Idebenone Ameliorates Rotenone-Induced Parkinson’s Disease in Rats Through Decreasing Lipid Peroxidation

Avcı, Bahattin; Günaydın, Caner; Güvenç, Tolga; Yavuz, Canan Kulcu; Kuruca, Nilüfer; Bilge, S. Sırrı

doi:10.1007/s11064-020-03186-w

Cited by 50 publications

(26 citation statements)

References 57 publications

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“… CoQ 10 administration was also able to prevent iron-induced apoptosis in cultured human dopaminergic (SK-N-SH) neurons, in metallothionein gene-manipulated mice, and in alpha-synuclein knockout ( alpha-synko ) mice [ 56 ]. CoQ 10 administration can prevent neurodegeneration and behavioral deterioration in rodents exposed to several toxins causing experimental parkinsonism, such as the pesticides paraquat [ 57 , 58 ], dichlorvos [ 59 ], and rotenone [ 60 , 61 ], and showed neuroprotective effects against rotenone in primary rat mesencephalic cultures [ 62 ] and human neuroblastoma cells [ 63 ]. Interestingly, the exposure of human neuroblastoma SH-SY5Y cells to commonly used organophosphate compounds, such as dichlorvos, methyl-parathion (parathion), and chlorpyrifos (CPF), induces an important decrease in CoQ 10 levels and complex II + III activity—both related to a decrease in neuronal cell viability.…”

Section: Discussionmentioning

confidence: 99%

Coenzyme Q10 and Parkinsonian Syndromes: A Systematic Review

Jiménez‐Jiménez

Alonso‐Navarro

García‐Martín

et al. 2022

JPM

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Coenzyme Q10 (CoQ10) has an important role as an antioxidant. Being that oxidative stress is one of the mechanisms involved in the pathogenesis of Parkinson’s disease (PD) and other neurodegenerative diseases, several studies addressed the concentrations of CoQ10 in the different tissues of patients with PD and other parkinsonian syndromes (PS), trying to elucidate their value as a marker of these diseases. Other studies addressed the potential therapeutic role of CoQ10 in PD and PS. We underwent a systematic review and a meta-analysis of studies measuring tissue CoQ10 concentrations which shows that, compared with controls, PD patients have decreased CoQ10 levels in the cerebellar cortex, platelets, and lymphocytes, increased total and oxidized CoQ10 levels in the cerebrospinal fluid and a non-significant trend toward decreased serum/plasma CoQ10 levels. Patients with multiple system atrophy (MSA) showed decreased CoQ10 levels in the cerebellar cortex, serum/plasma, cerebrospinal fluid, and skin fibroblasts. Patients with Lewy body dementia (LBD) showed decreased cerebellar cortex CoQ10, and those with progressive supranuclear palsy (PSP) had decreased CoQ10 levels in the cerebrospinal fluid. A previous meta-analysis of studies addressing the therapeutic effects of CoQ10 in PD showed a lack of improvement in patients with early PD. Results of the treatment with CoQ10 in PSP should be considered preliminary. The potential role of CoQ10 therapy in the MSA and selected groups of PD patients deserves future studies.

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Section: Discussionmentioning

confidence: 99%

Coenzyme Q10 and Parkinsonian Syndromes: A Systematic Review

Jiménez‐Jiménez

Alonso‐Navarro

García‐Martín

et al. 2022

JPM

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“…2) Analogs of coenzyme Q10 Idebenone is an analog of the well-known antioxidant coenzyme Q10 (CoQ10) and has been shown to mitigate motor impairment and to increase the neuron survival in PD model animals (56). Clinical trials of idebenone for protection against the development of PD in patients with REM sleep behavior disorder (SEASEiPPD study) and therapeutic effects on motor and non-motor symptoms in patients with early PD (ITEP study) are ongoing.…”

Section: ) Iron Chelatorsmentioning

confidence: 99%

Recent Advances in Drug Therapy for Parkinson's Disease

et al. 2023

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Parkinson's disease (PD) is a neurodegenerative disease manifesting with motor and non-motor symptoms. Current treatment mainly relies on medication as a symptomatic therapy modulating neurotransmitters. Dopamine replacement therapy has been established, and levodopa is the gold standard for treatment of PD. However, the emergence of motor complications, such as a wearing-off phenomenon, is a clinical problem. Both primary symptoms and motor complications have been targets for the development of treatments for PD. Recent progression in the management of motor complications is supported by newly developed agents and advances in device and formulation technology to deliver drugs continuously. Elucidation of the pathophysiology of PD and the development of disease-modifying therapy that affects the underlying fundamental pathophysiology of the disease are also progressing. In this review, we introduce current knowledge on developments concerning medications for patients with PD.

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“…There are many ways to inhibit ferroptosis, including reducing lipid ROS production {ferrostatin-1 [Fer-1 ( Chen et al, 2019 )], ADA-409-052}, blocking lipid peroxidation {vitamin E, coenzyme Q10 (CoQ10), idebenone ( Avcı et al, 2021 ), liproxstatin-1 [Lip-1 ( Cao et al, 2021 )]}, chelating iron (DFO and DFP), or iron oxide, and inhibiting 5-lipoxygenase.…”

Section: Inducers and Inhibitors Of Ferroptosismentioning

confidence: 99%

“…Ferroptosis has been shown to play an important role in the progression of numerous brain diseases, including PD ( Hou et al, 2019 ; Avcı et al, 2021 ), AD ( Hambright et al, 2017 ), ALS ( Devos et al, 2020 ), cerebral ischemia ( Lan et al, 2020 ; Cui et al, 2021a ), ICH ( Chen et al, 2019 ; Bai et al, 2020 ), SAH ( Qu et al, 2022 ), PMD ( Nobuta et al, 2019 ), PVL, MS, EAE ( Hu et al, 2019 ), SCI, TBI ( Rui et al, 2021 ), and depression ( Jiao et al, 2021 ). System Xc – blockade, GSH depletion, Gpx4 inactivity, lipoxygenase activation ( Figure 2 ), intracellular iron accumulation ( Figure 3 ), and some related signaling pathways ( Jiang et al, 2021 ) ( Figure 3 ) are common ferroptotic mechanisms in CNS diseases.…”

Section: Ferroptosis In Brain Diseasesmentioning

confidence: 99%

The emerging roles of ferroptosis in cells of the central nervous system

Xiao

Wang

2022

Front. Neurosci.

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Ferroptosis is morphologically characterized by shrunken mitochondria and biochemically characterized by iron overload, lipid peroxidation and lipid reactive oxygen species (ROS) accumulation; these phenomena are suppressed by iron chelation, genetic inhibition of cellular iron uptake, and intervention on other pathways such as lipid metabolism. The induction of ferroptosis may be related to pathological cellular conditions in the central nervous system (CNS); thus, ferroptosis may cause disability via CNS damage. Here, we review the role of ferroptosis in the main cells of the CNS, including glial cells, neurons, and pericytes; in various diseases of the CNS; and in the interaction of glia and neurons in CNS diseases. Some small molecules and traditional Chinese drugs which inhibit ferroptosis in cells of the CNS are shown as potential therapeutic strategies for neurological diseases.

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Idebenone Ameliorates Rotenone-Induced Parkinson’s Disease in Rats Through Decreasing Lipid Peroxidation

Cited by 50 publications

References 57 publications

Coenzyme Q10 and Parkinsonian Syndromes: A Systematic Review

Coenzyme Q10 and Parkinsonian Syndromes: A Systematic Review

Recent Advances in Drug Therapy for Parkinson's Disease

The emerging roles of ferroptosis in cells of the central nervous system

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