Role of lipid peroxidation in serotonin receptor injury and onset of epileptiform seizures during hyperoxia

Kagan, V. E.; Kopaladze, R. A.; Prilipko, L. L.; Savov, V.

doi:10.1007/bf00834297

Cited by 5 publications

(2 citation statements)

References 5 publications

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“…Free radicals have been shown to impair function of some membrane neurotransmitter receptors, such as muscarinic receptors (Abe et al, 1985), ␣-and ␤-adrenergic receptors (Kramer et al, 1987;Pruijn et al, 1989), and serotonergic receptor (Kagan et al, 1983), which may result from a disturbance of the membrane integrity induced by peroxidation of membrane lipids. We have recently observed that lipid peroxidation in cellular membranes can induce a reduction in [ 3 H]epibatidine binding of nAChRs in vitro (Guan et al, 2000a).…”

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confidence: 98%

Reduced expression of neuronal nicotinic acetylcholine receptors during the early stages of damage by oxidative stress in PC12 cells

Guan

Zhang

Mousavi

et al. 2001

J of Neuroscience Research

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The mechanism for a large loss of neuronal nicotinic acetylcholine receptors (nAChRs) in brains with neurodegenerative diseases remains unclear. Based on our previous results of [(3)H]epibatidine binding influenced by lipid peroxidation, we suggest that nAChR deficit in neurodegenerative diseases might be related to the neurons attacked by free radicals. To further understand how free radicals influence the expression of nAChRs, we detected [(125)I]alpha-bungarotoxin binding, nAChR subunit protein and mRNA during the early stage of damage by oxidative stress in PC12 cells in the present study. The results showed that free radical insult (FeSO(4)) within the concentration range (1 -100 microM) used in the study induced dose-dependent increases in lipid peroxidation and toxicity to PC12 cells, but did not result in apoptosis or necrosis. Significant reductions in [(125)I]alpha-bungarotoxin binding site, protein level for the alpha3 and alpha7 subunits, and mRNA level for the alpha7 subunit were observed in PC12 cells treated by FeSO(4) at the concentrations without inducing cell death compared to control. Pretreatment of cultural cells with antioxidant such as Vitamin E and reduced glutathione prevented the inhibiting effect of free radicals on [(125)I]alpha-bungarotoxin and [(3)H]epibatidine bindings. The present results further demonstrate that oxidative stress might reduce the number of [(125)I]alpha-bungarotoxin binding site and selectively suppress the expression of the nAChR subunits at protein and mRNA levels during the early stages of damage in PC12 cells.

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confidence: 98%

Reduced expression of neuronal nicotinic acetylcholine receptors during the early stages of damage by oxidative stress in PC12 cells

Guan

Zhang

Mousavi

et al. 2001

J of Neuroscience Research

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“…Free radicals have been implicated in the epileptic brain injury caused by prolonged seizures with resultant hypoxia. Hyperbaric oxygen induces convulsions in rats and mice (Jerret et al, 1973;Kagan et a]., 1983; Katz et al, 1987) and in humans (Behnke, 1940); these investigators also showed that hyperbaric oxygen-induced seizures could be prevented by prior administration of a-tocopherol. Vitamin E is an effective anticonvulsant in the ferrous chloride model (Rubin and Willmore, 1980;Rubin, 1981, 1984;Willmore et al, 1986;Levy et al, 1990), the topical penicillin model (Kryzhanovskii et al, 1980), and the hyperbaric oxygen model (Jerret et al, 1973).…”

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confidence: 99%

Randomized, Double‐Blind, Placebo‐Controlled, Clinical Trial of D‐α‐Tocopherol (Vitamin E) as Add‐on Therapy in Uncontrolled Epilepsy

et al. 1994

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In a double-blind, cross-over trial, vitamin E, and placebo were compared as add-on therapy in 43 patients with uncontrolled epilepsy. The study consisted of a 3-month baseline period followed by two treatment phases of vitamin E or placebo with cross-over to the second phase after 3 months. No significant side effects were noted during the study. Mean seizure frequency in the baseline period was 15.9 +/- 10.5 as compared with 11.8 +/- 10.9 during the placebo phase and 13.7 +/- 11.1 during the vitamin E phase. No significant change in seizure frequency was observed with vitamin E as compared with placebo (p > 0.1). Similar observation was noted in subgroups with generalized seizures (n = 25), partial with secondarily generalized seizures (n = 11), or complex partial seizures (CPS) (n = 7). This study did not corroborate the earlier claims of therapeutic efficacy of vitamin E as add-on therapy in refractory epilepsy in adults.

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Synthesis of GABA‐Valproic Acid Derivatives and Evaluation of Their Anticonvulsant and Antioxidant Activity

Rekatas

Tani

Demopoulos

et al. 1996

Archiv der Pharmazie

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The synthesis and the anticonvulsant activity of a number of GABA and valproic acid derivatives are reported. The lipophilicity of these compounds and their inhibitory effect on lipid peroxidation were also investigated, in an effort to correlate the anticonvulsant activity with lipophilicity and inhibitory effect on lipid peroxidation. The synthesized compounds exhibited anticonvulsant effects which were stronger for the more lipophilic derivatives. One of the active anticonvulsants showed appreciable antioxidant properties. Finally, a good correlation was found between the experimentally derived (RM) and calculated (sigma f and log PSK) lipophilicity for this series of compounds.

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Role of lipid peroxidation in serotonin receptor injury and onset of epileptiform seizures during hyperoxia

Cited by 5 publications

References 5 publications

Reduced expression of neuronal nicotinic acetylcholine receptors during the early stages of damage by oxidative stress in PC12 cells

Reduced expression of neuronal nicotinic acetylcholine receptors during the early stages of damage by oxidative stress in PC12 cells

Randomized, Double‐Blind, Placebo‐Controlled, Clinical Trial of D‐α‐Tocopherol (Vitamin E) as Add‐on Therapy in Uncontrolled Epilepsy

Synthesis of GABA‐Valproic Acid Derivatives and Evaluation of Their Anticonvulsant and Antioxidant Activity

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