Involvement of peroxynitrite and hydroxyradical generated from nitric oxide in hypoxia/reoxygenation injury in rat cerebrocortical slices

  title={Involvement of peroxynitrite and hydroxyradical generated from nitric oxide in hypoxia/reoxygenation injury in rat cerebrocortical slices},
  author={Michiko Oka and Masaaki Hirouchi and Yoshinori Itoh and Yojiro Ukai},

Effects of oxygen and glucose deprivation on the expression and distribution of neuronal and inducible nitric oxide synthases and on protein nitration in rat cerebral cortex

Prior and concurrent L‐NAME administration blocked the changes on diffusion MRI and attenuated the morphologic changes, suggesting that NO and consequent peroxynitrite formation during ischemia–reperfusion contributes to cerebral injury.

저산소-재산소화 손상에 미치는 Nitric Oxide에 대한 항산화제의 상호작용

Investigation of the effects of antioxidants on NO production, inducible nitric oxide synthase (iNOS) and the expression of p65, during the hypoxia-reoxygenation of VSMC cultures concluded that hypoxiarexygenation induced the iNOS protein, and the subsequent production of NO in the VSMC.

Acute hypercapnic hyperoxia stimulates reactive species production in the caudal solitary complex of rat brain slices but does not induce oxidative stress.

Overall, hyperoxia and HA do not result in increased production of markers of oxidative and nitrosative stress as expected, and it is postulate this is due to antioxidant and proteosomal removal of damaged lipids and proteins to maintain cell viability and avoid death during protractedhyperoxia.

Ischemia and reoxygenation induced amino acid release release and tissue damage in the slices of rat corpus striatum

More than one mechanisms probably support the ischemia-evoked accumulation of glutamate and other amino acids in the extracellular space, as indicated by the results of schemic incubation and reoxygenation of rat striatal slices.

Neuroprotective effect of peroxynitrite decomposition catalyst and poly(adenosine diphosphate-ribose) polymerase inhibitor alone and in combination in rats with focal cerebral ischemia.

Neuroprotection observed with FeTMPyP and ISO alone and in combination may be attributed to inhibition of the peroxynitrite-PARP cascade of cerebral ischemia/reperfusion injury.

Astroglial nitration after postnatal excitotoxic damage: correlation with nitric oxide sources, cytoskeletal, apoptotic and antioxidant proteins.

It is shown that nitrated astrocytes in vivo constitute a subpopulation of highly reactive astroCytes which display high resistance towards oxidative stress induced cell death.

Glucose exacerbates zinc-induced astrocyte death.



Apparent hydroxyl radical production by peroxynitrite: implications for endothelial injury from nitric oxide and superoxide.

It is proposed that superoxide dismutase may protect vascular tissue stimulated to produce superoxide and NO under pathological conditions by preventing the formation of peroxynitrite.

Oxidative Stress in Brain Ischemia

  • S. Love
  • Biology, Chemistry
    Brain pathology
  • 1999
The findings in recent animal studies are likely to lead to a range of further pharmacological strategies to limit brain injury in stroke patients and to prevent oxidative damage and its consequences after brain ischemia in man.

Neuronal expression of inducible nitric oxide synthase after oxygen and glucose deprivation in rat forebrain slices

The results demonstrate for the first time that iNOS is expressed in neurones after oxygen and glucose deprivation, and that this expression occurs in short periods of time, and suggest that NO can play an important pathogenic role in the tissue damage that occurs after cerebral ischaemia.

Peroxynitrite-mediated tyrosine nitration catalyzed by superoxide dismutase.

A redox-based mechanism for the neuroprotective and neurodestructive effects of nitric oxide and related nitroso-compounds

It is reported that NO.-mediated neurotoxicity is engendered, at least in part, by reaction with superoxide anion (O.-2), apparently leading to formation of peroxynitrite (ONOO−), and not by NO.

Marked Induction of Calcium-Independent Nitric Oxide Synthase Activity after Focal Cerebral Ischemia

The results suggest that the decline in calcium-dependent (cNOS) activity reflects loss of NOS neurons within the lesion, and sustained nitric oxide production by iNOS may contribute to the late phase of tissue damage in focal cerebral ischemia.

Nitric oxide mediates glutamate neurotoxicity in primary cortical cultures.

It is established that NO mediates the neurotoxicity of glutamate and Hemoglobin, which complexes NO, prevents neurotoxic effects of both N-methyl-D-aspartate and sodium nitroprusside.

Down‐Regulation of Neuronal Nitric Oxide Synthase by Nitric Oxide After Oxygen‐Glucose Deprivation in Rat Forebrain Slices

It is indicated that iNOS expression down‐regulates nNOS activity in rat brain slices exposed to OGD, suggesting important and complex interactions between NOS isoforms, the elucidation of which may provide further insights into the physiological and pathophysiological events that occur during and after cerebral ischemia.