Lamotrigine inhibition of rotenone- or 1-methyl-4-phenylpyridinium-induced mitochondrial damage and cell death

Kim, Yun Jeong; Ko, Hyun Hee; Han, Eun Sook; Lee, Chung Soo

doi:10.1016/j.brainresbull.2006.12.006

Cited by 39 publications

(19 citation statements)

References 39 publications

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“…With regard to BD, its etiopathogenesis may be associated with an impaired function of mitochondria, where particularly intense oxidative processes and increased production of free radicals take place. What supports this hypothesis is the comorbidity of BD and mitochondrial diseases as well as the occurrence of mutations in mitochondrial DNA or specific mitochondrial gene polymorphisms [7,8,9,10]. …”

Section: Introductionmentioning

confidence: 69%

Thiobarbituric Acid-Reactive Substances: Markers of an Acute Episode and a Late Stage of Bipolar Disorder

Siwek

Sowa-Kućma²,

Styczeń³

et al. 2016

Neuropsychobiology

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Background: Lowered antioxidant defense systems and increased oxidative stress are implicated in bipolar disorders (BD). Early and late stages of BD may present different biological features (including the level of oxidative stress) and may therefore require different treatment strategies. The aim of this study was to analyze serum levels of lipid peroxidation [measured as thiobarbituric acid-reactive substances (TBARS), a derivative of malondialdehyde] in BD patients at various stages and phases of the illness and compare their TBARS levels with those of healthy controls. Method: A total of 129 patients (58 in the depressive episode, 23 in the manic episode and 48 in remission) diagnosed with type I (n = 69) or type II (n = 60) BD and 50 healthy volunteers (control group) were enrolled in the study. The level of lipid peroxidation was measured in blood serum using a TBARS assay kit. Results: TBARS levels in the acute episode of mania/hypomania and depression (but not in remission) were significantly higher than in healthy controls. With regard to the BD stage, both early- and late-stage BD TBARS levels were significantly increased in patients in the depressive episode. In late-stage BD, the TBARS level in patients in remission remained elevated compared with controls. A multiple regression model confirmed the association between the TBARS level and BD stage or acute BD. Conclusion: Our findings indicate that TBARS levels reflect the oxidative stress state which increases both in the acute phase of BD (mania/hypomania and depression) and with BD progression (stage).

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Section: Introductionmentioning

confidence: 69%

Thiobarbituric Acid-Reactive Substances: Markers of an Acute Episode and a Late Stage of Bipolar Disorder

Siwek

Sowa-Kućma²,

Styczeń³

et al. 2016

Neuropsychobiology

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“…The mechanism of METH-induced apoptosis is not well known; this apoptosis might result from many factors such as oxidants, reactive oxygen, and NO oxidative stress and cell death [21]. It also prevents enhancement of NO generation and release [6,23].…”

Section: Discussionmentioning

confidence: 99%

Lamotrigine blocks apoptosis induced by repeated administration of high-dose methamphetamine in the medial prefrontal cortex of rats

Nakato

Abekawa

Ito

et al. 2011

Neuroscience Letters

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“…An antiepileptic drug, lamotrigine, similarly protected differentiated PC12 cells subjected to the complex I inhibitors, rotenone and MPP ? , which otherwise caused formation of ROS and depletion of GSH, nuclear damage, and OMM permeabilization leading to cytochrome c release and caspase-3 activation [73]. Lamotrigine was suggested to exert its protective effects by suppression of oxidative stress and, as a result, inhibition of MPT.…”

Section: Therapeutic Strategymentioning

confidence: 99%

Mitochondria as targets for chemotherapy

2009

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Mitochondrial malfunctioning is implicated in the pathogenesis of a variety of disorders, including cancer and multiple neurodegenerative diseases, such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease. Disturbance of mitochondrial vital functions, e.g., production of ATP, calcium buffering capacity, and generation of reactive oxygen species, can be potentially involved in disease pathogenesis. Neurological disorders caused by mitochondrial deterioration are often associated with cell loss within specific brain regions. In contrast, mitochondrial alterations in tumor cells and the "Warburg effect" might lead to cell survival and resistance of tumor cells to chemotherapy. This review is devoted to the role of mitochondria in neurodegeneration and tumor formation, and describes how targeting of mitochondria can be beneficial in the therapy of these diseases, which affect a large human population.

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Lamotrigine inhibition of rotenone- or 1-methyl-4-phenylpyridinium-induced mitochondrial damage and cell death

Cited by 39 publications

References 39 publications

Thiobarbituric Acid-Reactive Substances: Markers of an Acute Episode and a Late Stage of Bipolar Disorder

Thiobarbituric Acid-Reactive Substances: Markers of an Acute Episode and a Late Stage of Bipolar Disorder

Lamotrigine blocks apoptosis induced by repeated administration of high-dose methamphetamine in the medial prefrontal cortex of rats

Mitochondria as targets for chemotherapy

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