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Wyszukujesz frazę "NAD(P)H oxidase" wg kryterium: Temat


Wyświetlanie 1-2 z 2
Tytuł:
Endothelial NADH/NADPH-dependent enzymatic sources of superoxide production: relationship to endothelial dysfunction.
Autorzy:
Kalinowski, Leszek
Malinski, Tadeusz
Powiązania:
https://bibliotekanauki.pl/articles/1043282.pdf
Data publikacji:
2004
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
peroxynitrite
endothelial dysfunction
NAD(P)H oxidase
nitric oxide
superoxide
eNOS
Opis:
There is growing evidence that endothelial dysfunction, which is often defined as the decreased endothelial-derived nitric oxide (NO) bioavailability, is a crucial factor leading to vascular disease states such as hypertension, diabetes, atherosclerosis, heart failure and cigarette smoking. This is due to the fact that the lack of NO in endothelium-dependent vascular disorders contributes to impaired vascular relaxation, platelet aggregation, increased vascular smooth muscle proliferation, and enhanced leukocyte adhesion to the endothelium. During the last several years, it has become clear that reduction of NO bioavailability in the endothelium-impaired function disorders is associated with an increase in endothelial production of superoxide (O2̇̄). Because O2̇̄ rapidly scavenges NO within the endothelium, a reduction of bioactive NO might occur despite an increased NO generation. Among many enzymatic systems that are capable of producing O2̇̄, NAD(P)H oxidase and uncoupled endothelial NO synthase (eNOS) apparently are the main sources of O2̇̄ in the endothelial cells. It seems that O2̇̄ generated by NAD(P)H oxidase may trigger eNOS uncoupling and contribute to the endothelial balance between NO and O2̇̄. That is maintained at diverse levels.
Źródło:
Acta Biochimica Polonica; 2004, 51, 2; 459-469
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Metformin reduces NAD(P)H oxidase activity in mouse cultured podocytes through purinergic dependent mechanism by increasing extracellular ATP concentration
Autorzy:
Piwkowska, Agnieszka
Rogacka, Dorota
Jankowski, Maciej
Angielski, Stefan
Powiązania:
https://bibliotekanauki.pl/articles/1039452.pdf
Data publikacji:
2013
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
AMP-activated kinase
free radicals
metformin
NAD(P)H oxidase
podocytes
purinoceptors
Opis:
Hyperglycemia affects the functioning numbers of podocytes and leads to a gradual decline of renal function. The normalization of glucose level is a principle therapeutic goal in diabetic patients and metformin is a popular hypoglycemic drug used in type 2 diabetes mellitus. Metformin activates AMP-activated kinase (AMPK) and decreases NAD(P)H oxidase activity in podocytes leading to reduction of free radical generation. Similar effects are observed after activation of P2 receptors. Therefore, we investigated whether metformin increases extracellular ATP concentration and affects the activities of NAD(P)H oxidase and AMPK through P2 receptors. Experiments were performed on cultured mouse podocytes. NAD(P)H oxidase activity was measured by chemiluminescence and changes in AMPK activity were estimated by immunoblotting against AMPKα-Thr172-P. Metformin increased extracellular ATP concentration by reduction of ecto-ATPase activity, decreased NAD(P)H oxidase activity and increased AMPK phosphorylation. A P2 receptor antagonist, suramin (300 µM), prevented metformin action on NAD(P)H oxidase and AMPK phosphorylation. The data suggests a novel mechanism of metformin action, at least in podocytes. Metformin, which increases extracellular ATP concentration leads to activation of P2 receptors and consequent modulation of the podocytes' metabolism through AMPK and NAD(P)H oxidase which, in turn, may affect podocyte functioning.
Źródło:
Acta Biochimica Polonica; 2013, 60, 4; 607-612
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-2 z 2

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