Late-onset lipid peroxidation and neuronal cell death following transient forebrain ischemia in rat brain

Kondo, Yoichi; Asanuma, Masato; Nishibayashi, Sakiko; Iwata, Emi; Ogawa, Norio

doi:10.1016/s0006-8993(97)00836-6

Cited by 45 publications

(21 citation statements)

References 20 publications

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“…Levels of 4HN are increased in association with the neurodegenerative process in postmortem tissue samples from patients with Alzheimer's disease (45)(46)(47) and amyotrophic lateral sclerosis (48,49). Moreover, studies of experimental models of Alzheimer's disease (9 -11, 50, 51), stroke (52,53), and amyotrophic lateral sclerosis (54) suggest a pivotal role for 4HN in the neurodegenerative process. For each of these disorders, there is also evidence that excessive Ca 2ϩ influx contributes to the neurodegenerative process (21,55,56).…”

Section: Discussionmentioning

confidence: 99%

The Lipid Peroxidation Product 4-Hydroxynonenal Facilitates Opening of Voltage-dependent Ca2+ Channels in Neurons by Increasing Protein Tyrosine Phosphorylation

Lu¹,

Chan²,

Fu³

et al. 2002

Journal of Biological Chemistry

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Calcium influx through voltage-dependent calcium channels (VDCCs) mediates a variety of functions in neurons and other excitable cells, but excessive calcium influx through these channels can contribute to neuronal death in pathological settings. Oxyradical production and membrane lipid peroxidation occur in neurons in response to normal activity in neuronal circuits, whereas excessive lipid peroxidation is implicated in the pathogenesis of of neurodegenerative disorders. We now report on a specific mechanism whereby lipid peroxidation can modulate the activity of VDCCs. The lipid peroxidation product 4-hydroxy-2,3-nonenal (4HN) enhances dihydropyridine-sensitive whole-cell Ca 2؉ currents and increases depolarization-induced increases of intracellular Ca 2؉ levels in hippocampal neurons. Prolonged exposure to 4HN results in neuronal death, which is prevented by treatment with glutathione and attenuated by the L-type Ca 2؉ channel blocker nimodipine. Tyrosine phosphorylation of ␣1 VDCC subunits is increased in neurons exposed to 4HN, and studies using inhibitors of tyrosine kinases and phosphatases indicate a requirement for tyrosine phosphorylation in the enhancement of VDCC activity in response to 4HN. Phosphorylation-mediated modulation of Ca 2؉ channel activity in response to lipid peroxidation may play important roles in the responses of neurons to oxidative stress in both physiological and pathological settings.

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Section: Discussionmentioning

confidence: 99%

The Lipid Peroxidation Product 4-Hydroxynonenal Facilitates Opening of Voltage-dependent Ca2+ Channels in Neurons by Increasing Protein Tyrosine Phosphorylation

Lu¹,

Chan²,

Fu³

et al. 2002

Journal of Biological Chemistry

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“…Brain damage after TFI has been linked to enhanced leukocyte adhesion/infiltration, 19 free radical mechanisms, 20 upregulation of the inducible NOS (iNOS) isoform, 21 altered cerebral glucose transport, 22,23 and apoptosis. 24 Estrogens, E 2 in particular, have been shown to possess anti-inflammatory functions, 25 antioxidant actions, 26,27 an ability to block the induction of iNOS, 2 a capacity to improve glucose transport, 28 and antiapoptotic effects.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Provides Neuroprotection in Transient Forebrain Ischemia Through Perfusion-Independent Mechanisms in Rats

Wang

Santizo

Baughman

et al. 1999

Stroke

156

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Background and Purpose-Estrogen-related neuroprotection in association with animal models of transient forebrain and focal ischemia has been documented in several recent reports. Some of those studies indicated that part of that benefit was a function of improved intraischemic vasodilating capacity. In the present study we examined whether chronic estrogen depletion and repletion affected ischemic neuropathology through perfusion-independent mechanisms. Methods-Normal, ovariectomized (OVX), and OVX female rats treated with 17␤-estradiol (E 2 ) were subjected to 30 minutes of transient forebrain ischemia (right common carotid occlusion plus hemorrhagic hypotension) and reperfusion. Neurological function and brain histopathology were assessed over the 72-hour recovery period. In all rats, preischemic and intraischemic cortical cerebral blood flow (CBF) levels were monitored with laser-Doppler flowmetry.In additional rats, CBF changes in the striatum and hippocampus were also monitored with laser-Doppler flowmetry probes and radiolabeled microspheres. In each experiment, the level of ischemia was targeted to a 75% to 80% reduction in cortical CBF. Results-The similarity in ischemic severity among groups was supported by measurements of comparable patterns of electroencephalographic power changes during the ischemic period. Compared with normal females, OVX rats showed diminished neurological outcomes and more severe histopathology in the hippocampus and striatum. Two-week treatment of OVX rats with E 2 was accompanied by postischemic neuropathological changes similar to those seen in normal females. Intraischemic CBF reductions in the hippocampus and striatum were similar in all groups (to 35% to 50% of the preischemic value) but significantly less than the cortical CBF reductions. Conclusions-These findings indicate that estrogen provides ischemic neuroprotection through mechanisms unrelated to improvement of intraischemic cerebral perfusion. (Stroke. 1999;30:630-637.)

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“…Determination of its products, malondialdehyde (MDA) and 4-hydroxy-2(E)-nonenal (4-HNE), in brain tissues and plasma had been used to evaluate the severity of neuronal injury of ischemia (Bromont et al, 1989;Kondo et al, 1997;Re et al, 1997). Both MDA and 4-HNE are cytotoxic to cells but their reactivities to biomolecules are different (Cheeseman and Slater, 1993).…”

Section: Introductionmentioning

confidence: 99%

Effectiveness of multiple pre-ischemia electro-acupuncture on attenuating lipid peroxidation induced by cerebral ischemia in adult rats

Siu

Leung

2004

Life Sciences

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Late-onset lipid peroxidation and neuronal cell death following transient forebrain ischemia in rat brain

Cited by 45 publications

References 20 publications

The Lipid Peroxidation Product 4-Hydroxynonenal Facilitates Opening of Voltage-dependent Ca2+ Channels in Neurons by Increasing Protein Tyrosine Phosphorylation

The Lipid Peroxidation Product 4-Hydroxynonenal Facilitates Opening of Voltage-dependent Ca2+ Channels in Neurons by Increasing Protein Tyrosine Phosphorylation

Estrogen Provides Neuroprotection in Transient Forebrain Ischemia Through Perfusion-Independent Mechanisms in Rats

Effectiveness of multiple pre-ischemia electro-acupuncture on attenuating lipid peroxidation induced by cerebral ischemia in adult rats

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