INVESTIGADORES
GENARO Ana Maria
artículos
Título:
Role of Nitric Oxide Signaling Pathways in Brain Injuries
Autor/es:
MARÍA AURELIA ZORRILLA ZUBILETE; DAMIÁN MAUR; MARÍA LAURA PALUMBO; ANA MARÍA GENARO
Revista:
Current Chemical Biology
Editorial:
Bentham Science Publishers
Referencias:
Año: 2010 vol. 4 p. 250 - 261
ISSN:
1872-3136
Resumen:
Nitric oxide (NO) is involved in many physiological and pathological brain processes. NO is probably the
smallest and most versatile bioactive molecule identified. NO signaling in excitable tissues requires rapid and controlled
delivery of NO to specific cellular targets. This tight control of NO signaling is largely regulated at the level of its biosynthesis.
NO production might lead either to toxicity or to neuroprotection depending on the level of NO, the location of NO
production, the extent of oxidative stress and the type of neurodegenerative process. It has been suggested that NO directly
acts as an antioxidant. This protective effect is mediated by small fluxes of NO (<1 ìmol/L). This is consistent with
the fact that NO terminates lipid peroxidation reactions and suggests that the production of NO is a major protective
mechanism against oxidative stress in vivo. In fact it has been demonstrated, in vitro as well as in vivo, that during brain
insult NO might be part of the physiological response to injury. In general, it is accepted that a normal pathophysiologic
response of the damaged tissue may involve controlled NO production and the inhibition of this response may interfere
with the normal repair process. Nevertheless, it has been suggested that a high production of NO after the induction of
iNOS expression can interact with superoxide anion generated by the mitochondria or by other mechanisms, leading to the
formation of the potent oxidant species peroxynitrite. These events would result in cell damage and altered neuronal
physiological function. The present review focuses on the role of NO as an important neuromodulator that can exert both
neurotoxic and neuroprotective effects in different injuries.
insult NO might be part of the physiological response to injury. In general, it is accepted that a normal pathophysiologic
response of the damaged tissue may involve controlled NO production and the inhibition of this response may interfere
with the normal repair process. Nevertheless, it has been suggested that a high production of NO after the induction of
iNOS expression can interact with superoxide anion generated by the mitochondria or by other mechanisms, leading to the
formation of the potent oxidant species peroxynitrite. These events would result in cell damage and altered neuronal
physiological function. The present review focuses on the role of NO as an important neuromodulator that can exert both
neurotoxic and neuroprotective effects in different injuries.
the fact that NO terminates lipid peroxidation reactions and suggests that the production of NO is a major protective
mechanism against oxidative stress in vivo. In fact it has been demonstrated, in vitro as well as in vivo, that during brain
insult NO might be part of the physiological response to injury. In general, it is accepted that a normal pathophysiologic
response of the damaged tissue may involve controlled NO production and the inhibition of this response may interfere
with the normal repair process. Nevertheless, it has been suggested that a high production of NO after the induction of
iNOS expression can interact with superoxide anion generated by the mitochondria or by other mechanisms, leading to the
formation of the potent oxidant species peroxynitrite. These events would result in cell damage and altered neuronal
physiological function. The present review focuses on the role of NO as an important neuromodulator that can exert both
neurotoxic and neuroprotective effects in different injuries.
insult NO might be part of the physiological response to injury. In general, it is accepted that a normal pathophysiologic
response of the damaged tissue may involve controlled NO production and the inhibition of this response may interfere
with the normal repair process. Nevertheless, it has been suggested that a high production of NO after the induction of
iNOS expression can interact with superoxide anion generated by the mitochondria or by other mechanisms, leading to the
formation of the potent oxidant species peroxynitrite. These events would result in cell damage and altered neuronal
physiological function. The present review focuses on the role of NO as an important neuromodulator that can exert both
neurotoxic and neuroprotective effects in different injuries.
ìmol/L). This is consistent with
the fact that NO terminates lipid peroxidation reactions and suggests that the production of NO is a major protective
mechanism against oxidative stress in vivo. In fact it has been demonstrated, in vitro as well as in vivo, that during brain
insult NO might be part of the physiological response to injury. In general, it is accepted that a normal pathophysiologic
response of the damaged tissue may involve controlled NO production and the inhibition of this response may interfere
with the normal repair process. Nevertheless, it has been suggested that a high production of NO after the induction of
iNOS expression can interact with superoxide anion generated by the mitochondria or by other mechanisms, leading to the
formation of the potent oxidant species peroxynitrite. These events would result in cell damage and altered neuronal
physiological function. The present review focuses on the role of NO as an important neuromodulator that can exert both
neurotoxic and neuroprotective effects in different injuries.
insult NO might be part of the physiological response to injury. In general, it is accepted that a normal pathophysiologic
response of the damaged tissue may involve controlled NO production and the inhibition of this response may interfere
with the normal repair process. Nevertheless, it has been suggested that a high production of NO after the induction of
iNOS expression can interact with superoxide anion generated by the mitochondria or by other mechanisms, leading to the
formation of the potent oxidant species peroxynitrite. These events would result in cell damage and altered neuronal
physiological function. The present review focuses on the role of NO as an important neuromodulator that can exert both
neurotoxic and neuroprotective effects in different injuries.
in vivo. In fact it has been demonstrated, in vitro as well as in vivo, that during brain
insult NO might be part of the physiological response to injury. In general, it is accepted that a normal pathophysiologic
response of the damaged tissue may involve controlled NO production and the inhibition of this response may interfere
with the normal repair process. Nevertheless, it has been suggested that a high production of NO after the induction of
iNOS expression can interact with superoxide anion generated by the mitochondria or by other mechanisms, leading to the
formation of the potent oxidant species peroxynitrite. These events would result in cell damage and altered neuronal
physiological function. The present review focuses on the role of NO as an important neuromodulator that can exert both
neurotoxic and neuroprotective effects in different injuries.