituto de Investigaciones Químico-Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Edificio B-3. C.U., Morelia, Mich. 58030. México, Fax: 52-443-326-5788, E-mail: saavedra@zeus.umich.mx