ФарФаР - Фармацеутски факултет, репозиторијум
Универзитет у Београду, Фармацеутски факултет
    • English
    • Српски
    • Српски (Serbia)
  • Српски (ћирилица) 
    • Енглески
    • Српски (ћирилица)
    • Српски (латиница)
  • Пријава
Преглед записа 
  •   ФарФаР
  • Pharmacy
  • Radovi istraživača / Researchers’ publications
  • Преглед записа
  •   ФарФаР
  • Pharmacy
  • Radovi istraživača / Researchers’ publications
  • Преглед записа
JavaScript is disabled for your browser. Some features of this site may not work without it.

Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats

Efekti različitih inhibitora azot oksid sintaze na oštećenje neurona indukovano hinolinskom kiselinom kod pacova

Thumbnail
2004
560.pdf (76.87Kb)
Аутори
Vasiljević, Ivana
Jovanović, Marina
Čolić, Miodrag
Mihajlović, Rosa
Đukić, Mirjana
Ninković, Milica
Maličević, Živorad
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документу
Апстракт
The aetiology of neuronal death in neurodegenerative diseases, including Huntington-s disease, is still unknown. There could be a complex interplay among altered energy metabolism, excitotoxicity and oxidative stress. Our aim was to examine the effects of intrastriatal injection of a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, and a non-specific potent nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester, in order to study the possible involvement of glutathione, an important antioxidant, in quinolinic acid-induced striatal toxicity in the rat. Unilateral administration of quinolinic acid to rat striatum in a single dose of 150 nmol/L was used as a model of Huntington-s disease. The other group of animals were pretreated with 7- nitroindazole and Nw-nitro-L-arginine methyl ester, respectively. Control groups were treated with saline solution and olive oil, respectively. Content of total glutathione, was increased in the ipsi- and contralateral s...triatum, forebrain cortex, basal forebrain and hippocampus in the groups treated with nitric oxid synthase inhibitors and quinolinic acid compared to the quinolinic acid-treated animals. These results support the hypothesis that oxygen free radicals contribute to excitotoxic neuronal injury, and also that nitric oxide synthase inhibitors could be potential neuroprotective agents in Huntington-s disease.

Etiologija selektivnog umiranja neurona u neurodegenerativnim bolestima je nepoznata, iako postoje dokazi o defektu energetskog metabolizma, ekscitotoksičnosti i oksidativnom oštećenju. Verovatno je da ključnu ulogu ima kompleksna interakcija između ovih mehanizama. Cilj ovog rada bio je da se ispitaju efekti intrastrijatne primene selektivnog inhibitora neuronske azot oksid sintaze, 7-nitroindazola, kao i nespecifičnog inhibitora azot oksid sintaze, Nw-nitro-l-arginin metil estra, zbog moguće uključenosti glutationa, ključnog antioksidansa, u toksičnost strijatuma izazvanu hinolinskom kiselinom, kod pacova. Unilateralna aplikacija hinolinske kiseline, u strijatum pacova u pojedinačnoj dozi od 150 nmol/L korišćena je kao model Hantingtonove bolesti. Druge grupe životinja tretirane su 7-nitroindazolom, odnosno Nw-nitro-l-arginin metil estrom. Kontrolne grupe dobijale su fiziološki rastvor, odnosno maslinovo ulje. Sadržaj ukupnog glutationa je povećan u ipsi- i kontralateralnom strijatum...u, kori prednjeg mozga, bazalnom prednjem mozgu i hipokampusu grupa životinja koje su pored hinolinske kiseline primile i odgovarajući inhibitor neuronske azot oksid sintaze, u poređenju sa grupom tretiranom samo neurotoksinom. Ovi podaci pokazuju da kiseonični slobodni radikali učestvuju u ekscitotoksičnom oštećenju neurona, kao i da inhibitori azot oksid sintaze mogu biti potencijalni neuroprotektivni agensi u Hantingtonovoj bolesti.

Кључне речи:
Huntington-s disease / quinolinic acid / Nw-nitro-L-arginine methyl ester / 7-nitroindazole / glutathione / Hantingtonova bolest / hinolinska kiselina / Nw-nitro-l-arginin metil estar / 7-nitroindazol / glutation
Извор:
Jugoslovenska medicinska biohemija, 2004, 23, 1, 11-18
Издавач:
  • Društvo medicinskih biohemičara Srbije i Crne Gore, Beograd i Univerzitet u Beogradu - Farmaceutski fakultet, Beograd

DOI: 10.2298/JMH0401011V

ISSN: 0354-3447

Scopus: 2-s2.0-1842427441
[ Google Scholar ]
URI
https://farfar.pharmacy.bg.ac.rs/handle/123456789/562
Колекције
  • Radovi istraživača / Researchers’ publications
Институција/група
Pharmacy
TY  - JOUR
AU  - Vasiljević, Ivana
AU  - Jovanović, Marina
AU  - Čolić, Miodrag
AU  - Mihajlović, Rosa
AU  - Đukić, Mirjana
AU  - Ninković, Milica
AU  - Maličević, Živorad
PY  - 2004
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/562
AB  - The aetiology of neuronal death in neurodegenerative diseases, including Huntington-s disease, is still unknown. There could be a complex interplay among altered energy metabolism, excitotoxicity and oxidative stress. Our aim was to examine the effects of intrastriatal injection of a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, and a non-specific potent nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester, in order to study the possible involvement of glutathione, an important antioxidant, in quinolinic acid-induced striatal toxicity in the rat. Unilateral administration of quinolinic acid to rat striatum in a single dose of 150 nmol/L was used as a model of Huntington-s disease. The other group of animals were pretreated with 7- nitroindazole and Nw-nitro-L-arginine methyl ester, respectively. Control groups were treated with saline solution and olive oil, respectively. Content of total glutathione, was increased in the ipsi- and contralateral striatum, forebrain cortex, basal forebrain and hippocampus in the groups treated with nitric oxid synthase inhibitors and quinolinic acid compared to the quinolinic acid-treated animals. These results support the hypothesis that oxygen free radicals contribute to excitotoxic neuronal injury, and also that nitric oxide synthase inhibitors could be potential neuroprotective agents in Huntington-s disease.
AB  - Etiologija selektivnog umiranja neurona u neurodegenerativnim bolestima je nepoznata, iako postoje dokazi o defektu energetskog metabolizma, ekscitotoksičnosti i oksidativnom oštećenju. Verovatno je da ključnu ulogu ima kompleksna interakcija između ovih mehanizama. Cilj ovog rada bio je da se ispitaju efekti intrastrijatne primene selektivnog inhibitora neuronske azot oksid sintaze, 7-nitroindazola, kao i nespecifičnog inhibitora azot oksid sintaze, Nw-nitro-l-arginin metil estra, zbog moguće uključenosti glutationa, ključnog antioksidansa, u toksičnost strijatuma izazvanu hinolinskom kiselinom, kod pacova. Unilateralna aplikacija hinolinske kiseline, u strijatum pacova u pojedinačnoj dozi od 150 nmol/L korišćena je kao model Hantingtonove bolesti. Druge grupe životinja tretirane su 7-nitroindazolom, odnosno Nw-nitro-l-arginin metil estrom. Kontrolne grupe dobijale su fiziološki rastvor, odnosno maslinovo ulje. Sadržaj ukupnog glutationa je povećan u ipsi- i kontralateralnom strijatumu, kori prednjeg mozga, bazalnom prednjem mozgu i hipokampusu grupa životinja koje su pored hinolinske kiseline primile i odgovarajući inhibitor neuronske azot oksid sintaze, u poređenju sa grupom tretiranom samo neurotoksinom. Ovi podaci pokazuju da kiseonični slobodni radikali učestvuju u ekscitotoksičnom oštećenju neurona, kao i da inhibitori azot oksid sintaze mogu biti potencijalni neuroprotektivni agensi u Hantingtonovoj bolesti.
PB  - Društvo medicinskih biohemičara Srbije i Crne Gore, Beograd i Univerzitet u Beogradu - Farmaceutski fakultet, Beograd
T2  - Jugoslovenska medicinska biohemija
T1  - Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats
T1  - Efekti različitih inhibitora azot oksid sintaze na oštećenje neurona indukovano hinolinskom kiselinom kod pacova
VL  - 23
IS  - 1
SP  - 11
EP  - 18
DO  - 10.2298/JMH0401011V
UR  - conv_831
ER  - 
@article{
author = "Vasiljević, Ivana and Jovanović, Marina and Čolić, Miodrag and Mihajlović, Rosa and Đukić, Mirjana and Ninković, Milica and Maličević, Živorad",
year = "2004",
abstract = "The aetiology of neuronal death in neurodegenerative diseases, including Huntington-s disease, is still unknown. There could be a complex interplay among altered energy metabolism, excitotoxicity and oxidative stress. Our aim was to examine the effects of intrastriatal injection of a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, and a non-specific potent nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester, in order to study the possible involvement of glutathione, an important antioxidant, in quinolinic acid-induced striatal toxicity in the rat. Unilateral administration of quinolinic acid to rat striatum in a single dose of 150 nmol/L was used as a model of Huntington-s disease. The other group of animals were pretreated with 7- nitroindazole and Nw-nitro-L-arginine methyl ester, respectively. Control groups were treated with saline solution and olive oil, respectively. Content of total glutathione, was increased in the ipsi- and contralateral striatum, forebrain cortex, basal forebrain and hippocampus in the groups treated with nitric oxid synthase inhibitors and quinolinic acid compared to the quinolinic acid-treated animals. These results support the hypothesis that oxygen free radicals contribute to excitotoxic neuronal injury, and also that nitric oxide synthase inhibitors could be potential neuroprotective agents in Huntington-s disease., Etiologija selektivnog umiranja neurona u neurodegenerativnim bolestima je nepoznata, iako postoje dokazi o defektu energetskog metabolizma, ekscitotoksičnosti i oksidativnom oštećenju. Verovatno je da ključnu ulogu ima kompleksna interakcija između ovih mehanizama. Cilj ovog rada bio je da se ispitaju efekti intrastrijatne primene selektivnog inhibitora neuronske azot oksid sintaze, 7-nitroindazola, kao i nespecifičnog inhibitora azot oksid sintaze, Nw-nitro-l-arginin metil estra, zbog moguće uključenosti glutationa, ključnog antioksidansa, u toksičnost strijatuma izazvanu hinolinskom kiselinom, kod pacova. Unilateralna aplikacija hinolinske kiseline, u strijatum pacova u pojedinačnoj dozi od 150 nmol/L korišćena je kao model Hantingtonove bolesti. Druge grupe životinja tretirane su 7-nitroindazolom, odnosno Nw-nitro-l-arginin metil estrom. Kontrolne grupe dobijale su fiziološki rastvor, odnosno maslinovo ulje. Sadržaj ukupnog glutationa je povećan u ipsi- i kontralateralnom strijatumu, kori prednjeg mozga, bazalnom prednjem mozgu i hipokampusu grupa životinja koje su pored hinolinske kiseline primile i odgovarajući inhibitor neuronske azot oksid sintaze, u poređenju sa grupom tretiranom samo neurotoksinom. Ovi podaci pokazuju da kiseonični slobodni radikali učestvuju u ekscitotoksičnom oštećenju neurona, kao i da inhibitori azot oksid sintaze mogu biti potencijalni neuroprotektivni agensi u Hantingtonovoj bolesti.",
publisher = "Društvo medicinskih biohemičara Srbije i Crne Gore, Beograd i Univerzitet u Beogradu - Farmaceutski fakultet, Beograd",
journal = "Jugoslovenska medicinska biohemija",
title = "Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats, Efekti različitih inhibitora azot oksid sintaze na oštećenje neurona indukovano hinolinskom kiselinom kod pacova",
volume = "23",
number = "1",
pages = "11-18",
doi = "10.2298/JMH0401011V",
url = "conv_831"
}
Vasiljević, I., Jovanović, M., Čolić, M., Mihajlović, R., Đukić, M., Ninković, M.,& Maličević, Ž.. (2004). Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats. in Jugoslovenska medicinska biohemija
Društvo medicinskih biohemičara Srbije i Crne Gore, Beograd i Univerzitet u Beogradu - Farmaceutski fakultet, Beograd., 23(1), 11-18.
https://doi.org/10.2298/JMH0401011V
conv_831
Vasiljević I, Jovanović M, Čolić M, Mihajlović R, Đukić M, Ninković M, Maličević Ž. Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats. in Jugoslovenska medicinska biohemija. 2004;23(1):11-18.
doi:10.2298/JMH0401011V
conv_831 .
Vasiljević, Ivana, Jovanović, Marina, Čolić, Miodrag, Mihajlović, Rosa, Đukić, Mirjana, Ninković, Milica, Maličević, Živorad, "Effects of various nitric oxide synthase inhibitors on quinolinic acid-induced neuronal injury in rats" in Jugoslovenska medicinska biohemija, 23, no. 1 (2004):11-18,
https://doi.org/10.2298/JMH0401011V .,
conv_831 .

DSpace software copyright © 2002-2015  DuraSpace
О ФарФаР-у | Пошаљите запажања

OpenAIRERCUB
 

 

Комплетан репозиторијумИнституцијеАуториНасловиТемеОва институцијаАуториНасловиТеме

Статистика

Преглед статистика

DSpace software copyright © 2002-2015  DuraSpace
О ФарФаР-у | Пошаљите запажања

OpenAIRERCUB