The Role of Oxidative Stress in Early Brain Injury after
Subarachnoid Hemorrhage

J 2020

The Role of Oxidative Stress in Early Brain Injury after Subarachnoid Hemorrhage

JELÍNEK, Matyáš, Michal JURAJDA and Kamil ĎURIŠ

Basic information

Original name

The Role of Oxidative Stress in Early Brain Injury after Subarachnoid Hemorrhage

Authors

JELÍNEK, Matyáš (203 Czech Republic, belonging to the institution), Michal JURAJDA (203 Czech Republic, belonging to the institution) and Kamil ĎURIŠ (203 Czech Republic, guarantor, belonging to the institution)

Edition

Oxidative Medicine and Cellular Longevity, London, HINDAWI LTD, 2020, 1942-0900

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

10601 Cell biology

Country of publisher

United Kingdom of Great Britain and Northern Ireland

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

URL

Impact factor

Impact factor: 6.543

RIV identification code

RIV/00216224:14110/20:00117549

Organization unit

Faculty of Medicine

DOI

http://dx.doi.org/10.1155/2020/8877116

UT WoS

000596448900001

Keywords in English

Oxidative Stress; Early Brain Injury; Subarachnoid Hemorrhage

Abstract

V originále

This review focuses on the problem of oxidative stress in early brain injury (EBI) after spontaneous subarachnoid hemorrhage (SAH). EBI involves complex pathophysiological mechanisms, including oxidative stress. In the first section, we describe the main sources of free radicals in EBI. There are several sources of excessive generation of free radicals from mitochondrial free radicals' generation and endoplasmic reticulum stress, to hemoglobin and enzymatic free radicals' generation. The second part focuses on the disruption of antioxidant mechanisms in EBI. The third section describes some newly found molecular mechanisms and pathway involved in oxidative stress after EBI. The last section is dedicated to the pathophysiological mechanisms through which free radicals mediate early brain injury.

Links

MUNI/A/1453/2019, interní kód MU

Name: Příspěvek ke studiu molekulární, buněčné, tkáňové a systémové patofyziologie vybraných komplexních nemocí

Investor: Masaryk University, Category A

MUNI/11/SUP/24/2020, interní kód MU

Name: Pilotní studie ke studiu role cytokinů z rodiny interleukinu 6 a možnosti potlačení zánětu pomocí stimulace nervus vagus u experimentálního modelu subarachnoidálního krvácení a sepse (Acronym: Rodina IL-6 a SAH)

Investor: Masaryk University

Citovat

JELÍNEK, Matyáš, Michal JURAJDA and Kamil ĎURIŠ. The Role of Oxidative Stress in Early Brain Injury after Subarachnoid Hemorrhage. Oxidative Medicine and Cellular Longevity. London: HINDAWI LTD, 2020, vol. 2020, NOV 2020, p. 1-9. ISSN 1942-0900. Available from: https://dx.doi.org/10.1155/2020/8877116.

@article{1718796,
   author = {Jelínek, Matyáš and Jurajda, Michal and Ďuriš, Kamil},
   article_location = {London},
   article_number = {NOV 2020},
   doi = {http://dx.doi.org/10.1155/2020/8877116},
   keywords = {Oxidative Stress; Early Brain Injury; Subarachnoid Hemorrhage},
   language = {eng},
   issn = {1942-0900},
   journal = {Oxidative Medicine and Cellular Longevity},
   title = {The Role of Oxidative Stress in Early Brain Injury after Subarachnoid Hemorrhage},
   url = {https://www.hindawi.com/journals/omcl/2020/8877116/},
   volume = {2020},
   year = {2020}
}

TY  - JOUR
ID  - 1718796
AU  - Jelínek, Matyáš - Jurajda, Michal - Ďuriš, Kamil
PY  - 2020
TI  - The Role of Oxidative Stress in Early Brain Injury after Subarachnoid Hemorrhage
JF  - Oxidative Medicine and Cellular Longevity
VL  - 2020
IS  - NOV 2020
SP  - 1-9
EP  - 1-9
PB  - HINDAWI LTD
SN  - 19420900
KW  - Oxidative Stress
KW  - Early Brain Injury
KW  - Subarachnoid Hemorrhage
UR  - https://www.hindawi.com/journals/omcl/2020/8877116/
L2  - https://www.hindawi.com/journals/omcl/2020/8877116/
N2  - This review focuses on the problem of oxidative stress in early brain injury (EBI) after spontaneous subarachnoid hemorrhage (SAH). EBI involves complex pathophysiological mechanisms, including oxidative stress. In the first section, we describe the main sources of free radicals in EBI. There are several sources of excessive generation of free radicals from mitochondrial free radicals' generation and endoplasmic reticulum stress, to hemoglobin and enzymatic free radicals' generation. The second part focuses on the disruption of antioxidant mechanisms in EBI. The third section describes some newly found molecular mechanisms and pathway involved in oxidative stress after EBI. The last section is dedicated to the pathophysiological mechanisms through which free radicals mediate early brain injury.
ER  -

JELÍNEK, Matyáš, Michal JURAJDA and Kamil ĎURIŠ. The Role of Oxidative Stress in Early Brain Injury after Subarachnoid Hemorrhage. \textit{Oxidative Medicine and Cellular Longevity}. London: HINDAWI LTD, 2020, vol.~2020, NOV 2020, p.~1-9. ISSN~1942-0900. Available from: https://dx.doi.org/10.1155/2020/8877116.

Detailed Information on Publication Record