RT Journal Article
T1 Acute hypoxia produces a superoxide burst in cells
A1 Hernansanz-Agustín, Pablo
A1 Izquierdo-Álvarez, Alicia
A1 Sánchez-Gómez, Francisco J.
A1 Ramos, Elena
A1 Villa-Piña, Tamara
A1 Lamas, Santiago
A1 Bogdanova, Anna
A1 Martínez Ruiz, Antonio
AB Oxygen is a key molecule for cell metabolism. Eukaryotic cells sense the reduction in oxygen availability (hypoxia) and trigger a series of cellular and systemic responses to adapt to hypoxia, including the optimization of oxygen consumption. Many of these responses are mediated by a genetic program induced by the hypoxia-inducible transcription factors (HIFs), regulated by a family of prolyl hydroxylases (PHD or EGLN) that use oxygen as a substrate producing HIF hydroxylation. In parallel to these oxygen sensors modulating gene expression within hours, acute modulation of protein function in response to hypoxia is known to occur within minutes. Free radicals acting as second messengers, and oxidative posttranslational modifications, have been implied in both groups of responses. Localization and speciation of the paradoxical increase in reactive oxygen sp+ecies production in hypoxia remain debatable. We have observed that several cell types respond to acute hypoxia with a transient increase in superoxide production for about 10 min, probably originating in the mitochondria. This may explain in part the apparently divergent results found by various groups that have not taken into account the time frame of hypoxic ROS production. We propose that this acute and transient hypoxia-induced superoxide burst may be translated into oxidative signals contributing to hypoxic adaptation and preconditioning
SN 0891-5849
YR 2014
FD 2014-06
LK https://hdl.handle.net/20.500.14352/103813
UL https://hdl.handle.net/20.500.14352/103813
LA eng
NO Gobierno de España
NO Swiss National Science Foundation
NO Instituto de Salud Carlos III
NO Instituto de Investigación Sanitaria Princesa
NO Ministerio de Educación y Cultura
DS Docta Complutense
RD 2 sept 2024