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

@article{Oka2000InvolvementOP,
  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},
  journal={Neuropharmacology},
  year={2000},
  volume={39},
  pages={1319-1330}
}

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.

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