Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Wyszukujesz frazę "neurotoxicity" wg kryterium: Temat


Wyświetlanie 1-10 z 10
Tytuł:
Pretreatment with diallylsulphide modulates mercury-induced neurotoxicity in male rats
Autorzy:
Ansar, Sabah
Powiązania:
https://bibliotekanauki.pl/articles/1039013.pdf
Data publikacji:
2015
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
diallylsulphide
metal toxicity
neurotoxicity
antioxidants
Opis:
Many studies have reported on the toxicity and related oxidative stress of mercury. Antioxidants play an important role in counteracting metal-induced neurotoxicity under in vivo conditions. In this study, the effect of diallylsulphide (DAS) was evaluated on mercuric chloride induced activities of catalase, superoxide dismutase, glutathione peroxidase and glutathione content in brains of rats. Pretreatment of rats with DAS in the Hg-treated group also inhibited an increase in lipid peroxidation and elevated acetyl cholinesterase and glutathione content. Activities of antioxidant enzymes were also restored concomitantly when compared to the control rats after DAS administration. DAS also caused a decrease in tumor necrosis factor-α level which was higher in HgCl2-treated group. The results indicate that DAS augments antioxidant defense with anti-inflammatory response against HgCl2-induced neurotoxicity. The increased level of antioxidant enzymes enhances the antioxidant potential of the organ to reduce oxidative stress.
Źródło:
Acta Biochimica Polonica; 2015, 62, 3; 599-603
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Effect of amyloid beta peptide on poly(ADP-ribose) polymerase activity in adult and aged rat hippocampus.
Autorzy:
Strosznajder, Joanna
Jęśko, Henryk
Strosznajder, Robert
Powiązania:
https://bibliotekanauki.pl/articles/1044342.pdf
Data publikacji:
2000
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
aging
amyloid
poly(ADP-ribose) polymerase
hippocampus
neurotoxicity
Opis:
It is suggested that the fibrillar amyloid beta peptide (Aβ) in brain plays a direct role in neurodegeneration in Alzheimer's disease, probably through activation of reactive oxygen species formation. Free radicals and numerous neurotoxins elicit DNA damage that subsequently activates poly(ADP-ribose) polymerase (PARP, EC 2.4.2.30). In this study the effect of neurotoxic fragment (25-35) of full length Aβ peptide on PARP activity in adult and aged rat hippocampus was investigated. In adult (4 month old) rat hippocampus the Aβ 25-35 peptide significantly enhanced PARP activity by about 80% but had no effect on PARP activity in cerebral cortex and in hippocampus from aged (24-27 month old) rats. The effect of Aβ peptide was reduced by half by the nitric oxide synthase inhibitor N-nitro-L-arginine. Stimulation of glutamate receptor(s) itself enhanced PARP activity by about 80% in adult hippocampus. However, Aβ 25-35 did not exert any additional stimulatory effect. These results indicate that Aβ, through NO and probably other free radicals, induces activation of DNA bound PARP activity exclusively in adult but not in aged hippocampus.
Źródło:
Acta Biochimica Polonica; 2000, 47, 3; 847-854
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Severe vascular and neurological complications after hematopoietic stem cell transplantation with reduced intensity conditioning
Autorzy:
Czyżewski, Krzysztof
Nierychlewska, Paulina
Richert-Przygońska, Monika
Cieściński, Jakub
Styczyński, Jan
Powiązania:
https://bibliotekanauki.pl/articles/1035762.pdf
Data publikacji:
2019
Wydawca:
Medical Education
Tematy:
ALLO-HSCT
PRES
fludarabine
neurotoxicity
reduced intensity conditioning
Opis:
It is well established that the benefit of myeloablative ALLO-HSCT can be associated with a potential high risk of procedure-related toxicity. The objective of this report is the analysis of complications in a 17-year-old girl with AML previously treated for medulloblastoma and myelodysplastic syndrome. Thiotepa, fludarabine, treosulfan and thymoglobuline were used in conditioning regimen. During conditioning neurological complications have occurred. MRI and CT scan results revealed the coexistence of PRES with the left internal carotid artery thrombosis. The effect of fludarabine on endothelial cells could possibly contribute to irreversible CNS damage and death in presented case.
Źródło:
OncoReview; 2019, 9, 1; 27-30
2450-6125
Pojawia się w:
OncoReview
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Convulsions and hypoglycemia due to tetramethyl succinonitrile intoxication in the polyvinyl chloride (PVC) industry: A 4-year follow-up
Autorzy:
Enssli, Angela
Koller, Michael
Powiązania:
https://bibliotekanauki.pl/articles/2178819.pdf
Data publikacji:
2014-05-17
Wydawca:
Instytut Medycyny Pracy im. prof. dra Jerzego Nofera w Łodzi
Tematy:
tetramethyl succinonitrile
neurotoxicity
convulsion
Epilepsy
occupational exposure
hypoglycemia
Opis:
Objectives: Exposure and clinical data concerning cases of toxic convulsions and hypoglycemia due to tetramethyl succinonitrile (TMSN) exposure are reported. Material and Methods: Forty-four workers exposed to TMSN in the PVC production plant participated in occupational health medical check-ups including medical history, clinical examination and clinical chemistry. A 4-year follow-up was performed. To evaluate occupational exposure, measurements of TMSN in the ambient air as well as personal air sampling were conducted. Results: Four workers suffered from convulsions with reversible pathologic EEG and 16 other persons were hypoglycemic. Other frequent symptoms included headaches, dizziness and unpleasant taste sensations. TMSN levels had been clearly above the Swiss occupational exposure limit value (MAK). Occupational hygiene interventions resulted in a reduction of the TMSN concentration below the MAK value. TMSN related symptoms have not been observed anymore in the 4-year follow-up. Conclusion: TMSN is a convulsive substance which in humans has also a hypoglycemic effect.
Źródło:
International Journal of Occupational Medicine and Environmental Health; 2014, 27, 2; 188-195
1232-1087
1896-494X
Pojawia się w:
International Journal of Occupational Medicine and Environmental Health
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Molecular mechanisms initiating amyloid β-fibril formation in Alzheimers disease
Autorzy:
Kirkitadze, Marina
Kowalska, Anna
Powiązania:
https://bibliotekanauki.pl/articles/1041422.pdf
Data publikacji:
2005
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
protein aggregation
fibrillogenesis
Alzheimer's disease
neurotoxicity
amyloid-β
APP mutations
Opis:
The deposition of aggregated amyloid β-protein (Aβ) in the human brain is a major lesion in Alzheimer' disease (AD). The process of Aβ fibril formation is associated with a cascade of neuropathogenic events that induces brain neurodegeneration leading to the cognitive and behavioral decline characteristic of AD. Although a detailed knowledge of Aβ assembly is crucial for the development of new therapeutic approaches, our understanding of the molecular mechanisms underlying the initiation of Aβ fibril formation remains very incomplete. The genetic defects responsible for familial AD influence fibrillogenesis. In a majority of familial cases determined by amyloid precursor protein (APP) and presenilin (PS) mutations, a significant overproduction of Aβ and an increase in the Aβ42/Aβ40 ratio are observed. Recently, it was shown that the two main alloforms of Aβ have distinct biological activity and behaviour at the earliest stage of assembly. In vitro studies demonstrated that Aβ42 monomers, but not Aβ40, form initial and minimal structures (pentamer/hexamer units called paranuclei) that can oligomerize to larger forms. It is now apparent that Aβ oligomers and protofibrils are more neurotoxic than mature Aβ fibrils or amyloid plaques. The neurotoxicity of the prefibrillar aggregates appears to result from their ability to impair fundamental cellular processes by interacting with the cellular membrane, causing oxidative stress and increasing free Ca^(2+)that eventually lead to apoptotic cell death.
Źródło:
Acta Biochimica Polonica; 2005, 52, 2; 417-423
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Neurotoxicity of cyanobacterial toxins
Autorzy:
Florczyk, M.
Łakomiak, A.
Woźny, M.
Brzuzan, P.
Powiązania:
https://bibliotekanauki.pl/articles/363222.pdf
Data publikacji:
2014
Wydawca:
Uniwersytet Warmińsko-Mazurski w Olsztynie
Tematy:
blue-green algae
cyanotoxins
drug
medicine
microcystin
neurotoxicity
sinice
cyjanotoksyny
lek
mikrocystyna
neurotoksyczność
Opis:
Eutrophication of marine and fresh waters can lead to excessive development of cyanobacterial blooms, which may contain strains that produce toxins. These toxins are secondary metabolites which can accumulate in the food chain and contaminate drinking water, thus posing a potential threat to the health of humans and aquatic organisms. These toxins include a variety of compounds with different mechanisms; this review focuses on the neurotoxicity of microcystin and other cyanotoxins. Although the hepatotoxic action of microcystins is commonly known, its neurotoxic effects have also been described, e.g. oxidative stress, cytoskeletal changes and changes in protein phosphatase activity. These effects have been partially explained by the discovery in the blood brain barrier of the same membrane transporters involved in microcystins hepatotoxic mechanisms. Additionally, this paper reviews other cyanotoxins that are known or suspected to target cholinergic synapses and voltage gated channels, including anatoxin a, anatoxin a(s), antillatoxins, cylindrospermopsin, homoanatoxin a, jamaicamide, kalkitoxin and saxitoxins. The neurotoxic and cytotoxic effects of the cyanotoxins discussed here are of particular interest because of their pharmacological potential. This review also discusses the potential of these compounds to serve as drugs for cancer and central nervous system failure.
Źródło:
Environmental Biotechnology; 2014, 10, 1; 26-43
1734-4964
Pojawia się w:
Environmental Biotechnology
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Effects of 17-beta estradiol and estriol on NMDA-induced toxicity and apoptosis in primary cultures of rat cortical neurons
Autorzy:
Kajta, M.
Budziszewska, B.
Marszal, M.
Lason, W.
Powiązania:
https://bibliotekanauki.pl/articles/70785.pdf
Data publikacji:
2001
Wydawca:
Polskie Towarzystwo Fizjologiczne
Tematy:
cortical neuron
oestriol
oestriadol-17beta
estrogen
toxicity
estrogen receptor
neurotoxicity
apoptosis
hypoglycemia
rat
Źródło:
Journal of Physiology and Pharmacology; 2001, 52, 3
0867-5910
Pojawia się w:
Journal of Physiology and Pharmacology
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The role of nitric oxide in paraquat-induced oxidative stress in rat striatum
Autorzy:
Djukic, M
Jovanovic, M.C.
Ninkovic, M.
Vasiljevic, I.
Jovanovic, M.
Powiązania:
https://bibliotekanauki.pl/articles/49779.pdf
Data publikacji:
2007
Wydawca:
Instytut Medycyny Wsi
Tematy:
Wistar rat
brain
nitric oxide
paraquat
oxidative stress
pesticide
herbicide
neurotoxicity
exposure
rat
Opis:
The role of nitric oxide (NO) in paraquat (PQ)-induced neurotoxicity is still not fully understood. In this study we used NG-nitro-L-arginine methyl ester (L-NAME), a non-selective nitric oxide synthase (NOS) inhibitor, in order to examine the effects of NO, reactive oxygen species (ROS) generation and lipid peroxidation (LPO) development during PQ-mediated neurotoxicity. Oxidative stress development in the striatum of Wistar rats intrastriatally (i.s.) poisoned with PQ (and in some cases pre-treated with L-NAME) was investigated by measuring superoxide anion (O2 •ˉ), malondialdehyde (MDA) and nitrate (NO3ˉ), 30 min, 24 hours and 7 days after treatment. L-NAME pretreatment provided the possibility to distinguish the role of ROS from reactive nitrogen species (RNS) in oxidative stress development induced by PQ. Our results confi rm the involvement of NO in PQ-mediated neurotoxicity and reduced LPO by L-NAME pretreatment implying that the latter has a protective role.
Źródło:
Annals of Agricultural and Environmental Medicine; 2007, 14, 2
1232-1966
Pojawia się w:
Annals of Agricultural and Environmental Medicine
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Evaluation of neurotoxicity of repeated dermal application of chlorpyrifos on hippocampus of adult mice
Autorzy:
Mitra, N K
Siong, H.H.
Nadarajah, V.D.
Powiązania:
https://bibliotekanauki.pl/articles/51858.pdf
Data publikacji:
2008
Wydawca:
Instytut Medycyny Wsi
Tematy:
histomorphometry
adult mouse
pesticide
mouse
repeated exposure
mice
dermal toxicity
chlorpyrifos
neurotoxicity
hippocampus
cholinesterase inhibition
Źródło:
Annals of Agricultural and Environmental Medicine; 2008, 15, 2
1232-1966
Pojawia się w:
Annals of Agricultural and Environmental Medicine
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Przemijający deficyt neurologiczny spowodowany neurotoksycznym działaniem środka kontrastowego użytego do zabiegu koronarografii
Transient neurological deficit due to neurotoxicity of contrast medium used for coronary angiography
Autorzy:
Wilczewska, Renata
Kułakowska, Alina
Korneluk-Sadzyńska, Alicja
Borowik, Helena
Drozdowski, Wiesław
Powiązania:
https://bibliotekanauki.pl/articles/1058124.pdf
Data publikacji:
2010
Wydawca:
Medical Communications
Tematy:
complication
contrast medium
coronary angiography
neurotoxicity
transient neurological deficit
koronarografia
powikłanie
środek kontrastowy
neurotoksyczność
przemijający deficyt neurologiczny
Opis:
Coronary angiography is an invasive procedure and may lead to complications. The most common of them are: myocardial infarction, embolism (e.g. cerebral embolism), dysrhythmia and acute circulatory insufficiency. Damage to the artery and subsequent major bleeding or thrombosis, vasovagal reaction and allergic reactions may also occur. Neurological deficits caused by contrast medium neurotoxicity are very rare complications of percutaneous coronary interventions. Contrast medium infiltrates blood-brain barrier and produces transient disturbances of neural membranes function. The neurotoxicity depends on its ionic properties, osmolality and solubility. Contrast medium neurotoxicity usually concerns occipital lobes and transient cortical blindness is its most common clinical manifestation. Transient pyramidal deficits due to contrast medium neurotoxicity are very rarely observed. The authors present a case of 70-yearold woman who developed left-sided hemiparesis and conjugate deviation of the eyes to the right after coronary angiography with subsequent right coronary artery angioplasty and stenting. Computed tomography (CT) of the brain performed just after occurrence of the neurological deficit revealed hyperintensive areas in sulci of the cerebral convexities and in the right frontal lobe. Control brain CT done after 24 hours did not show hyperintensive areas mentioned above. All symptoms of neurological deficit withdrew during 72 hours. Neurotoxicity of contrast medium seems to be responsible for occurrence of neurological deficit symptoms in a presented case.
Koronarografia jest badaniem inwazyjnym i niesie ze sobą ryzyko wystąpienia powikłań. Najczęstszymi z nich są: zawały serca, incydenty zatorowe (w tym zatory tętnic mózgowych), zaburzenia rytmu serca i ostra niewydolność krążenia. Zdarzają się także uszkodzenia tętnicy i miejscowe krwawienia, reakcje naczyniowo-błędne i odczyny alergiczne. Deficyty neurologiczne spowodowane neurotoksycznym działaniem środka kontrastowego są bardzo rzadkim powikłaniem przezskórnych interwencji wieńcowych. Kontrast przenika przez barierę krew-mózg i powoduje przejściowe zaburzenia funkcji błon neuronalnych. Neurotoksyczne działanie środka kontrastowego zależy od jego właściwości jonowych, osmolalności i rozpuszczalności. Neurotoksyczność kontrastu dotyczy zazwyczaj płatów potylicznych, a jej najczęstszą manifestacją kliniczną jest przemijająca ślepota korowa. Przejściowe deficyty piramidowe wywołane działaniem środka kontrastowego są bardzo rzadko obserwowane. Autorzy przedstawiają przypadek 70-letniej kobiety, u której po zabiegu koronarografii oraz angioplastyki i stentowania prawej tętnicy wieńcowej wystąpił deficyt neurologiczny pod postacią niedowładu połowiczego lewostronnego oraz przymusowego skierowania gałek ocznych w stronę prawą. Wykonana bezpośrednio po wystąpieniu objawów klinicznych tomografia komputerowa (TK) mózgu ujawniła obecność hiperintensywnych ognisk w bruzdach mózgowych na sklepistości półkul mózgu oraz w prawym płacie czołowym. Kontrolna TK wykonana po upływie 24 godzin nie uwidoczniła wspomnianych ognisk. Objawy neurologiczne całkowicie wycofały się w ciągu 72 godzin od zachorowania. Wydaje się, iż działanie neurotoksyczne środka kontrastowego jest odpowiedzialne za objawy deficytu neurologicznego, które wystąpiły w prezentowanym przypadku.
Źródło:
Aktualności Neurologiczne; 2010, 10, 3; 172-175
1641-9227
2451-0696
Pojawia się w:
Aktualności Neurologiczne
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-10 z 10

    Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies