Effect of an NMDA receptor antagonist and a ganglioside GM1 derivative upon ethanol-induced modification of parameters of oxidative stress in several brain regions

Bondy, Stephen C.; Guo, Shirley X.

doi:10.1016/0006-8993(96)00008-x

Cited by 10 publications

(7 citation statements)

References 32 publications

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“…Numerous reports associate ethanol and free radical formation [ 11. Our finding that an ethanolcontaining vehicle decreases GPX activity in the cortex of rats with LiPi-induced status epilepticus is in keeping with reports by Bondy and Guo [2]. According to them ethanol causes a decrease in GSH and Cu/Zn-SOD levels in the rat cerebral cortex, cerebellum, midbrain and striatum [2].…”

Section: Discussionsupporting

confidence: 90%

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The influence of calcium channel blockers on the brain free fatty acid level and glutathione peroxidase activity in rats with lithium and pilocarpine‐induced status epilepticus

Eraković¹,

Župan²,

Varljen³

et al. 2002

Neuroscience Res Communica

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The aim of this study was to investigate possible therapeutic approach to neuronal damage caused by status epilepticus. The effects of the L-type voltage-sensitive calcium channel blockers (nimodipine, nicardipine) and NMDA blockers (ifenprodil and MK-801) on the brain free fatty acid (FFA) level and glutathione peroxidase (GPX) activity in rats with lithium and pilocarpine (LiPi) -induced status epilepticus were examined. Vehicle or various doses of calcium channel and NMDA blockers had been injected i.p. 30 min after the pilocarpine application. Tested doses of nicardipine and MK-801 did not influence the increase in the brain FFA level. Nimodipine and ifenprodil revealed a tendency to reduce FFA level. The inhibition of L-type voltage-sensitive Ca2' channels or NMDA receptor -associated channels was not sufficient for significant attenuation of an increase in the rat brain FFA content and a decrease GPX activity associated with LiPi -induced status epilepticus. Individual compounds have shown to prevent FFA increase, suggesting some alternative or additional mechanism of action. The prevention of FFA accumulation was not followed by the prevention of GPX decrease indicating the activation of non FFA-related mechanisms of cell damage.

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Section: Discussionsupporting

confidence: 90%

“…According to them ethanol causes a decrease in GSH and Cu/Zn-SOD levels in the rat cerebral cortex, cerebellum, midbrain and striatum [2]. In the presence of oxidants and proteases, subtoxic doses of ethanol can cause cell death [ 121.…”

Section: Discussionmentioning

confidence: 99%

The influence of calcium channel blockers on the brain free fatty acid level and glutathione peroxidase activity in rats with lithium and pilocarpine‐induced status epilepticus

Eraković¹,

Župan²,

Varljen³

et al. 2002

Neuroscience Res Communica

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“…In addition, our data showed that chronic AL treatment significantly increased concentrations of MDA but failed to significantly affect any other marker of oxidative stress. In line with the present study, it has been reported that AL exposure causes an increase of MDA levels, without changing the SOD and GPX activities in the hippocampus [90,91]. Although according to some studies, increased oxidative stress in hippocampus due to ethanol treatment results in memory disorders [92], however, we detected no such correlation.…”

Section: Effect Of Ma And/or Al On Spatial Learning and Memory And Oxsupporting

confidence: 89%

The Effect of Escalating Dose, Multiple Binge Methamphetamine Regimen and Alcohol Combination on Spatial Memory and Oxidative Stress Markers in Rat Brain

M¹

2014

J Alcohol Drug Depend

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Polydrug abuse is a major problem around the world. Methamphetamine (MA) and alcohol (AL) are two abused drugs which are frequently used together. Chronic abuse of either MA or AL causes oxidative stress in the brain and is associated with impairments in cognitive functions including various aspects of memory and learning. The present study examined the effect of escalating dose, multiple binge MA regimen, AL and MA-AL combination on spatial memory and the induction of oxidative stress in the hippocampus. Adult male Wistar rats were exposed to ethanol, an escalating dose of MA either individually or in combination for 28 consecutive days. In order to examine the short-and long-term effects of chronic exposure to the drugs, each group was then subdivided into two further groups. Thereafter, spatial memory was tested using a Morris water maze, either one day or 14 days after the drugs were withdrawn. At the end of the behavioral testing, oxidative stress markers including Superoxide Dismutase (SOD), Glutathione Peroxidase (GPX), Catalase (CAT), and Malondialdehyde (MDA) were measured. Our results showed that MA, but not AL, impaired spatial memory. Although AL alone had no effect, it exacerbated the impairment due to MA when the drugs were co-administered. In addition, while both drugs significantly induced oxidative stress in the hippocampus when given alone, co-administration of these drugs resulted in a greater oxidative stress and an impairment of the antioxidant enzyme glutathione peroxidase in rat hippocampus. Taken together, this study demonstrates that MA in combination with AL has synergistic effects on increased oxidative stress in the hippocampus, as well as spatial memory impairment.

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“…Chronic ethanol has been shown to increase SOD activity (Montoliu et al, 1994;Somani et al, 1996), as well as to depress its activity in the rat brain (Bondy and Guo, 1996). SOD activity in the liver after chronic ethanol treatment has also been reported as either a decrease (Chen et al, 1995) or no change (Matsuyama et al, 1987;Perera et al, 1995).…”

Section: Discussionmentioning

confidence: 96%

Chronic Ethanol and Iron Administration on Iron Content, Neuronal Nitric Oxide Synthase, and Superoxide Dismutase in Rat Cerebellum

Xia

Simonyi

Sun

1999

Alcoholism Clin & Exp Res

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Excessive chronic ethanol administration to animals has been shown to cause oxidative insults to many body organs, including the liver and brain. In many instances, iron supplementation to the diet may further aggravate ethanol-induced liver damage. However, whether increased dietary iron can enhance the damage in the brain is unknown. In this study, four groups of Sprague-Dawley rats were fed a Lieber-DeCarli liquid diet containing 5% (w/v) ethanol or isocaloric amount of maltase and/or 0.25% (w/v) carbonyl iron for 2 months. At the end of the feeding regimen, iron contents were determined in the plasma, liver, cerebral cortex, and cerebellum. Cerebellar superoxide dismutase (SOD) and nitric oxide synthase (NOS) activities were measured and mRNA levels of MnSOD, CuZnSOD, and nNOS in the cerebellar granule cell layer were quantitated by in situ hybridization. Ethanol treatment alone caused an increase in iron levels in plasma, no change in the liver and cerebral cortex, but a decrease in the cerebellum. Iron supplementation increased liver iron >4-fold but did not alter iron contents in the cerebellum and cortex. All of the mRNA species examined and SOD activity were not affected by either iron or ethanol administration. However, NOS activity in the cerebellum was significantly enhanced by ethanol, whereas iron supplementation had an opposite effect. Our results indicate that iron supplementation to animals consuming ethanol may have tissue-specific effects. Furthermore, ethanol-induced increase in NOS activity in the cerebellum may explain the sensitivity of cerebellar neurons to oxidative insult.

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Effect of an NMDA receptor antagonist and a ganglioside GM1 derivative upon ethanol-induced modification of parameters of oxidative stress in several brain regions

Cited by 10 publications

References 32 publications

The influence of calcium channel blockers on the brain free fatty acid level and glutathione peroxidase activity in rats with lithium and pilocarpine‐induced status epilepticus

The influence of calcium channel blockers on the brain free fatty acid level and glutathione peroxidase activity in rats with lithium and pilocarpine‐induced status epilepticus

The Effect of Escalating Dose, Multiple Binge Methamphetamine Regimen and Alcohol Combination on Spatial Memory and Oxidative Stress Markers in Rat Brain

Chronic Ethanol and Iron Administration on Iron Content, Neuronal Nitric Oxide Synthase, and Superoxide Dismutase in Rat Cerebellum

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