bluuebunny/crossref_metadata_2025_split huggingface dataset:
Coenzyme Q10 administration increases antibody titer in hepatitis B vaccinated volunteers — A single blind placebo‐ controlled and randomized clinical study
Authors: Barbieri Bruno , Lund Bernt , Lundström Bengt , Scaglione Francesco 
Published: December 2008

AbstractPersons involved in the study, 21 per treatment arm, were consuming ubiquinone (Q10), 90 mg/day, 180 mg/day or placebo, for two weeks prior to hepatitis B vaccination. After 30 days this vaccination was repeated. Q10 was given as soft gelatin capsules containing 30 mg each. The consumption was continued throughout the study conducted for 90 days. Clinical observations and laboratory tests were performed throughout the study and no adverse effects were observed in any of the groups.Already after 30 days the two groups receiving Q10 showed a slightly higher titer of antibodies to hepatitis B surface antigen then the placebo group. This difference escalated and the immunopotentiating effect of Q10 was even more clear‐cut in the residual part of the study. In addition, a dose response did also seem to be present when comparing the 90 mg group with the 180 mg group. Statistics revealed that Q10 in the dose 180 mg/day is able to increase antibody response in vivo in humans vaccinated against hepatitis B with up to 57% (p=0.011).
Clinical implications of the correlation between coenzyme Q10 and vitamin B6 status
Authors: Willis R. , Anthony M. , Sun L. , Honse Y. , Qiao G. 
Published: December 2008

AbstractThe endogenous biosynthesis of the quinone nucleus of coenzyme Q10 (CoQ10) from tyrosine is dependent on adequate vitamin B6 nutriture. Lowered blood and tissue levels of CoQ10 have been observed in a number of clinical conditions. Many of these clinical conditions are most prevalent among the elderly. Kalen et al. have shown that blood levels of CoQ10 decline with age. Similarly, Kant et al. have shown that indicators of vitamin B6 status also decline with age. Blood samples were collected from 29 patients who were not currently being supplemented with either CoQ10 or vitamin B6. Mean CoQ10 concentrations was 1.1 ± 0.3 μg/ml of blood. Mean specific activities of EGOT was 0.30 ± 0.13 μmol pyruvate/hr/108 erythrocytes and the mean percent saturation of EGOT with PLP was 78.2 ± 13.9%. Means for all parameters were within normal ranges. Strong positive correlation was found between CoQ10 and the specific activity of EGOT (r =0.5787, p <0.001) and between CoQ10 and the percent saturation of EGOT with PLP (r =0.4174, p <0.024). Studies are currently in progress to determine the effect of supplementation with vitamin B6 of blood CoQ10 levels. It appears prudent to recommend that patients receiving supplemental CoQ10 be concurrently supplemented with vitamin B6 to provide for better endogenous synthesis of CoQ10 along with the exogenous CoQ10.
Manganese deficiency and toxicity: Are high or low dietary amounts of manganese cause for concern?
Authors: Finley John Weldon , Davis Cindy D. 
Published: December 2008

AbstractManganese is an essential trace element that is required for the activity of several enzymes. Manganese is also quite toxic when ingested in large amounts, such as the inhalation of Mn‐laden dust by miners. This review examines Mn intake by way of the food supply and poses the question: Is there reason to be concerned with Mn toxicity or deficiency in free‐living populations in North America? Although much remains to be learned of the functions of Mn, at present there are only a few vaguely described cases of Mn deficiency in the medical literature. Given the heterogeneity of the North American food supply, it is difficult to see the possibility of more than greatly isolated and unique instances of Mn deficiency. However, low Mn‐dependent superoxide dismutase activity may be associated with cancer susceptibility, and deserves further study. There may be reasons, however, to be concerned about Mn toxicity under some very specialized conditions. Increasing numbers of young people are adopting a vegetarian lifestyle which may greatly increase Mn intake. Iron deficiency may increase Mn absorption and further increase the body‐burden of Mn, especially in vegetarians. Mn is eliminated primarily through the bile, and hepatic dysfunction could depress Mn excretion and further contribute to the body burden. Would such a combination of events predispose substantial numbers of people to chronic Mn toxicity? At present, there is no definite proof of this occurring, but given the state of knowledge at the present time, more studies with longer time‐frames and more sensitive methods of analysis are needed.
Production and characterization of monoclonal antibodies to porcine brain pyridoxal kinase
Authors: Choi Soo Young , Kwok Francis , Bahn Jae Hoon , Jeon Seong Gyu , Ahn Yoon Kyung , Yoon Byung Hak , Lee Byung Ryong , Choi Kyung Soon , Gao G. Z. 
Published: December 2008

AbstractSix monoclonal antibodies that recognize porcine brain pyridoxal kinase have been selected and designated as PK67, PK86, PK91, PK144, PK252 and PK275. A total of six monoclonal antibodies recognizing different epitopes of the enzyme were obtained, of which four inhibited the enzyme activity. When total proteins of porcine brain homogenate separated by SDS‐PAGE were subjected to monoclonal antibodies, a single reactive protein band of molecular weight 39 kDa which comigrated with purified porcine pyridoxal kinase was detected. Using the anti‐pyridoxal kinase antibodies as probes, the cross reactivities of brain pyridoxal kinase from human and other mammalian tissues and from avian sources were also investigated. Among human and all animal tissues tested, immunoreactive bands on Western blots appeared to have the same molecular mass of 39 kDa. These results indicate that mammalian brains contain only one major type of immunologically similar pyridoxal kinase, although some properties of the enzymes reported previously differed from one another.
Vanadium and diabetes
Authors: Thompson Katherine H. 
Published: December 2008

AbstractVanadium is an ultratrace element, widely distributed in nature, yet with no presently known specific physiological function in mammals. The apparent role of vanadium in regulation of intracellular signaling, as a cofactor of enzymes essential in energy metabolism, and as a possible therapeutic agent in diabetes is of increasing interest as more and more research reports present evidence of vanadium's potentially unique biological function. In this mini‐review, the author summarizes current knowledge of the bioinorganic chemistry of vanadium, the basic features of diabetes mellitus and its metabolic sequelae, and the in vitro and in vivo effects of both inorganic and organically‐chelated vanadium compounds. Results of clinical trials to date, as well as kinetic studies of tissue uptake are covered. Examples of ways to enhance the positive effects of vanadium as an oral therapeutic adjunct in diabetic control, while minimizing potential toxicity, are compared with regard to desirable features and possible drawbacks.
Copper and signal transduction: Platelets as a model to determine the role of copper in stimulus‐response coupling
Authors: Thomas Johnson W. 
Published: December 2008

AbstractPlatelets from copper‐deficient rats have been used as a model to investigate the role of copper in receptor‐mediated cellular responses. Copper deficiency doubles the rate of dense granule secretion and increases myosin association with the platelet cytoskeleton following thrombin stimulation. Mechanisms underlying the effects of copper deficiency on thrombin‐ induced signals that elicit dense granule secretion involve suppression of protein kinase C activity and impairment of Ca2+ release from intracellular stores. Copper deficiency also reduces the cellular GTP content of platelets. This may limit receptor effector coupling through GTP‐dependent regulatory proteins leading to protein kinase C activation and the release of Ca2+ from intracellular stores. The reduction in GTP content during copper deficiency results from its utilization to maintain cellular ATP levels in response to severely inhibited cytochrome c oxidase activity in platelet mitochondria. Thus, the role of copper in maintaining normal signal transduction may be indirectly related to its biological function in mitochondria.
Influence of dietary nucleotides on plasma immunoglobulin levels and lymphocyte subsets of preterm infants
Authors: Navarro J. , Maldonado J. , Narbona E. , Ruiz‐Bravo A. , García Salmerón J. L. , Molina J. A. , Gil A. 
Published: December 2008

AbstractWe examined the effects of nucleotide supplementation to a preterm adapted milk formula on the lymphocyte subsets and plasma IgG, IgM and IgA levels in preterm infants for the first three months of life. Two groups of preterm infants received a milk formula or the same formula supplemented with CMP, AMP, UMP, GMP and IMP to mimic the concentration of acid‐soluble nucleotides found in human milk. Blood samples were obtained at birth, 10 days, 20—30 days and 3 months of age. Preterm infants fed the nucleotide formula exhibited higher plasma levels of IgM in all postnatal study periods than neonates fed the standard formula; moreover, IgA was also higher at 3 months of age in nucleotide formula fed infants. No major differences were seen between groups for IgG levels and lymphocyte subsets. Thus, dietary nucleotides appear to exert actions on immature human neonate lymphocytes enhancing the in vivo production of Ig which may have a role in the defense capacity of neonates.
Lipid soluble vitamins in gene regulation
Authors: Carlberg Carsten 
Published: December 2008

AbstractVitamin A (retinol) and vitamin D are lipid soluble vitamins that are precursors of the nuclear hormones all‐trans retinoic acid (RA) and 1α,25‐dihydroxyvitamin D3 (VD) that bind with high affinity to their cognate nuclear receptors, referred to as retinoic acid receptor (RAR) and vitamin D receptor (VDR). Both types of nuclear receptors are structurally related and belong to the same subclass of the nuclear receptor superfamily, a large family of ligand‐inducible transcription factors. Both RAR and VDR form heterodimers preferentially with the nuclear receptor for 9‐cis RA, referred to as the retinoid X receptor (RXR), but functional RAR‐VDR heterodimers have also been observed. Moreover, both types of nuclear receptors interact in a ligand‐dependent fashion with members of the same class of co‐activator, co‐repressor and co‐integrator proteins. These similar molecular mechanisms of action provide several possibilities for an interaction of RARs with VDR that are all based on allosteric protein—protein interactions. These interactions can result in either an additive or a transrepressive functional interference between RA and VD. The two remaining lipid soluble vitamins, vitamins E and K, are not known to interact with nuclear receptors, but their structure does not exclude this possibility. Moreover, for vitamin E modulatory effects on transcription factors, such as AP‐1, have been described. This review will discuss briefly gene regulation by the four lipid soluble vitamins.
Ubiquinone redox cycle as a cellular antioxidant defense system
Authors: Kishi Takeo , Takahashi Takayuki , Usui Akinori , Okamoto Tadashi 
Published: December 2008

AbstractUbiquinone (UQ) reductase responsible for reduction of non‐mitochondrial UQ was investigated in rats toward demonstrating an antioxidant role of UQ. In the liver, most of cellular UQ‐10 reductase activity was attributable to a novel NADPH‐UQ reductase in cytosol. The enzyme was not inhibited by dicumarol and rotenone, and had a Km of 19 μM for NADPH and 307 μM for NADH at the optimum pH 7.4. The enzyme was purified 300‐fold to apparent homogeneity from the liver cytosol by an affinity chromatographic method. The purified enzyme reduced UQ‐10 in lecithin liposomes, and protected the liposomes from lipid peroxidation. Furthermore, supplementation of rats with UQ‐10 was observed to increase the enzyme level in their livers without affecting levels of other antioxidant factors. The observations suggested that cytosolic NADPH‐UQ reductase is responsible for cellular UQ redox cycle as an endogenous antioxidant.
Effect of vitamin E on production of macrophage migration inhibitory factor (MIF) by macrophages
Authors: Sakamoto Wataru , Nishihira Jun , Fujie Katsutoshi , Iizuka Tadashi , Handa Hiroshi , Ozaki Mitsuru , Yukawa Susumu 
Published: December 2008

AbstractMacrophage migration inhibitory factor (MIF), a putative cytokine involved in inflammatory and immune responses, was identified in rat peritoneal macrophages by Western blot analysis and its secretion into culture medium by enzyme‐linked immunosorbent assay. To clarify the possibility of vitamin E as an immune modulator, we investigated the effect of vitamin E on MIF production in macrophages in response to calcium ionophore A23187 and lipopolysaccharide (LPS). Intraperitoneal injections of vitamin E (5 mg per rat) for 6 successive days resulted in a significant increase of α‐tocopherol content in peritoneal macrophages. α‐Tocopherol content of macrophages in vitamin E‐treated rats was 478.3 ± 90.7 ng/106 cells, whereas in control rats it was 1.5 ± 0.5 ng/106 cells. For the control macrophages, total MIF content of the medium (2.5 × 106 cells/18 ml) without stimulation was 40.7 ± 3.6 ng after 14 h culture, whereas stimulation with calcium ionophore A23187 (400 nM) and LPS (5.0 μg/ml) induced the elevation of MIF content to 65.9 ± 7.5 ng and 74.3 ± 10.4 ng, respectively (p<0.05, n=3). On the other hand, vitamin E‐enriched macrophages without stimulation showed less MIF content (14.0 ± 4.2 ng) than the control (p<0.05, n=3). Similarly, the increase of MIF of vitamin E‐treated macrophages was significantly suppressed after stimulation with calcium ionophore A23187 or LPS, compared with the control macrophages (p<0.01, n=3). From analysis of intracellular MIF content by Western blot, we found no alteration of intracellular MIF content of vitamin E‐macrophages, in contrast to the decreased content of control stimulated‐macrophages, showing that vitamin E suppressed MIF secretion into the culture medium. Taken together, these results indicate that vitamin E may contribute to the regulation of inflammatory and immune responses through regulation of MIF secretion, possibly by modulating macrophage‐membrane architecture.
Interleukin‐1 signaling is dependent on free thiols
Authors: Böl Gaby‐Fleur , Tewes Frank , Brigelius‐Flohé Regina 
Published: December 2008

AbstractStimulation of the Interleukin‐1 receptor type I (IL‐1‐RI) with IL‐1 activates an associated serine/threonine kinase, IRAK, which phosphorylates downstream targets, resulting in NF/kappaB activation. The signaling cascade is accompanied by oxidative processes and contains putative targets for redox regulation. Preincubation of the murine T cell line EL‐4 and the human umbilical cord vein endothelial cell line ECV 304 with thiol modifying compounds like diamide, menadione or phenylarsine oxide inhibited the IL‐1‐induced phosphorylation of an endogenous substrate with a molecular mass of 60 kD. In the endothelial cell line, a second target of about 85 kD was phosphorylated after IL‐1 stimulation, which was also inhibited by thiol modification. These data suggest that IL‐1 signal transduction depends on free thiols which might be targets for redox regulation not only in lymphocytes, but also in endothelial cells.
Biosynthesis of selenophosphate
Authors: Lacourciere Gerard M. 
Published: December 2008

AbstractSelenophosphate synthetase, the product of the selD gene, produces the highly active selenium donor, monoselenophosphate, from selenide and ATP. Positional isotope exchange experiments have shown hydrolysis of ATP occurs by way of a phosphoryl‐enzyme intermediate. Although, mutagenesis studies have demonstrated Cys17 in the Escherichia coli enzyme is essential for catalytic activity the nucleophile in catalysis has not been identified. Recently, selenophosphate synthetase enzymes have been identified from other organisms. The human enzyme which contains a threonine residue corresponding to Cys17 in the E. coli enzyme, has been overexpressed in E. coli. The purified enzyme shows no detectable activity in the in vitro selenophosphate synthetase assay. In contrast, when the human enzyme is expressed to complement a selD mutation in E. coli, in the presence of 75Se, incorporation of 75Se into bacterial selenoproteins is observed. The inactive purified human enzyme together with the very low determined specific activity of the E. coli enzyme (83 nmol/min/mg) suggest an essential component for the formation of selenophosphate has not been identified.
Iodine and brain development
Authors: Bernal Juan 
Published: December 2008

AbstractThe development of the brain is critically dependent on an adequate supply of iodine. Iodine is an integral part of thyroid hormone, which acts on brain development by regulating the expression of target genes. The active thyroid hormone, T3, is generated in part in the thyroid gland, but about 80% of T3 in brain is formed locally from T4 deiodination mainly by the action of a specific iodothyronine deiodinase. This enzyme is highly expressed in astrocytes, which take up T4 from the blood and deliver T3 for neuronal use. In the target cells T3 binds to nuclear receptors which are transcription factors. The T3 receptors are expressed in the brain before fetal thyroid gland function and may be activated by maternal thyroid hormone during midgestation. Although a group of thyroid hormone target genes has been identified in recent years, many basic questions of thyroid hormone action in the brain remain to be elucidated.
Relationship between dietary copper concentration and acetylcholine‐induced vasodilation in the microcirculation of rats
Authors: Schuschke D. A. , Percival S. S. , Saari J. T. , Miller F. N. 
Published: December 2008

AbstractDietary copper deficiency has been shown to significantly reduce acetylcholine (Ach)‐induced vascular smooth muscle relaxation. The current study was designed to examine the relative relationship between dietary copper and the vasodilator response to Ach in the microcirculation of the rat. Male weanling rats were fed a purified basal diet supplemented with 6.0, 3.0, 1.5 or 0.0 μg Cu/g diet for 4 weeks to provide an adequate, two marginal, and deficient intakes of dietary copper. Arteriole dilation in response to increasing concentrations of acetylcholine (10−1 to 10−4 M) was measured in the in vivo cremaster muscle microcirculation for each dietary group. Liver copper and both aortic and erythrocyte Cu,Zn‐SOD activity were used as indices of systemic copper status. Dilation to the increasing concentrations of Ach was only different in the 0 μg Cu supplemented group compared to the copper‐adequate control values. However, the combined results showed an exponential increase in 10−5 M Ach‐induced vasodilation as liver copper concentration increases from 0 μg Cu/g dry wt. This relationship suggests that dilation is attenuated at liver Cu concentrations below 5 μg/g dry wt. The results indicate that Ach‐induced vasodilation is copper‐dependent but that the pathway is not very sensitive to short‐term marginal restriction of copper intake.
The role of 4′‐phosphopantetheine in the biosynthesis of fatty acids, polyketides and peptides
Authors: Kleinkauf Horst 
Published: December 2008

AbstractThe peptide part of CoA, 4′‐phosphopantetheine, has been identified as an essential cofactor in in the biosynthesis of fatty acids, polyketides, depsipeptides, peptides, and compounds derived from both carboxylic and amino acid precursors, like rapamycin. The cofactor is attached to a unique protein moiety, referred to as acyl carrier protein, aminoacyl carrier protein, or peptidyl carrier protein. These carrier proteins are either associated to enzyme complexes (type II) or integrated within multifunctional polypeptide chains (type I). The cofactor is added in a post‐translational modification reaction by highly specific transferases, acting on CoA. The functions of carrier proteins in directed condensation reactions are: (1) the selection of substrates to be attached as thioesters, (2) the stabilization of intermediates, (3) the presentation of intermediates for modification by associated enyzme activities, (4) facilitation of the directed condensation reactions of two adjacent intermediates, and (5) assistance in the termination reaction(s) leading to product release.
Effect of dietary vitamin B6 contents on antibody production
Authors: Inubushi T. , Okada M. , Matsui A. , Hanba J. , Murata E. , Katunuma N. 
Published: December 2008

AbstractWhen mice were placed on diets extreme deficient in vitamin B6, ovalbumin‐dependent antibody productions (IgE, IgG1, IgG2a) were significantly suppressed, and alanine aminotransferase activity in the liver was also significantly decreased.In the case of pyridoxine excess (6 mg% = about ten times standard amount) in a 70% casein diet, ovalbumin‐dependent antibody productions were also considerably suppressed. These responses were weaker in a low casein (5%) or normal casein (20%) diet than in a 70% casein diet.The administration of high doses of pyridoxine (6 mg%) resulted in the suppression of hepatic cathepsin B activity. Therefore, we conclude that ovalbumin‐dependent antibody productions (IgG1, IgE) were suppressed by pyridoxine excess diet (6 mg%), because hepatic cathepsin B activity was suppressed by the excess pyridoxine in diet.
Ecto‐diadenosine 5′,5‴‐P1,P4‐tetraphosphate (Ap4A)‐hydrolase is expressed as an ectoenzyme in a variety of mammalian and human cells and adds ne
Authors: Drygalski Annette Von , Ogilvie Adaling 
Published: December 2008

AbstractAp4A and other dinucleotides participate in the regulation of hemostasis and blood pressure control. With the exception of two previously reported surface anchored ectoAp4A‐hydrolases on bovine aortic endothelial and chromaffine cells, all Ap4A‐hydrolases reported are intracellular or freely soluble. We demonstrated that ectoAp4A‐hydrolases are present on a broad variety of cell types of different species: rat mesangial, bovine corneal epithelial, human Hep‐G2 and peridontal cells. Ectoenzyme properties were evaluated on rat mesangium cells. Chromatography of purified plasma membranes on Sephacel 300 resulted in enrichment of ectoAp4A‐hydrolase and in separation from ectoATPase. In contrast to ATPase, Ap4A‐hydrolase was stable at room temperature. EctoAp4A‐hydrolase also recognized ATP as substrate, and therefore is not highly specific. The molecular weight was 180 kD. Unlike ectoAMPase ectoAp4A‐hydrolase was not attached via a glycosyl‐phosphatidylinositol (GPI)‐moiety. Concentrations of PI‐PLC 10–100‐fold higher than effective for ectoAMPase cleavage (10–100 mU/ml) plus extensively extended incubation times up to eight hours did not result in cleavage of ectoAp4A‐hydrolase. The enzyme ectoAp4A‐hydrolase might presage a direction for pharmaceutical manipulation in the control of blood pressure and hemostasis.