In vivo evidence of hydroxyl radical formation induced by elevation of extracellular glutamate after cerebral ischemia in the cortex of anesthetized rats

Yang, Chung‐Shi; Lin, Nai-Nu; Tsai, Perng Jy; Liu, Lin; Kuo, Jon‐Son

doi:10.1016/0891-5849(95)02042-x

Cited by 55 publications

(22 citation statements)

References 24 publications

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“…Previous studies documented that excitotoxicity plays a role in mediating neuronal injury in bacterial meningitis (13,55). The production of excitotoxic neuronal injury is tightly linked to the generation of ROI, in that stimulation of neurons with excitatory amino acids leads to the production of ROI (15,40), and that induction of oxidative injury in the hippocampus by exposure to ROI-generating substrates leads to the release of excitatory amino acids (42). Furthermore, activation of glial cells, an early event in bacterial meningitis (Leib, S.L., and M.G.…”

Section: Discussionmentioning

confidence: 99%

“…ROI have been implicated as mediators of brain injury in a wide variety of disease processes, including chemically induced cerebral inflammation (1), ischemia/reperfusion injury (6, 7, 22), brain edema (12,35), neuronal apoptosis (36-39), and excitotoxic neuronal injury (4,(40)(41)(42). Pathophysiologic processes characteristic of bacterial meningitis, such as vascular endothelial cell activation and neutrophil adherence, subarachnoid space inflammation, blood-brain barrier disruption, brain edema, and excitotoxicity may also involve the generation of ROI (1,35,39,43,44).…”

Section: Discussionmentioning

confidence: 99%

“…Cerebral ischemia leads to an increase in extracellular concentrations of excitatory amino acids, which results in excessive activation of neuronal receptors and excitotoxic cell death (40,42). Previous studies documented that excitotoxicity plays a role in mediating neuronal injury in bacterial meningitis (13,55).…”

Section: Discussionmentioning

confidence: 99%

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Reactive oxygen intermediates contribute to necrotic and apoptotic neuronal injury in an infant rat model of bacterial meningitis due to group B streptococci.

Leib¹,

Kim²,

Chow³

et al. 1996

J. Clin. Invest.

219

159

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Reactive oxygen intermediates contribute to necrotic and apoptotic neuronal injury in an infant rat model of bacterial meningitis due to group B streptococci.

Leib¹,

Kim²,

Chow³

et al. 1996

J. Clin. Invest.

219

159

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“…Furthermore, damage to the brain is also observed during reperfusion after ischemia (when the oxygen supply is restored to the brain) and may be attributed primarily to the presence of reactive oxygen species that can induce oxidative stress (3). The sources of reactive oxygen species include: a) products from the arachidonic acid cascade, b) metabolism of xanthine by xanthine oxidase (4), and c) release of excitatory amino acids (5).…”

Section: Introductionmentioning

confidence: 99%

Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats

Frassetto

Schetinger

Webber

et al. 1999

Braz J Med Biol Res

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Brain ischemia followed by reperfusion causes neuronal death related to oxidative damage. Furthermore, it has been reported that subjects suffering from ischemic cerebrovascular disorders exhibit changes in circulating platelet aggregation, a characteristic that might be important for their clinical outcome. In the present investigation we studied tert-butyl hydroperoxide-initiated plasma chemiluminescence and thiol content as measures of peripheral oxidative damage in naive and preconditioned rats submitted to forebrain ischemia produced by the 4-vessel occlusion method. Rats were submitted to 2 or 10 min of global transient forebrain ischemia followed by 60 min or 1, 2, 5, 10 or 30 days of reperfusion. Preconditioned rats were submitted to a 10-min ischemic episode 1 day after a 2-min ischemic event (2 + 10 min), followed by 60 min or 1 or 2 days of reperfusion. It has been demonstrated that such preconditioning protects against neuronal death in rats and gerbils submitted to a lethal (10 min) ischemic episode. The results show that both 2 and 10 min of ischemia cause an increase of plasma chemiluminescence when compared to control and sham rats. In the 2-min ischemic group, the effect was not present after reperfusion. In the 10-min ischemic group, the increase was present up to 1 day after recirculation and values returned to control levels after 2 days. However, rats preconditioned to ischemia (2 + 10 min) and reperfusion showed no differences in plasma chemiluminescence when compared to controls. We also analyzed plasma thiol content since it has been described that sulfhydryl (SH) groups significantly contribute to the antioxidant capacity of plasma. There was a significant decrease of plasma thiol content after 2, 10 and 2 + 10 min of ischemia followed by reperfusion when compared to controls. We conclude that ischemia may cause, along with brain oxidative damage and cell death, a peripheral oxidative damage that is reduced by the preconditioning phenomenon.

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“…Both the retinal and cerebral injuries involve excitotoxicity due to increases in extracellular glutamate and calcium influx. [9][10][11] Other common mechanisms include altered aquaporin expression, 12,13 oxidative stress, 14,15 and increases in proapoptotic and decreases in antiapoptotic markers. 16,17 Increased inflammation occurs in both conditions, including increased activation of glial cells and macrophages, 18,19 increased levels of inflammatory cytokines (IL-6, TNF-a, and so on), 20,21 and nuclear factor kappa-light-chain-enhancer of active B cells (NF-jB) pathway activation.…”

mentioning

confidence: 99%

Progesterone Treatment in Two Rat Models of Ocular Ischemia

Allen

Olsen

Sayeed

et al. 2015

Invest. Ophthalmol. Vis. Sci.

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Citation: Allen RS, Olsen TW, Sayeed I, et al. Progesterone treatment in two rat models of ocular ischemia. Invest Ophthalmol Vis Sci. 2015;56:2880-2891. DOI:10.1167/iovs.14-16070 PURPOSE. To determine whether the neurosteroid progesterone, shown to have protective effects in animal models of traumatic brain injury, stroke, and spinal cord injury, is also protective in ocular ischemia animal models.METHODS. Progesterone treatment was tested in two ocular ischemia models in rats: a rodent anterior ischemic optic neuropathy (rAION) model, which induces permanent monocular optic nerve stroke, and the middle cerebral artery occlusion (MCAO) model, which causes transient ischemia in both the retina and brain due to an intraluminal filament that blocks the ophthalmic and middle cerebral arteries. Visual function and retinal histology were assessed to determine whether progesterone attenuated retinal injury in these models. Additionally, behavioral testing and 2% 2,3,5-triphenyltetrazolium chloride (TTC) staining in brains were used to compare progesterone's neuroprotective effects in both retina and brain using the MCAO model. RESULTS.Progesterone treatment showed no effect on visual evoked potential (VEP) reduction and retinal ganglion cell loss in the permanent rAION model. In the transient MCAO model, progesterone treatment reduced (1) electroretinogram (ERG) deficits, (2) MCAO-induced upregulation of glutamine synthetase (GS) and glial fibrillary acidic protein (GFAP), and (3) retinal ganglion cell loss. As expected, progesterone treatment also had significant protective effects in behavioral tests and a reduction in infarct size in the brain. CONCLUSIONS.Progesterone treatment showed protective effects in the retina following MCAO but not rAION injury, which may result from mechanistic differences with injury type and the therapeutic action of progesterone.

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In vivo evidence of hydroxyl radical formation induced by elevation of extracellular glutamate after cerebral ischemia in the cortex of anesthetized rats

Cited by 55 publications

References 24 publications

Reactive oxygen intermediates contribute to necrotic and apoptotic neuronal injury in an infant rat model of bacterial meningitis due to group B streptococci.

Reactive oxygen intermediates contribute to necrotic and apoptotic neuronal injury in an infant rat model of bacterial meningitis due to group B streptococci.

Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats

Progesterone Treatment in Two Rat Models of Ocular Ischemia

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