Protein thiol oxidation by haloperidol results in inhibition of mitochondrial complex I in brain regions: comparison with atypical antipsychotics

Balijepalli, Sadguna Y.; Kenchappa, Rajappa S.; Boyd, Michael R.; Ravindranath, Vijayalakshmi

doi:10.1016/s0197-0186(00)00108-x

Cited by 85 publications

(47 citation statements)

References 31 publications

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“…In addition, research on neuroleptics has indicated that typical and atypical antipsychotics have substantially different effects on respiratory enzyme activity levels. 142 Although typical agents inhibit Complex I of the electron transport chain 143,144 and thus may cause significant reductions in synaptic ATP synthesis and mitochondrial respiration, 145 atypical agents have comparatively no effect on electron transfer activities. 142 Consideration of the possible mitochondrial factors underlying bipolar disorder may thus prove valuable in the choice and prescription of such antipsychotic treatments.…”

Section: Resultsmentioning

confidence: 99%

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

2005

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Magnetic resonance spectroscopy (MRS) affords a noninvasive window on in vivo brain chemistry and, as such, provides a unique opportunity to gain insight into the biochemical pathology of bipolar disorder. Studies utilizing proton ( 1 H) MRS have identified changes in cerebral concentrations of N-acetyl aspartate, glutamate/glutamine, choline-containing compounds, myo-inositol, and lactate in bipolar subjects compared to normal controls, while studies using phosphorus ( 31 P) MRS have examined additional alterations in levels of phosphocreatine, phosphomonoesters, and intracellular pH. We hypothesize that the majority of MRS findings in bipolar subjects can be fit into a more cohesive bioenergetic and neurochemical model of bipolar illness that is both novel and yet in concordance with findings from complementary methodological approaches. In this review, we propose a hypothesis of mitochondrial dysfunction in bipolar disorder that involves impaired oxidative phosphorylation, a resultant shift toward glycolytic energy production, a decrease in total energy production and/or substrate availability, and altered phospholipid metabolism. Molecular Psychiatry (2005) 10, 900-919.

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Section: Resultsmentioning

confidence: 99%

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

2005

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“…Numerous reports indicate that an excessive production of free radicals is associated with neuroleptic administration in rodents [59]. This abnormal free radical production is often related with a reduction of GSH content and detoxifying enzymes activity as well as higher thiobarbituric acid reactive substances as a result of increased LPO [60,61].…”

Section: Haloperidol-induced Oxidative Stressmentioning

confidence: 99%

Neuroprotective effect of naphtha[1,2-d]thiazol-2-amine in an animal model of Parkinson's disease

Azam¹,

Barodia

Anwer

et al. 2009

Journal of Enzyme Inhibition and Medicinal Chemistry

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“…[119] Antipsikotik alan olguların dopaminden zengin olan prefrontal kortekste kompleks I aktivasyonunda azalma olduğu görülmüşken; nondopaminerjik bölge olan ventral parietooksipital alanda aktivasyonda artış gözlenmiştir. [121,122] Beyindeki bu bölgesel farklılıklar, kompleks I alt bölüm ekspresyonlarının beyinde farklı bölgelerde hem endojen (dopamin) hem de ekzojen (antipsikotik tedavi) faktörlerden etkilendiğini göster-mektedir. [121,122] Hangi antipsikotiğin solunum zincirini ne ölçüde etkilediği açık değildir.…”

Section: Antipsikotik Tedavinin Mitokondrial Solunum Zinciri üZerine unclassified

Schizophrenia and Mitochondrial Dysfunction

Akarsu¹

2014

Psikiyatride Guncel Yaklasimlar - Current Approaches in Psychia

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ÖzetEtyolojisi net olarak bilinmeyen şizofreninin oluşumunda genetik faktörler önemli rol oynamaktadır. Ancak, bu bozukluğun spesifik kalıtımsal mekanizması henüz açıklanamamıştır. Şizofreni kalıtımı-nın poligenik veya multifaktöryel olabileceği düşünülmektedir. Son dönemde yapılan çalışmalarda, şizofreni olgularında mitokondrial fonksiyon ve serebral enerji metabolizmasında anormallikler tespit edilmiştir. Mitokondri fonksiyonlarındaki bozulma ile nöronal plastisite ve beyin devreleri etkilenerek, şizofreninin klinik tablosunda da belirgin olarak rastlanabilen davranış anormallikleri ve bilişsel defisitler gelişebilir. Şizofreni olgularının hem beyin hem de periferal dokularının incelendiği araştırmalarda, şizofreni olgularında sağlıklı olgulara göre bazı değişiklikler saptanmıştır. Ayrıca şizofreni tedavisinde kullanılan antipsikotiklerin solunum zinciri inhibisyonu yaparak mitokondrinin oksidatif fosforilasyon kapasitesinde progresif olarak azalmaya neden olabileceği görülmüştür. Bu çalışmalarda, özellikle periferal dokulardan elde edilen bulguların, şizofreni tanısında biyolojik bir belirteç olarak kullanılabileceği önerilmiştir. Plateletlerin kendi DNA'sı olmadığı için, platelet mitokondrisinde gerçekleşen değişiklikler nöronlar için periferal bir model olarak kabul edilmektedir. Bu değişiklikler çeşitli nöropsikiyatrik rahatsızlıklarda beyindeki bulguları yansıtmaktadır. Günümüzde şizofreni tanısının klinik ölçütlere dayalı olması, şizofreni için periferal biyolojik bir belirteç gerekliliğini ortaya koymaktadır. Bu nedenle mitokondrial elektron transport zincirindeki değişikliklerin şizofreni ile ilişkisini araştıran daha sistematik çalışmaların yapılması gereklidir.Anahtar sözcükler: Şizofreni, mitokondrial disfonksiyon, biyolojik belirteç. AbstractGenetic factors play an important role in the development of schizophrenia that the etiology is clearly not known. However, specific inheritance mechanism of this disorder is still unclear. Inheritance of schizophrenia is thought to be polygenic or multifactorial. In the recent studies, mitochondrial function and cerebral energy metabolism abnormalities have been identified in patients with schizophrenia. Cognitive deficits and behavioral abnormalities evident as typically found in the clinical course of schizophrenia may develop due to the affection of neuronal plasticity and brain circuits by impaired function of mitochondria. Some changes were found in patients with schizophrenia compared with control subjects in the researches examining both brain and peripheral tissues. Also, it was seen that antipsychotics used in the treatment of schizophrenia might lead to a progressive reduction in oxidative phosphorylation capacity of mitochondria by inhibition of respiratory chain. Especially the findings of the peripheral tissues in patients with schizophrenia were considered to be used as a biological marker for schizophrenia in these studies. Changes in the mitochondria of platelets are considered as a peripheral model for the neurons because of the lack of the pl...

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Protein thiol oxidation by haloperidol results in inhibition of mitochondrial complex I in brain regions: comparison with atypical antipsychotics

Cited by 85 publications

References 31 publications

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

Mitochondrial dysfunction in bipolar disorder: evidence from magnetic resonance spectroscopy research

Neuroprotective effect of naphtha[1,2-d]thiazol-2-amine in an animal model of Parkinson's disease

Schizophrenia and Mitochondrial Dysfunction

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