Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: STROSZNAJDER
Liczba odnalezionych rekordów: 2



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Tytuł oryginału: Inhibition of N-methyl-D-aspartic acid-nitric oxide synthase in rat hippocampal slices by ethanol. Evidence for the involvement of tetrahydrobiopterin but not lipid peroxidation.
Autorzy: Czapski Grzegorz A., Sun Grace Y., Strosznajder Joanna B.
Źródło: J. Biomed. Sci. 2002: 9 (1) s.3-9, il., tab., bibliogr. 30 poz.
Sygnatura GBL: 313,488

Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

    Typ dokumentu:
  • praca doświadczalna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: The ionotropic glutamatergic receptor system, especially the subtype mediated by N-methyl-D-aspartic acid (NMDA), is known to exhibit special sensitivity to the effect of ethanol. This is due partly to the ability of ethanol to modulate the production of nitric oxide through the NMDA-nitric oxide synthase (NOS) pathway. In this study, we examined the effects of ethanol on basal and NMDA-stimulated NOS activity in rat hippocampal slices by measuring the conversion of [**14C]-arginine into [**14C]-citrulline in an incubation system containing the necessary cofactors. Stimulation of hippocampal slices with NMDA (100 ćM) enhanced NOS activity by 43 p.c. (n = 12). Although ethanol did not alter NOS activity when added to the incubation system during NMDA stimulation, it dose-dependently inhibited NMDA-NOS activity when added to the slices during the 90-min preincubation period. Further assay of NOS activity with brain cytosolic fraction indicated an inhibitory effect of ethanol (200 mM) when the assay was carried out in the absence of exogenous tetrahydrobiopterin (BH4), a redox-active cofactor for NOS. Incubation of brain homogenates resulted in a time-dependent increase in the levels of lipid peroxidation products, but ethanol did not further enhance these products. Taken together, these results providence evidence for the role of BH4 but not oxidative stress in the inhibitory effect of ethanol on NMDA-NOS activity in rat hippocampal slices.

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    Tytuł oryginału: Poly(ADP-ribose) polymerase activity in the cat carotid body in hypoxia and hyperoxia.
    Autorzy: Strosznajder R. P., Jesko H., Pokorski M.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (3) s.491-496, il., bibliogr. 16 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • pulmonologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • koty
  • płeć męska
  • płeć żeńska

    Streszczenie angielskie: Reactive oxygen species (ROS) induce DNA damage with the ensuing activation of the chromosomal repair enzyme poly(ADP-ribose) polymerase (PARP). ROS also interact with the function of carotid body chemoreceptor cells. The possibility arises that PARP is part of the carotid chemosensing process. This study seeks to determine the presence of PARP and its changes in response to contrasting chemical stimuli, hypoxia and hyperoxia, both capable of generating ROS, in cat carotid bodies. The organs were dissected from anesthetized cats exposed in vivo to acute normoxic (PaO2 ÷ 25 mmHg), and hyperoxic (PaO2 400 mmHg) conditions. Carotid body homogenate was the source of PARP and [adenine 14C] NAD was the substrate in the assay. Specimens of the superior cervical ganglion and brainstem were used as reference tissues. We found that PARP activity amounted to 27 pmol/mg protein/min in the normoxic carotid body. The activity level more than doubled in both hypoxic and hyperoxic carotid bodies. Changes of PARP in the reference tissues were qualitatively similar. We conclude that PARP is present in the carotid body but the augmentation of the enzyme activity in both hypoxia and hyperoxia reflects DNA damage, induced likely by ROS and being universal for neural tissues, rather than a specific involvement of PARP in the chemosensing process.

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