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Title
molybdenum-cofactor deficiency: CT and MR findings.
Author
Schuierer G; Kurlemann G; Bick U; Stephani U
Address
Institut f ur Klinische Radiologie' Westf alische-Wilhelms-Universit
at' Kiel' Germany.
Source
Neuropediatrics, 26(1):51-4 1995 Feb
Abstract
We describe the CT and MR findings in molybdenum-cofactor deficiency' a
rare metabolic disorder which is caused by the defect of a
molybdenum-containing enzyme cofactor. The CT (3 patients) and/or MR
studies (3 patients) of 4 children' which became symptomatic with
intractable seizures within the first days after birth and finally
turned out to have molybdenum cofactor deficiency' were reviewed. All
patients showed multicystic leukencephalopathy and a normal newborn
pattern of myelination of the brainstem. A striking finding in some
studies was an abnormal shape of the frontal horns of the dilated
ventricles caused by severe volume loss of the basal ganglia'
especially of the caudate nucleus' and of the corpus callosum. MRI was
superior to CT in the demonstration of these lesions. In
molybdenum-cofactor deficiency' which can be diagnosed by a typical
laboratory pattern' CT and MR show the findings of severe perinatal
brain damage. The abnormal shape of the frontal horns' although
possibly not specific' may even suggest molybdenum-cofactor deficiency
in newborns with intractable seizures.
Language
Eng
Unique Identifier
95312162
Publication Type
JOURNAL ARTICLE
ISSN
0174-304X
Country of Publication
GERMANY




Title
Suppressive effect of molybdenum on hepatotoxicity of
N-nitrosodiethylamine in rats.
Author
Koizumi T; TaJima K; Emi N; Hara A; Suzuki KT
Address
Faculty of Pharmaceutical Sciences' Chiba University' Japan.
Source
Biol Pharm Bull, 18(3):460-2 1995 Mar
Abstract
In order to elucidate the mechanism by which molybdenum prevents the
carcinogenesis of N-nitroso compounds' the effects of
Na2MoO4-pretreatment on N-nitrosodiethylamine (NDEA)-induced DNA strand
breaks' fluctuation in cation contents and lipid peroxidation levels in
rat liver were examined. Male Wistar rats weighing 170-190 g were
pretreated with Na2MoO4 (1.24 mmol/kg body weight' i.p.' once a day)
for 3 d and on day 4' they were exposed to NDEA (50 mg/kg body weight'
once' i.p.). Three days after exposure to NDEA' the nitroso compound
caused DNA strand breaks and disrupted potassium (K) and calcium (Ca)
metabolism in the liver but did not affect lipid peroxidation levels.
Na2MoO4-pretreatment prevented both NDEA-induced DNA damage and
disruption of the metabolism of those cations but rather enhanced lipid
peroxidation. These results suggest that Mo prevented NDEA-induced DNA
damage by preventing disruption of intracellular Ca metabolism while
stimulating the metabolism of the nitroso compound via a nontoxic
pathway.
Language
Eng
Unique Identifier
96031331
Publication Type
JOURNAL ARTICLE
ISSN
0918-6158
Country of Publication
JAPAN




Title
Proton activation analysis of stable isotopes for a molybdenum
biokinetics study in humans.
Author
Cantone MC; de Bartolo D; Gambarini G; Giussani A; Ottolenghi A; Pirola
L; Hansen C; Roth P; Werner E
Address
Universit`a degli Studi' Dipartimento di Fisica' Milano' Italy.
Source
Med Phys, 22(8):1293-8 1995 Aug
Abstract
molybdenum is a trace element essential to life. Nevertheless' little
information is available on its metabolism in humans. A methodology
based on stable isotope administration that combines compartmental
analysis' simultaneous use of two tracers' and proton nuclear
activation (PNA) is presented. A four-compartment metabolic model was
adopted. The compartments are stomach' small intestine' transfer
compartment' and unquantified tissue pool. The employment of two
different stable isotopes of the element under investigation as tracers
was made possible by PNA. Optimization of the technique for molybdenum
determination in plasma led to the choice of 95Mo and 96Mo as tracers.
Their concentrations in plasma can be determined measuring the
disintegration gamma lines of the corresponding technetium
radioisotopes produced via (p'n) reaction. In the adopted experimental
conditions' a minimum detectable concentration of 2 ng isotope/ml
plasma was attained. A kinetics study was performed on two healthy
volunteers. To both subJects one tracer was orally administered' and
the other intravenously inJected. Venous blood samples were withdrawn
at different postinJection times and the concentrations for both
isotopes determined. The model parameters describing molybdenum
kinetics were obtained for the two individuals. Total absorbed fraction
was found to be 0.84 +/- 0.03 and 0.86 +/- 0.07' respectively.
Language
Eng
Unique Identifier
96027033
Publication Type
JOURNAL ARTICLE
ISSN
0094-2405
Country of Publication
UNITED STATES




Title
molybdenum-cofactor-containing enzymes: structure and mechanism.
Author
Kisker C; Schindelin H; Rees DC
Address
Division of Chemistry and Chemical Engineering' California Institute of
Technology' Pasadena 91125' USA.
Source
Annu Rev Biochem, 66():233-67 1997
Abstract
molybdenum-containing enzymes catalyze basic metabolic reactions in the
nitrogen' sulfur' and carbon cycles. With the exception of the
nitrogenase cofactor' molybdenum is incorporated into proteins as the
molybdenum cofactor that contains a mononuclear molybdenum atom
coordinated to the sulfur atoms of a pterin derivative named
molybdopterin. Certain microorganisms can also utilize tungsten in a
similar fashion. molybdenum-cofactor-containing enzymes catalyze the
transfer of an oxygen atom' ultimately derived from or incorporated
into water' to or from a substrate in a two-electron redox reaction. On
the basis of sequence alignments and spectroscopic properties' four
families of molybdenum-cofactor-containing enzymes have been
identified. The available crystallographic structures for members of
these families are discussed within the framework of the active site
structure and catalytic mechanisms of molybdenum-cofactor-containing
enzymes. Although the function of the molybdopterin ligand has not yet
been conclusively established' interactions of this ligand with the
coordinated metal are sensitive to the oxidation state' indicating that
the molybdopterin may be directly involved in the enzymatic mechanism.
Language
Eng
Unique Identifier
97386817
Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW' TUTORIAL
ISSN
0066-4154
Country of Publication
UNITED STATES
Database: med95-97 -- Record 5 of 8 selected.




Title
Improvement of glucose and lipid metabolism in diabetic rats treated
with molybdate.
Author
Ozcelikay AT; Becker DJ; Ongemba LN; Pottier AM; Henquin JC; Brichard
SM
Address
Endocrinology and Metabolism Unit' Faculty of Medicine' University of
Louvain' Brussels' Belgium.
Source
Am J Physiol, 270(2 Pt 1):E344-52 1996 Feb
Abstract
molybdenum mimics certain insulin actions in vitro. We have
investigated the effects of oral administration of Na2MoO4 (Mo) for 8
wk on carbohydrate and lipid metabolism in streptozotocin-diabetic
rats. Mo decreased hyperglycemia and glucosuria by 75% and corrected
the elevation of plasma nonesterified fatty acids. Tolerance to glucose
loads was improved' and glycogen stores were replenished. These effects
were not due to a rise of insulinemia. In liver' Mo restored the
blunted mRNA and activity of glucokinase and pyruvate kinase and
decreased to normal phosphoenolpyruvate carboxykinase values. Finally'
Mo totally reversed the low expression and activity of acetyl-CoA
carboxylase and fatty acid synthase in liver' but not in white adipose
tissue. In conclusion' Mo exerts a marked blood glucose-lowering effect
in diabetic rats by an insulin-like action. This effect results in part
from a restoration of hepatic glucose metabolism and is associated with
a tissue-specific correction of lipogenic enzyme gene expression' both
processes being essentially mediated by reversal of impaired
pretranslational regulatory mechanisms. These observations raise new
therapeutic perspectives in diabetes' particularly in the
insulin-resistant condition.
Language
Eng
Unique Identifier
96373667
Publication Type
JOURNAL ARTICLE
ISSN
0002-9513
Country of Publication
UNITED STATES




Title
Defective molybdopterin biosynthesis: clinical heterogeneity associated
with molybdenum cofactor deficiency.
Author
Mize C; Johnson JL; RaJagopalan KV
Address
Department of Pediatrics' University of Texas Southwestern' Dallas
75235-9063' USA.
Source
J Inherit Metab Dis, 18(3):283-90 1995
Abstract
A patient with molybdenum cofactor deficiency (producing the
biochemical abnormalities associated with deficiencies of sulphite
oxidase and xanthine dehydrogenase) clinically expressed Marfan-like
habitus with dislocated lenses' vertebral abnormality' learning
disability' moderate hemiplegia' increased medial lentiform MRI signal
and intermittent microscopic haematuria. S-Sulphocysteine was present
in plasma and urine' and the oxidized derivative of a molybdopterin
precursor (precursor Z)' together with xanthine and hypoxanthine' were
elevated in urine. Blood uric acid was < 1 mg/dl' while urinary
urothione was not detected. These data indicate a functionally
inadequate terminal enzyme for converting precursor Z to active
molybdopterin (complementation group B of general molybdenum cofactor
deficiency). Although the biochemical parameters were indicative of a
severe deficiency state' the patient has survived into the third decade
with a less severe clinical spectrum than has generally been associated
with this disease.
Language
Eng
Unique Identifier
96086549
Publication Type
JOURNAL ARTICLE
ISSN
0141-8955
Country of Publication
NETHERLANDS




Title
molybdenum cofactor deficiency-phenotypic variability in a family with
a late-onset variant.
Author
Hughes EF; Fairbanks L; Simmonds HA; Robinson RO
Address
Department of Paediatric Neurology, Newcomen Centre, Guy's Hospital,
London, UK.
Source
Dev Med Child Neurol, 40(1):57-61 1998 Jan
Abstract
In a family with molybdenum cofactor deficiency, the onset in the index
case was delayed until 1 year of age, when the patient presented with
an episode of lethargy and inconsolable crying culminating in a
seizure. By 17 months she showed mild motor delay, regression in
language skills, and feeding difficulties. Progressive global
deterioration followed, associated with sustained irritability,
dystonic posturing, and further seizures, before her condition
subsequently plateaued. Low plasma uric acid, raised urinary xanthine
and hypoxanthine, and positive urinary sulphite were found, which,
coupled with assay of sulphite oxidase activity in cultured
fibroblasts, confirmed the diagnosis. A sibling had isolated lens
dislocation and an identical biochemical profile. MRI in both children
was strikingly abnormal. molybdenum cofactor deficiency may present as
a late-onset variant with considerable phenotypic variability.
Language
Eng
Unique Identifier
98119306
Publication Type
JOURNAL ARTICLE
ISSN
0012-1622
Country of Publication
ENGLAND




Title
[molybdenum cofactor deficiency. Clinical symptoms and diagnostic
strategy
Author
H Jberg AS; Hertz B; Christensen T; Christensen E; Taudorf K
Address
B rneafdelingen' Viborg Sygehus.
Source
Ugeskr Laeger, 157(38):5255-7 1995 Sep 18
Abstract
The clinical' neuroradiological and biochemical findings in two
siblings with molybdenum cofactor deficiency are presented. A search
for this deficiency is advocated in each case of unexplained refractory
neonatal convulsions. Early diagnosis is prompted by the often rapid
fatal outcome and the availability of methods for prenatal diagnosis.
Diagnosis may be missed or delayed on standard metabolic screening for
several reasons discussed. Magnetic resonance imaging in this condition
seems to be rather characteristic.
Language
Dan
Unique Identifier
96075147
Publication Type
JOURNAL ARTICLE
ISSN
0041-5782
Country of Publication
DENMARK

 

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