Increased infarct size and exacerbated apoptosis in the glutathione peroxidase‐1 (Gpx‐1) knockout mouse brain in response to ischemia/reperfusion injury

Glutathione peroxidase is an antioxidant enzyme that is involved in the control of cellular oxidative state. Recently, unregulated oxidative state has been implicated as detrimental to neural cell viability and involved in both acute and chronic neurodegeneration. In this study we have addressed the...

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Veröffentlicht in:Journal of neurochemistry 2001-09, Vol.78 (6), p.1389-1399
Hauptverfasser: Crack, Peter J., Taylor, Juliet M., Flentjar, Nicole J., De Haan, Judy, Hertzog, Paul, Iannello, Rocco C., Kola, Ismail
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container_end_page 1399
container_issue 6
container_start_page 1389
container_title Journal of neurochemistry
container_volume 78
creator Crack, Peter J.
Taylor, Juliet M.
Flentjar, Nicole J.
De Haan, Judy
Hertzog, Paul
Iannello, Rocco C.
Kola, Ismail
description Glutathione peroxidase is an antioxidant enzyme that is involved in the control of cellular oxidative state. Recently, unregulated oxidative state has been implicated as detrimental to neural cell viability and involved in both acute and chronic neurodegeneration. In this study we have addressed the importance of a functional glutathione peroxidase in a mouse ischemia/reperfusion model. Two hours of focal cerebral ischemia followed by 24 h of reperfusion was induced via the intraluminal suture method. Infarct volume was increased three‐fold in the glutathione peroxidase‐1 (Gpx‐1) –/– mouse compared with the wild‐type mouse; this was mirrored by an increase in the level of apoptosis found at 24 h in the Gpx‐1 –/– mouse compared with the wild‐type mouse. Neuronal deficit scores correlated to the histologic data. We also found that activated caspase‐3 expression is present at an earlier time point in the Gpx‐1 –/– mice when compared with the wild‐type mice, which suggests an enhanced susceptibility to apoptosis in the Gpx‐1 –/– mouse. This is the first known report of such a dramatic increase, both temporally and in level of apoptosis in a mouse stroke model. Our results suggest that Gpx‐1 plays an important regulatory role in the protection of neural cells in response to the extreme oxidative stress that is released during ischemia/reperfusion injury.
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Recently, unregulated oxidative state has been implicated as detrimental to neural cell viability and involved in both acute and chronic neurodegeneration. In this study we have addressed the importance of a functional glutathione peroxidase in a mouse ischemia/reperfusion model. Two hours of focal cerebral ischemia followed by 24 h of reperfusion was induced via the intraluminal suture method. Infarct volume was increased three‐fold in the glutathione peroxidase‐1 (Gpx‐1) –/– mouse compared with the wild‐type mouse; this was mirrored by an increase in the level of apoptosis found at 24 h in the Gpx‐1 –/– mouse compared with the wild‐type mouse. Neuronal deficit scores correlated to the histologic data. We also found that activated caspase‐3 expression is present at an earlier time point in the Gpx‐1 –/– mice when compared with the wild‐type mice, which suggests an enhanced susceptibility to apoptosis in the Gpx‐1 –/– mouse. 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This is the first known report of such a dramatic increase, both temporally and in level of apoptosis in a mouse stroke model. 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subjects Animals
Apoptosis
Biological and medical sciences
Brain - pathology
Brain - physiopathology
Brain Ischemia - pathology
Brain Ischemia - physiopathology
Caspase 3
Caspases - metabolism
Cerebral Infarction - pathology
Cerebral Infarction - physiopathology
cerebral ischemia
Enzyme Activation - physiology
Glutathione Peroxidase - genetics
Glutathione Peroxidase - physiology
glutathione peroxidase‐1
knockout mouse
Lipid Peroxides - metabolism
Medical sciences
Mice
Mice, Knockout - genetics
Neurology
Neurons - physiology
oxidative stress
Reperfusion Injury - pathology
Reperfusion Injury - physiopathology
Vascular diseases and vascular malformations of the nervous system
title Increased infarct size and exacerbated apoptosis in the glutathione peroxidase‐1 (Gpx‐1) knockout mouse brain in response to ischemia/reperfusion injury
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