JavaScript NENÍ povolen !

Prosím povolte JavaScript.

* Zobrazit nápovědu

Reset

MeSH: lipofuscin-metabolismus

14 záznamů v Medvik Filtry

Článek

Diagnosis and misdiagnosis of adult neuronal ceroid lipofuscinosis (Kufs disease)

Berkovic, Samuel F
Autor Berkovic, Samuel F From the Epilepsy Research Centre, Department of Medicine (S.F.B., K.L.O., J.A.D., M.S.H.), University of Melbourne, Austin Health, Heidelberg, Australia Biogen, Inc. (J.F.S.), Cambridge, MA Department of Pathology (S.C.), Centro Hospitalar São João, Porto, Portugal Institute of Inherited Metabolic Disorders (S.K., I.J., A.P.), First Faculty of Medicine, Charles University in Prague General University Hospital in Prague (S.K.), Czech Republic Great Ormond Street Hospital for Children NHS Foundation Trust (G.W.A.), London, UK Center for Human Genetic Research and Department of Neurology (K.B.S., S.L.C.), Harvard Medical School, Massachusetts General Hospital, Boston Population Health and Immunity Division (M.B., K.R.S.), The Walter and Eliza Hall Institute of Medical Research Departments of Mathematics and Statistics and Medical Biology (M.B.), University of Melbourne, Australia Centre de Recherche du Centre Hospitalier de l'Université de Montréal (M.C.-D., P.C.), University of Montreal, Canada and MRC Laboratory for Cell Biology (S.E.M.), Department of Genetics, Evolution & Environment and UCL Institute of Child Health, University College London, UK. s.berkovic@unimelb.edu.au
Staropoli, John F
Autor Staropoli, John F From the Epilepsy Research Centre, Department of Medicine (S.F.B., K.L.O., J.A.D., M.S.H.), University of Melbourne, Austin Health, Heidelberg, Australia Biogen, Inc. (J.F.S.), Cambridge, MA Department of Pathology (S.C.), Centro Hospitalar São João, Porto, Portugal Institute of Inherited Metabolic Disorders (S.K., I.J., A.P.), First Faculty of Medicine, Charles University in Prague General University Hospital in Prague (S.K.), Czech Republic Great Ormond Street Hospital for Children NHS Foundation Trust (G.W.A.), London, UK Center for Human Genetic Research and Department of Neurology (K.B.S., S.L.C.), Harvard Medical School, Massachusetts General Hospital, Boston Population Health and Immunity Division (M.B., K.R.S.), The Walter and Eliza Hall Institute of Medical Research Departments of Mathematics and Statistics and Medical Biology (M.B.), University of Melbourne, Australia Centre de Recherche du Centre Hospitalier de l'Université de Montréal (M.C.-D., P.C.), University of Montreal, Canada and MRC Laboratory for Cell Biology (S.E.M.), Department of Genetics, Evolution & Environment and UCL Institute of Child Health, University College London, UK
Carpenter, Stirling
Autor Carpenter, Stirling From the Epilepsy Research Centre, Department of Medicine (S.F.B., K.L.O., J.A.D., M.S.H.), University of Melbourne, Austin Health, Heidelberg, Australia Biogen, Inc. (J.F.S.), Cambridge, MA Department of Pathology (S.C.), Centro Hospitalar São João, Porto, Portugal Institute of Inherited Metabolic Disorders (S.K., I.J., A.P.), First Faculty of Medicine, Charles University in Prague General University Hospital in Prague (S.K.), Czech Republic Great Ormond Street Hospital for Children NHS Foundation Trust (G.W.A.), London, UK Center for Human Genetic Research and Department of Neurology (K.B.S., S.L.C.), Harvard Medical School, Massachusetts General Hospital, Boston Population Health and Immunity Division (M.B., K.R.S.), The Walter and Eliza Hall Institute of Medical Research Departments of Mathematics and Statistics and Medical Biology (M.B.), University of Melbourne, Australia Centre de Recherche du Centre Hospitalier de l'Université de Montréal (M.C.-D., P.C.), University of Montreal, Canada and MRC Laboratory for Cell Biology (S.E.M.), Department of Genetics, Evolution & Environment and UCL Institute of Child Health, University College London, UK
Oliver, Karen L
Autor Oliver, Karen L From the Epilepsy Research Centre, Department of Medicine (S.F.B., K.L.O., J.A.D., M.S.H.), University of Melbourne, Austin Health, Heidelberg, Australia Biogen, Inc. (J.F.S.), Cambridge, MA Department of Pathology (S.C.), Centro Hospitalar São João, Porto, Portugal Institute of Inherited Metabolic Disorders (S.K., I.J., A.P.), First Faculty of Medicine, Charles University in Prague General University Hospital in Prague (S.K.), Czech Republic Great Ormond Street Hospital for Children NHS Foundation Trust (G.W.A.), London, UK Center for Human Genetic Research and Department of Neurology (K.B.S., S.L.C.), Harvard Medical School, Massachusetts General Hospital, Boston Population Health and Immunity Division (M.B., K.R.S.), The Walter and Eliza Hall Institute of Medical Research Departments of Mathematics and Statistics and Medical Biology (M.B.), University of Melbourne, Australia Centre de Recherche du Centre Hospitalier de l'Université de Montréal (M.C.-D., P.C.), University of Montreal, Canada and MRC Laboratory for Cell Biology (S.E.M.), Department of Genetics, Evolution & Environment and UCL Institute of Child Health, University College London, UK
Kmoch, Stanislav
Autor Kmoch, Stanislav From the Epilepsy Research Centre, Department of Medicine (S.F.B., K.L.O., J.A.D., M.S.H.), University of Melbourne, Austin Health, Heidelberg, Australia Biogen, Inc. (J.F.S.), Cambridge, MA Department of Pathology (S.C.), Centro Hospitalar São João, Porto, Portugal Institute of Inherited Metabolic Disorders (S.K., I.J., A.P.), First Faculty of Medicine, Charles University in Prague General University Hospital in Prague (S.K.), Czech Republic Great Ormond Street Hospital for Children NHS Foundation Trust (G.W.A.), London, UK Center for Human Genetic Research and Department of Neurology (K.B.S., S.L.C.), Harvard Medical School, Massachusetts General Hospital, Boston Population Health and Immunity Division (M.B., K.R.S.), The Walter and Eliza Hall Institute of Medical Research Departments of Mathematics and Statistics and Medical Biology (M.B.), University of Melbourne, Australia Centre de Recherche du Centre Hospitalier de l'Université de Montréal (M.C.-D., P.C.), University of Montreal, Canada and MRC Laboratory for Cell Biology (S.E.M.), Department of Genetics, Evolution & Environment and UCL Institute of Child Health, University College London, UK
Anderson, Glenn W
Autor Anderson, Glenn W From the Epilepsy Research Centre, Department of Medicine (S.F.B., K.L.O., J.A.D., M.S.H.), University of Melbourne, Austin Health, Heidelberg, Australia Biogen, Inc. (J.F.S.), Cambridge, MA Department of Pathology (S.C.), Centro Hospitalar São João, Porto, Portugal Institute of Inherited Metabolic Disorders (S.K., I.J., A.P.), First Faculty of Medicine, Charles University in Prague General University Hospital in Prague (S.K.), Czech Republic Great Ormond Street Hospital for Children NHS Foundation Trust (G.W.A.), London, UK Center for Human Genetic Research and Department of Neurology (K.B.S., S.L.C.), Harvard Medical School, Massachusetts General Hospital, Boston Population Health and Immunity Division (M.B., K.R.S.), The Walter and Eliza Hall Institute of Medical Research Departments of Mathematics and Statistics and Medical Biology (M.B.), University of Melbourne, Australia Centre de Recherche du Centre Hospitalier de l'Université de Montréal (M.C.-D., P.C.), University of Montreal, Canada and MRC Laboratory for Cell Biology (S.E.M.), Department of Genetics, Evolution & Environment and UCL Institute of Child Health, University College London, UK
Damiano, John A
Autor Damiano, John A From the Epilepsy Research Centre, Department of Medicine (S.F.B., K.L.O., J.A.D., M.S.H.), University of Melbourne, Austin Health, Heidelberg, Australia Biogen, Inc. (J.F.S.), Cambridge, MA Department of Pathology (S.C.), Centro Hospitalar São João, Porto, Portugal Institute of Inherited Metabolic Disorders (S.K., I.J., A.P.), First Faculty of Medicine, Charles University in Prague General University Hospital in Prague (S.K.), Czech Republic Great Ormond Street Hospital for Children NHS Foundation Trust (G.W.A.), London, UK Center for Human Genetic Research and Department of Neurology (K.B.S., S.L.C.), Harvard Medical School, Massachusetts General Hospital, Boston Population Health and Immunity Division (M.B., K.R.S.), The Walter and Eliza Hall Institute of Medical Research Departments of Mathematics and Statistics and Medical Biology (M.B.), University of Melbourne, Australia Centre de Recherche du Centre Hospitalier de l'Université de Montréal (M.C.-D., P.C.), University of Montreal, Canada and MRC Laboratory for Cell Biology (S.E.M.), Department of Genetics, Evolution & Environment and UCL Institute of Child Health, University College London, UK
Hildebrand, Michael S
Autor Hildebrand, Michael S From the Epilepsy Research Centre, Department of Medicine (S.F.B., K.L.O., J.A.D., M.S.H.), University of Melbourne, Austin Health, Heidelberg, Australia Biogen, Inc. (J.F.S.), Cambridge, MA Department of Pathology (S.C.), Centro Hospitalar São João, Porto, Portugal Institute of Inherited Metabolic Disorders (S.K., I.J., A.P.), First Faculty of Medicine, Charles University in Prague General University Hospital in Prague (S.K.), Czech Republic Great Ormond Street Hospital for Children NHS Foundation Trust (G.W.A.), London, UK Center for Human Genetic Research and Department of Neurology (K.B.S., S.L.C.), Harvard Medical School, Massachusetts General Hospital, Boston Population Health and Immunity Division (M.B., K.R.S.), The Walter and Eliza Hall Institute of Medical Research Departments of Mathematics and Statistics and Medical Biology (M.B.), University of Melbourne, Australia Centre de Recherche du Centre Hospitalier de l'Université de Montréal (M.C.-D., P.C.), University of Montreal, Canada and MRC Laboratory for Cell Biology (S.E.M.), Department of Genetics, Evolution & Environment and UCL Institute of Child Health, University College London, UK
Sims, Katherine B
Autor Sims, Katherine B From the Epilepsy Research Centre, Department of Medicine (S.F.B., K.L.O., J.A.D., M.S.H.), University of Melbourne, Austin Health, Heidelberg, Australia Biogen, Inc. (J.F.S.), Cambridge, MA Department of Pathology (S.C.), Centro Hospitalar São João, Porto, Portugal Institute of Inherited Metabolic Disorders (S.K., I.J., A.P.), First Faculty of Medicine, Charles University in Prague General University Hospital in Prague (S.K.), Czech Republic Great Ormond Street Hospital for Children NHS Foundation Trust (G.W.A.), London, UK Center for Human Genetic Research and Department of Neurology (K.B.S., S.L.C.), Harvard Medical School, Massachusetts General Hospital, Boston Population Health and Immunity Division (M.B., K.R.S.), The Walter and Eliza Hall Institute of Medical Research Departments of Mathematics and Statistics and Medical Biology (M.B.), University of Melbourne, Australia Centre de Recherche du Centre Hospitalier de l'Université de Montréal (M.C.-D., P.C.), University of Montreal, Canada and MRC Laboratory for Cell Biology (S.E.M.), Department of Genetics, Evolution & Environment and UCL Institute of Child Health, University College London, UK
Cotman, Susan L
Autor Cotman, Susan L From the Epilepsy Research Centre, Department of Medicine (S.F.B., K.L.O., J.A.D., M.S.H.), University of Melbourne, Austin Health, Heidelberg, Australia Biogen, Inc. (J.F.S.), Cambridge, MA Department of Pathology (S.C.), Centro Hospitalar São João, Porto, Portugal Institute of Inherited Metabolic Disorders (S.K., I.J., A.P.), First Faculty of Medicine, Charles University in Prague General University Hospital in Prague (S.K.), Czech Republic Great Ormond Street Hospital for Children NHS Foundation Trust (G.W.A.), London, UK Center for Human Genetic Research and Department of Neurology (K.B.S., S.L.C.), Harvard Medical School, Massachusetts General Hospital, Boston Population Health and Immunity Division (M.B., K.R.S.), The Walter and Eliza Hall Institute of Medical Research Departments of Mathematics and Statistics and Medical Biology (M.B.), University of Melbourne, Australia Centre de Recherche du Centre Hospitalier de l'Université de Montréal (M.C.-D., P.C.), University of Montreal, Canada and MRC Laboratory for Cell Biology (S.E.M.), Department of Genetics, Evolution & Environment and UCL Institute of Child Health, University College London, UK

Neurology. 2016 ; 87 (6) : 579-84. [pub] 20160713

ISSN 1526-632X
Medvik
Zdroj

OBJECTIVE: To critically re-evaluate cases diagnosed as adult neuronal ceroid lipofuscinosis (ANCL) in order to aid clinicopathologic diagnosis as a route to further gene discovery. METHODS: Through establishment of an international consortium we pooled 47 unsolved cases regarded by referring centers as ANCL. Clinical and neuropathologic experts within the Consortium established diagnostic criteria for ANCL based on the literature to assess each case. A panel of 3 neuropathologists independently reviewed source pathologic data. Cases were given a final clinicopathologic classification of definite ANCL, probable ANCL, possible ANCL, or not ANCL. RESULTS: Of the 47 cases, only 16 fulfilled the Consortium's criteria of ANCL (5 definite, 2 probable, 9 possible). Definitive alternate diagnoses were made in 10, including Huntington disease, early-onset Alzheimer disease, Niemann-Pick disease, neuroserpinopathy, prion disease, and neurodegeneration with brain iron accumulation. Six cases had features suggesting an alternate diagnosis, but no specific condition was identified; in 15, the data were inadequate for classification. Misinterpretation of normal lipofuscin as abnormal storage material was the commonest cause of misdiagnosis. CONCLUSIONS: Diagnosis of ANCL remains challenging; expert pathologic analysis and recent molecular genetic advances revealed misdiagnoses in >1/3 of cases. We now have a refined group of cases that will facilitate identification of new causative genes.

MeSH
chybná diagnóza * MeSH
dospělí MeSH
lidé MeSH
lipofuscin metabolismus MeSH
mladiství MeSH
mladý dospělý MeSH
neuronální ceroidlipofuscinózy klasifikace diagnóza genetika metabolismus MeSH
neurony metabolismus ultrastruktura MeSH
věk při počátku nemoci MeSH
Check Tag
dospělí MeSH
lidé MeSH
mladiství MeSH
mladý dospělý MeSH
Publikační typ
časopisecké články MeSH

Článek

Changes in the composition of fatty acids and lipofuscin-like pigments during development of rat heart

Physiological research. 2015 ; 64 (5) : 643-651. [pub] 2015Mar24

Physiol. Res. (Print)
ISSN 1802-9973
Medvik
Zdroj

Postnatal heart development is characterized by critical periods of heart remodeling. In order to characterize the changes in the lipophilic fraction induced by free radicals, fatty acids and their oxidized products, lipofuscin-like pigments (LFP), were investigated. Fatty acids were analyzed by gas chromatography and LFP were studied by fluorescence techniques. A fluorophore characterized by spectral methods was further resolved by HPLC. Major changes in the composition of fatty acids occurred immediately after birth and then during maturation. Fluorescence of LFP changed markedly on postnatal days 1, 4, 8, and 14, and differed from the adult animals. LFP comprise several fluorophores that were present since fetal state till adulthood. No new major fluorophores were formed during development, just the abundances of individual fluorophores have been modulated which produced changes in the shape of the spectral arrays. HPLC resolved the fluorophore with excitation maximum at 360 nm and emission maximum at 410 nm. New chromatographically distinct species appeared immediately on postnatal day 1, and then on days 30 and 60. Consumption of polyunsaturated fatty acids immediately after birth and subsequent formation of LFP suggests that oxidative stress is involved in normal heart development.

Článek

Sodium Orthovanadate and Trigonella Foenum Graecum Prevents Neuronal Parameters Decline and Impaired Glucose Homeostasis in Alloxan Diabetic Rats

Prague Medical Report. 2015 ; 116 (2) : 122-138.

Prague Med. Rep.
ISSN 1214-6994
Medvik
Zdroj

Hyperglycemia is the most important contributor in the onset and progress of diabetic complications mainly by producing oxidative stress. The present study was carried out to observe, the antihyperglycemic effect of sodium orthovanadate (SOV) and Trigonella foenum graecum seed powder (TSP) administration on blood glucose and insulin levels, membrane linked enzymes (monoamine oxidase, acetylcholinesterase, Ca2+ATPase), intracellular calcium (Ca2+) levels, lipid peroxidation, membrane fluidity and neurolipofuscin accumulation in brain of the alloxan induced diabetic rats and to see whether the treatment with SOV and TSP was capable of reversing the diabetic effects. Diabetes was induced by administration of alloxan monohydrate (15 mg/100 g body weight) and rats were treated with 2 IU insulin, 0.6 mg/ml SOV, 5% TSP in the diet and a combination of 0.2 mg/ml SOV and 5% TSP separately for three weeks. Diabetic rats showed hyperglycemia with almost four fold high blood glucose levels. Activities of acetylcholinesterase and Ca2+ATPase decreased in diabetic rat brain. Diabetic rats exhibited an increased level of intracellular Ca2+ levels, lipid peroxidation, neurolipofuscin accumulations and monoamine oxidase activity. Treatment of diabetic rats with insulin, TSP, SOV and a combined therapy of lower dose of SOV with TSP revived normoglycemia and restored the altered level of membrane bound enzymes, lipid peroxidation and neurolipofuscin accumulation. Our results showed that lower doses of SOV (0.2 mg/ml) could be used in combination with TSP in normalization of altered metabolic parameters and membrane linked enzymes without any harmful side effect.

MeSH
experimentální diabetes mellitus farmakoterapie MeSH
inzulin krev MeSH
krevní glukóza analýza MeSH
krysa rodu rattus MeSH
lipofuscin metabolismus MeSH
monoaminoxidasa metabolismus MeSH
mozek - chemie MeSH
oxidační stres MeSH
peroxidace lipidů MeSH
potkani Wistar MeSH
rostlinné extrakty aplikace a dávkování farmakologie MeSH
semena rostlinná chemie MeSH
Trigonella chemie MeSH
vanadáty aplikace a dávkování farmakologie MeSH
vápník analýza MeSH
zvířata MeSH
Check Tag
krysa rodu rattus MeSH
ženské pohlaví MeSH
zvířata MeSH
Publikační typ
časopisecké články MeSH
práce podpořená grantem MeSH

Článek

End products of lipid peroxidation in erythrocyte membranes in Alzheimer's disease

Cell biochemistry and function. 2012 ; 30 (3) : 205-10.

Cell Biochem Funct
ISSN 1099-0844
Medvik
Zdroj

Alzheimer's disease (AD) is accompanied by oxidative stress in the brain. Because the brain tissue is rich in polyunsaturated fatty acids, it is prone to the free radical attack resulting in lipid peroxidation. Intermediates of lipid peroxidation may diffuse from the primary site, cross the blood-brain barrier and modify erythrocyte membranes in the bloodstream. We exposed isolated erythrocyte membranes from patients with AD and the control group to in vitro free radical damage and monitored the accumulation of the end products of lipid peroxidation, lipofuscin-like pigments (LFPs), by fluorescence spectroscopy. LFPs were analyzed by means of tridimensional and synchronous fluorescence spectroscopy. The levels of LFP formed during in vitro peroxidation were significantly higher in erythrocyte membranes from patients with AD compared with the control group. Furthermore, the chemical composition of LFP in AD was different from the control group. The analysis of the specific modifications of erythrocyte membranes in AD is of great medical importance regarding the need of a diagnostic blood biomarker.

MeSH
Alzheimerova nemoc metabolismus MeSH
erytrocytární membrána metabolismus MeSH
lidé MeSH
lipofuscin metabolismus MeSH
oxidační stres MeSH
peroxidace lipidů MeSH
senioři nad 80 let MeSH
senioři MeSH
studie případů a kontrol MeSH
Check Tag
lidé MeSH
mužské pohlaví MeSH
senioři nad 80 let MeSH
senioři MeSH
ženské pohlaví MeSH
Publikační typ
časopisecké články MeSH
práce podpořená grantem MeSH

Článek

Ontogenetic changes of lipofuscin-like pigments in the rat heart

Physiological research. 2012 ; 61 (Suppl 1) : S173-S179.

Physiol. Res. (Print)
ISSN 1802-9973
Medvik
Zdroj

The developmental origin of the important human diseases. 2012 ; 61 (Suppl 1) : S173-S179.

ISSN 1802-9973
Medvik
Zdroj

Increased generation of reactive oxygen species results in the formation of fluorescent end-products of lipid peroxidation - lipofuscin-like pigments (LFP). LFP increased up to six-fold from the fetal value in the rat heart immediately after birth. In the experimental design of this study the fetuses were sampled 1 day before birth, and then the samples were collected on postnatal days 1, 4, 7, 10, 15, 30, and 60. Males and females were compared on day 30 and 60 when the difference between right and left ventricle was studied as well. Four LFP fluorophores were analyzed: F355/440, F310/470, F350/450, F315/450 (excitation/emission, nm). All fluorophores decreased on day 4 relative to day 1, subsequent transient increases ended in a significant decrease on day 60. However, the LFP levels on day 60 are still about threefold higher than those in fetuses. Differences between male and female hearts were observed on day 30. The corresponding male ventricles contained by one third higher concentration of LFP than the female counterparts. The increase in LFP concentration in male ventricles on day 30 was only transient, no difference between corresponding male and female ventricles was found on day 60. The most distinguished feature in the male heart was a sharp LFP decrease in the right ventricle on day 60.

Článek

Evaluation of lipofuscin-like pigments as an index of lead-induced oxidative damage in the brain

Experimental and toxicologic pathology. 2012 ; 64 (1-2) : 51-56.

Exp Toxicol Pathol
ISSN 1618-1433
Medvik
Zdroj

This study was carried out to investigate the role of lead in the development of oxidative stress in the brain. We examined the rate of lipid peroxidation and we determined lipid fluorescence products (lipofuscin-like pigments - LFP) as a marker of lipid peroxidation after short in vitro incubation of rat brain homogenates with lead acetate (10(-2), 10(-4), 10(-6) M lead acetate, 2 h). Simultaneously we examined by the same method in vivo indices of oxidative stress in brains of mice exposed for 12 weeks to 0.2% lead acetate in drinking water. The results show that the concentration of LFP in rat brain homogenates increased significantly after 2 h incubation with 10(-2) M lead acetate as compared to controls (P<0.0001). This effect was not observed in lower doses of lead acetate (10(-4) and 10(-6) M). After the long-term exposure of mice to 0.2% lead acetate, pronounced accumulation of lead and significantly increased concentration of LFP (P<0.004) in the brains of exposed animals as compared to controls were observed. The evidence for the formation of specific fluorophores originating from oxidative damage was shown also in qualitative changes in 3D spectral arrays and synchronous spectra. The presented results proved the influence of lead on the activation of radical reactions in the brain after short in vitro exposure of rat brain as well as within long-term in vivo exposure in mice using lipofuscin-like pigments as an indicator of oxidative stress.

Článek

Early postnatal development of rat brain is accompanied by generation of lipofuscin-like pigments

Molecular and cellular biochemistry. 2011 ; 347 (1-2) : 157-162.

Mol Cell Biochem
ISSN 1573-4919
Medvik
Zdroj

The increased generation of free radicals results in the formation of fluorescent end-products of lipid peroxidation, lipofuscin-like pigments (LFPs). The authors observed that LFPs are generated in rat brain after a normal birth during 5 postnatal days. The experimental design of the study comprised 10 groups of animals. The authors measured prenatal values 1 day and 7 days before birth, and then the animals were sampled on postnatal day 1, 2, 5, 10, 15, 25, 35, and 90. Maximum LFP concentration is achieved on the postnatal day 2. Starting from postnatal day 10, LFP concentration returns to prenatal values. A new rise in LFP concentration is observed at 3 months of age. This is associated with the beginning of the aging process. LFPs were characterized by fluorescence spectroscopy using tridimensional excitation spectra, synchronous spectra and their derivatives, and HPLC with fluorescence detection. It was possible to discern several tens of fluorescent compounds of unknown structure that are generated and metabolized during early development. The authors suggest that LFPs are formed after respiratory burst of microglia phagocytosing apoptotic cells.

MeSH
fluorescenční spektrometrie MeSH
krysa rodu rattus MeSH
lipofuscin metabolismus MeSH
mozek růst a vývoj metabolismus MeSH
novorozená zvířata MeSH
potkani Wistar MeSH
vysokoúčinná kapalinová chromatografie MeSH
zvířata MeSH
Check Tag
krysa rodu rattus MeSH
ženské pohlaví MeSH
zvířata MeSH
Publikační typ
časopisecké články MeSH
práce podpořená grantem MeSH

Článek

The lipid peroxidation products as possible markers of Alzheimer's disease in blood

Experimental gerontology. 2011 ; 46 (1) : 38-42.

Exp Gerontol
ISSN 1873-6815
Medvik
Zdroj

Oxidative stress, which is present in Alzheimer's disease (AD), results in the formation of various end-products of free radical reactions with proteins and lipids. At present there are no reliable diagnostic biomarkers of AD in the blood. Therefore, specific products of lipid peroxidation in the blood of AD patients were investigated. Lipophilic extracts of erythrocytes in the group of patients with AD (n = 44) and age-matched controls (n = 16) were studied. The end-products of lipid peroxidation, so called lipofuscin-like pigments (LFP), were analysed by fluorescence spectroscopy. It was found that the level of these products is significantly increased in erythrocytes of AD patients compared to controls. LFP were further separated by means of HPLC into individual fractions to study their composition in AD and controls. The specific fraction of LFP in AD patients, which was isolated, might represent a disease-specific product in the blood.

MeSH
Alzheimerova nemoc diagnóza metabolismus MeSH
biologické markery metabolismus MeSH
erytrocyty metabolismus MeSH
fluorescenční spektrometrie MeSH
lidé MeSH
lipofuscin metabolismus MeSH
oxidační stres fyziologie MeSH
peroxidace lipidů fyziologie MeSH
senioři nad 80 let MeSH
senioři MeSH
vysokoúčinná kapalinová chromatografie MeSH
Check Tag
lidé MeSH
mužské pohlaví MeSH
senioři nad 80 let MeSH
senioři MeSH
ženské pohlaví MeSH
Publikační typ
časopisecké články MeSH
práce podpořená grantem MeSH

Článek

Lipofuscin-like pigments in the rat heart during early postnatal development: effect of selenium supplementation

Ošťádalová, Ivana, 1940-
Autor Autorita
Charvátová, Zuzana
Autor Autorita
Wilhelm, Jiří, 1950-
Autor Autorita

Physiological research. 2010 ; 59 (6) : 881-886.

Medvik
Zdroj

The aim of the study was to characterize a) the lipofuscin-like pigment (LFP) accumulation (an indicator of ROS production) in the rat heart during early postnatal period and b) possible antioxidative role of selenium. Experimental animals received Na2SeO3 in drinking water during gravidity and up to day 15 post partum. Two fluorophores of LFP in the hearts of 1-, 4-, 7- and 15-day-old rats were evaluated by fluorescent analysis. The highest level of heart/body weight ratio in control rats was observed on day 4, in the Se-supplemented rats on day 7. Cardiac LFP content in controls increased from postnatal day 4, in the hearts of Se-supplemented rats the LFP content increased already from day 1. As compared with the Se-supplemented group the LFP content of control hearts was significantly higher on day 1 but significantly lower on day 4. LFP concentration in control hearts decreased from postnatal day 1 to 4; this decrease was followed by significant increase until day 7 and decrease to day 15. LFP concentration in the Se-supplemented hearts was the highest on postnatal day 7; it differed from controls on day 1 and 4. Significant changes of LFP suggest an important role of ROS during critical ontogenetic period.

MeSH
financování organizované MeSH
krysa rodu rattus MeSH
lipofuscin metabolismus MeSH
myokard metabolismus MeSH
potkani Wistar MeSH
potravní doplňky MeSH
selen aplikace a dávkování farmakologie MeSH
srdce růst a vývoj účinky léků MeSH
tělesná hmotnost účinky léků MeSH
zvířata MeSH
Check Tag
krysa rodu rattus MeSH
ženské pohlaví MeSH
zvířata MeSH

Článek

Selenium protects the immature rat heart against ischemia/reperfusion injury

Ošťádalová, Ivana, 1940-
Autor Autorita
Vobecký, Miloslav, 1929-
Autor Autorita
Chvojková, Zuzana, 1978-
Autor Autorita
Miková, Dana, 1962-
Autor Autorita
Hampl, Václav, 1962-
Autor Autorita ORCID
Wilhelm, Jiří, 1950-
Autor Autorita
Ošťádal, Bohuslav, 1940-
Autor Autorita

Molecular and cellular biochemistry. 2007 ; 300 (1-2) : 259-267.

ISSN 0300-8177
Medvik
Zdroj

The aim of the study was to find out whether administration of selenium (Se) will protect the immature heart against ischemia/reperfusion.The control pregnant rats were fed laboratory diet (0.237 mg Se/kg diet); experimental rats received 2 ppm Na(2)SeO(3) in the drinking water from the first day of pregnancy until day 10 post partum. The concentration of Se in the serum and heart tissue was determined by activation analysis, the serum concentration of NO by chemiluminescence, cardiac concentration of lipofuscin-like pigment by fluorescence analysis. The 10 day-old hearts were perfused (Langendorff); recovery of developed force (DF) was measured after 40 min of global ischemia. In acute experiments, 10 day-old hearts were perfused with selenium (75 nmol/l) before or after global ischemia. Sensitivity to isoproterenol (ISO, pD(50)) was assessed as a response of DF to increasing cumulative dose.Se supplementation elevated serum concentration of Se by 16%. Se increased ischemic tolerance (recovery of DF, 32.28 +/- 2.37 vs. 41.82 +/- 2.91%, P < 0.05). Similar results were obtained after acute administration of Se during post-ischemic reperfusion (32.28 +/- 2.37 vs. 49.73 +/- 4.40%, P < 0.01). The pre-ischemic treatment, however, attenuated the recovery (23.08 +/- 3.04 vs. 32.28 +/- 2.37%, P < 0.05). Moreover, Se supplementation increased the sensitivity to the inotropic effect of ISO, decreased cardiac concentration of lipofuscin-like pigment and serum concentration of NO. Our results suggest that Se protects the immature heart against ischemia/reperfusion injury. It seems therefore, that ROS may affect the function of the neonatal heart, similarly as in adults.

Kolekce

Publikováno

Filtry

Filtry

* Zobrazit nápovědu

* Zobrazit nápovědu

Upřesnit dle MeSH