scholarly journals Role of cytosolic rat liver aldehyde dehydrogenase in the oxidation of acetaldehyde during ethanol metabolism in vivo

1975 ◽  
Vol 152 (3) ◽  
pp. 709-712 ◽  
Author(s):  
C J Eriksson ◽  
M Marselos ◽  
T Koivula
Keyword(s):  
Aldehyde Dehydrogenase ◽  
Oxidation Rate ◽  
Ethanol Metabolism ◽  
Minor Role ◽  
Liver Cytosol ◽  
A Minor ◽  
Liver Aldehyde Dehydrogenase ◽  
Phenobarbital Induction

The activity of a high-Km aldehyde dehydrogenase in the liver cytosol was increased by phenobarbital induction. No corresponding increase in the oxidation rate of acetaldehyde in vivo was found, and it is concluded that cytosolic aldehyde dehydrogenase plays only a minor role in the oxidation of acetaldehyde during ethanol metabolism.

scholarly journals Aldehyde dehydrogenase is essential for both adult and larval ethanol resistance in Drosophila melanogaster

2006 ◽  
Vol 87 (2) ◽  
pp. 87-92 ◽  
Author(s):  
JAMES D. FRY ◽  
MOLLY SAWEIKIS
Keyword(s):  
Aldehyde Dehydrogenase ◽  
Ethanol Metabolism ◽  
Minor Role ◽  
Ethanol Sensitivity ◽  
Fruit Breeding ◽  
Structural Locus ◽  
Ethanol Resistance ◽  
A Minor

The enzyme aldehyde dehydrogenase (ALDH) is essential for ethanol metabolism in mammals, converting the highly toxic intermediate acetaldehyde to acetate. The role of ALDH in Drosophila has been debated, with some authors arguing that, at least in larvae, acetaldehyde detoxification is carried out mainly by alcohol dehydrogenase (ADH), the enzyme responsible for converting ethanol to acetaldehyde. Here, we report the creation and characterization of four null mutants of Aldh, the putative structural locus for ALDH. Aldh null larvae and adults are poisoned by ethanol concentrations easily tolerated by wild-types; their ethanol sensitivity is in fact comparable to that of Adh nulls. The results refute the view that ALDH plays only a minor role in ethanol detoxification in larvae, and suggest that Aldh and Adh may be equally important players in the evolution of ethanol resistance in fruit-breeding Drosophila.

scholarly journals A minor role of WNK3 in regulating phosphorylation of renal NKCC2 and NCC co-transporters in vivo

Biology Open ◽  
2011 ◽  
Vol 1 (2) ◽  
pp. 120-127 ◽  
Author(s):  
K. Oi ◽  
E. Sohara ◽  
T. Rai ◽  
M. Misawa ◽  
M. Chiga ◽  
...  
Keyword(s):  
Minor Role ◽  
A Minor

scholarly journals Deep Sequencing Reveals New Roles for MuB in Transposition Immunity and Target-capture, and Redefines the Insular Ter Region of E. coli

2020 ◽  
Author(s):  
David M Walker ◽  
Rasika Harshey
Keyword(s):  
High Efficiency ◽  
Active Regions ◽  
Minor Role ◽  
Entire Genome ◽  
E Coli ◽  
Target Capture ◽  
Mu Transposition ◽  
A Minor

Abstract Background The target capture protein MuB is responsible for the high efficiency of phage Mu transposition within the E. coli genome. However, some targets are off-limits, such as regions immediately outside the Mu ends (cis-immunity) as well as the entire ~37 kb genome of Mu (Mu genome immunity). Paradoxically, MuB is responsible for cis-immunity and is also implicated in Mu genome immunity, but via different mechanisms. This study was undertaken to dissect the role of MuB in target choice in vivo.Results We tracked Mu transposition from six different starting locations on the E. coli genome, in the presence and absence of MuB. The data reveal that Mu’s ability to sample the entire genome during a single hop in a clonal population is independent of MuB, and that MuB is responsible for cis-immunity, plays a minor role in Mu genome immunity, and facilitates insertions into transcriptionally active regions. Unexpectedly, transposition patterns in the absence of MuB have helped extend the boundaries of the insular Ter segment of the E. coli genome.Conclusions The results in this study demonstrate unambiguously the operation of two distinct mechanisms of Mu target immunity, only one of which is wholly dependent on MuB. The study also reveals several interesting and hitherto unknown aspects of Mu target choice in vivo, particularly the role of MuB in facilitating the capture of promoter and translation start site targets, likely by displacing macromolecular complexes engaged in gene expression. So also, MuB facilitates transposition into the restricted Ter region of the genome.

scholarly journals Chronic treatment with exendin(9–39)amide indicates a minor role for endogenous glucagon-like peptide-1 in metabolic abnormalities of obesity-related diabetes in ob/ob mice

2005 ◽  
Vol 185 (2) ◽  
pp. 307-317 ◽  
Author(s):  
B D Green ◽  
N Irwin ◽  
V A Gault ◽  
C J Bailey ◽  
F P M O’Harte ◽  
...  
Keyword(s):  
Feeding Activity ◽  
Minor Role ◽  
Metabolic Abnormalities ◽  
Similar Treatment ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Glucose Stimulated Insulin Secretion ◽  
A Minor

Glucagon-like peptide-1 (GLP-1) is a potent insulinotropic hormone proposed to play a role in both the pathophysiology and treatment of type 2 diabetes. This study has employed the GLP-1 receptor antagonist, exendin-4(9–39)amide (Ex(9–39)) to evaluate the role of endogenous GLP-1 in genetic obesity-related diabetes and related metabolic abnormalities using ob/ob and normal mice. Acute in vivo antagonistic potency of Ex(9–39) was confirmed in ob/ob mice by blockade of the insulin-releasing and anti-hyperglycaemic actions of intraperitoneal GLP-1. In longer term studies, ob/ob mice were given once daily injections of Ex(9–39) or vehicle for 11 days. Feeding activity, body weight, and both basal and glucose-stimulated insulin secretion were not significantly affected by chronic Ex(9–39) treatment. However, significantly elevated basal glucose concentrations and impaired glucose tolerance were evident at 11 days. These disturbances in glucose homeostasis were independent of changes of insulin sensitivity and reversed by discontinuation of the Ex(9–39) for 9 days. Similar treatment of normal mice did not affect any of the parameters measured. These findings illustrate the physiological extrapancreatic glucose-lowering actions of GLP-1 in ob/ob mice and suggest that the endogenous hormone plays a minor role in the metabolic abnormalities associated with obesity-related diabetes.

scholarly journals Complement Activation Selectively Potentiates the Pathogenicity of the IgG2b and IgG3 Isotypes of a High Affinity Anti-Erythrocyte Autoantibody

2002 ◽  
Vol 195 (6) ◽  
pp. 665-672 ◽  
Author(s):  
Samareh Azeredo da Silveira ◽  
Shuichi Kikuchi ◽  
Liliane Fossati-Jimack ◽  
Thomas Moll ◽  
Takashi Saito ◽  
...  
Keyword(s):  
Affinity Maturation ◽  
Minor Role ◽  
Binding Affinities ◽  
Effector Cells ◽  
High Affinity ◽  
Erythrocyte Binding ◽  
Igg Isotypes ◽  
A Minor

By generating four IgG isotype-switch variants of the high affinity 34–3C anti-erythrocyte autoantibody, and comparing them to the IgG variants of the low affinity 4C8 anti-erythrocyte autoantibody that we have previously studied, we evaluated in this study how high affinity binding to erythrocytes influences the pathogenicity of each IgG isotype in relation to the respective contributions of Fcγ receptor (FcγR) and complement. The 34–3C autoantibody opsonizing extensively circulating erythrocytes efficiently activated complement in vivo (IgG2a = IgG2b > IgG3), except for the IgG1 isotype, while the 4C8 IgG autoantibody failed to activate complement. The pathogenicity of the 34–3C autoantibody of IgG2b and IgG3 isotypes was dramatically higher (>200-fold) than that of the corresponding isotypes of the 4C8 antibody. This enhanced activity was highly (IgG2b) or totally (IgG3) dependent on complement. In contrast, erythrocyte-binding affinities only played a minor role in in vivo hemolytic activities of the IgG1 and IgG2a isotypes of 34–3C and 4C8 antibodies, where complement was not or only partially involved, respectively. The remarkably different capacities of four different IgG isotypes of low and high affinity anti-erythrocyte autoantibodies to activate FcγR-bearing effector cells and complement in vivo demonstrate the role of autoantibody affinity maturation and of IgG isotype switching in autoantibody-mediated pathology.

Role of Thromboxane A2 as a Mediator of Platelet-Activating-Factor-Induced Aggregation of Human Platelets

1989 ◽  
Vol 77 (1) ◽  
pp. 99-103 ◽  
Author(s):  
R. K. McCulloch ◽  
J. Summers ◽  
R. Vandongen ◽  
I. L. Rouse
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activating Factor ◽  
Thromboxane A2 ◽  
Human Platelets ◽  
Minor Role ◽  
A Minor ◽  
Induced Aggregation

1. At present it is unclear whether platelet-activating-factor (PAF)-induced aggregation is mediated by thromboxane. To obtain further information about this event we have compared the affects of aspirin on platelet aggregation and secretion induced by PAF and collagen. 2. Collagen and PAF induced aggregation and secretion in human platelets in a dose-related manner. 3. Aspirin inhibited the magnitude of both platelet aggregation and secretion induced by PAF and collagen, but the degree of inhibition was much greater for collagen. 4. Aspirin strongly inhibited the aggregation rate of collagen-induced platelet aggregation, but had no measurable effect on the rate of PAF-induced aggregation. 5. Inconsistencies reported in previous studies of the effect of aspirin on PAF-induced platelet aggregation may be explained, in part, by the doses of PAF used and the method of inactivating cyclo-oxygenase (in vitro compared with in vivo). 6. Our results suggest that the initial events of PAF-induced aggregation are independent of thromboxane A2 formation and that thromboxane A2 plays only a minor role in the later phase of PAF-induced aggregation.

Thrombocytopenia Induced in Mice by Thromboplastin Infusion – Essential Role of the Third Complement Component

1978 ◽  
Vol 39 (03) ◽  
pp. 733-742
Author(s):  
Luis A Giraudo ◽  
Agustin P Dalmasso
Keyword(s):  
Blood Platelet ◽  
Total Serum ◽  
Minor Role ◽  
Slight Reduction ◽  
Experimental Conditions ◽  
Slow Infusion ◽  
A Minor ◽  
Deficient Mice

SummaryStudies were performed in mice to investigate the effects of the slow infusion of brain thromboplastin (tissue factor) on blood platelet levels. Thromboplastin caused pronounced thrombocytopenia in all strains of mice tested without histological evidence of intravascular coagulation. The role of the complement system in the thrombocytopenic response to thromboplastin administration was evaluated by using complement-deficient animals. Depending on experimental conditions, the degree of platelet reduction in C5-deficient mice was similar to or significantly lower than in normocomplementemic animals. C5-deficient mice reconstituted with mouse plasma or purified human C5 had a thrombocytopenic reaction identical to that of normocomplementemic controls. The thrombocytopenic response of B10.D2/new and old line mice could be abrogated by inactivating C3 with cobra venom factor prior to the administration of thromboplastin. We conclude that in mice C3 plays a central role in the thrombocytopenia induced by thromboplastin infusion, while C5 (and/or other late acting components) plays only a minor role. In vivo activation of complement by thromboplastin was indicated by the finding that thromboplastin infusion in B10.D2/new mice caused a significant reduction in total serum hemolytic complement and a slight reduction in C3 measured immunochemically. The platelet counts of uninjected B10.D2/new mice were slightly but significantly higher than in B10.D2/old mice.

The Effect of Path Length and Display Size on Memory for Spatial Information

2012 ◽  
Vol 59 (3) ◽  
pp. 147-152 ◽  
Author(s):  
Katherine Guérard ◽  
Sébastien Tremblay
Keyword(s):  
Path Length ◽  
Potential Role ◽  
Spatial Information ◽  
Recall Performance ◽  
Minor Role ◽  
Length Effect ◽  
Serial Memory ◽  
Fixed Reference ◽  
A Minor

In serial memory for spatial information, some studies showed that recall performance suffers when the distance between successive locations increases relatively to the size of the display in which they are presented (the path length effect; e.g., Parmentier et al., 2005) but not when distance is increased by enlarging the size of the display (e.g., Smyth & Scholey, 1994). In the present study, we examined the effect of varying the absolute and relative distance between to-be-remembered items on memory for spatial information. We manipulated path length using small (15″) and large (64″) screens within the same design. In two experiments, we showed that distance was disruptive mainly when it is varied relatively to a fixed reference frame, though increasing the size of the display also had a small deleterious effect on recall. The insertion of a retention interval did not influence these effects, suggesting that rehearsal plays a minor role in mediating the effects of distance on serial spatial memory. We discuss the potential role of perceptual organization in light of the pattern of results.

Ethanol Metabolism in Vivo and the Role of Hepatic Microsomal Ethanol Oxidation

1972 ◽  
Vol 33 (3) ◽  
pp. 751-755 ◽  
Author(s):  
Mary K. Roach ◽  
Myrna Khan ◽  
Marguerite Knapp ◽  
W. N. Reese
Keyword(s):  
Ethanol Oxidation ◽  
Ethanol Metabolism

Effects of Myo-inositol Alone and in Combination with Seleno-Lmethionine on Cadmium-Induced Testicular Damage in Mice

2019 ◽  
Vol 12 (4) ◽  
pp. 311-323 ◽  
Author(s):  
Salvatore Benvenga ◽  
Antonio Micali ◽  
Giovanni Pallio ◽  
Roberto Vita ◽  
Consuelo Malta ◽  
...  
Keyword(s):  
Structural Changes ◽  
Natural Antioxidants ◽  
Minor Role ◽  
Positive Role ◽  
Testosterone Levels ◽  
Tnf Α ◽  
Testicular Lesions ◽  
A Minor ◽  
Immunohistochemical Analyses

Background: Cadmium (Cd) impairs gametogenesis and damages the blood-testis barrier. Objective: As the primary mechanism of Cd-induced damage is oxidative stress, the effects of two natural antioxidants, myo-inositol (MI) and seleno-L-methionine (Se), were evaluated in mice testes. Methods: Eighty-four male C57 BL/6J mice were divided into twelve groups: 0.9% NaCl (vehicle; 1 ml/kg/day i.p.); Se (0.2 mg/kg/day per os); Se (0.4 mg/kg/day per os); MI (360 mg/kg/day per os); MI plus Se (0.2 mg/kg/day); MI plus Se (0.4 mg/kg/day); CdCl2 (2 mg/kg/day i.p.) plus vehicle; CdCl2 plus MI; CdCl2 plus Se (0.2 mg/kg/day); CdCl2 plus Se (0.4 mg/kg/day); CdCl2 plus MI plus Se (0.2 mg/kg/day); and CdCl2 plus MI plus Se (0.4 mg/kg/day). After 14 days, testes were processed for biochemical, structural and immunohistochemical analyses. Results: CdCl2 increased iNOS and TNF-α expression and Malondialdehyde (MDA) levels, lowered glutathione (GSH) and testosterone, induced testicular lesions, and almost eliminated claudin-11 immunoreactivity. Se administration at 0.2 or 0.4 mg/kg significantly reduced iNOS and TNF-α expression, maintained GSH, MDA and testosterone levels, structural changes and low claudin-11 immunoreactivity. MI alone or associated with Se at 0.2 or 0.4 mg/kg significantly reduced iNOS and TNF-α expression and MDA levels, increased GSH and testosterone levels, ameliorated structural organization and increased claudin-11 patches number. Conclusion: We demonstrated a protective effect of MI, a minor role of Se and an evident positive role of the association between MI and Se on Cd-induced damages of the testis. MI alone or associated with Se might protect testes in subjects exposed to toxicants, at least to those with behavior similar to Cd.

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