Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease

Valdez, Laura B.; Zaobornyj, Tamara; Bández, Manuel J.; López-Cepero, J.M.; Boveris, Alberto; Navarro, Ana

doi:10.1016/j.freeradbiomed.2019.03.001

Cited by 22 publications

(14 citation statements)

References 61 publications

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“…Similar to our study, Vijayalakshmi et al (22) reported signi cant decrease in locomotion in Open eld test in rotenone-treated Wister rats. Similarly, Valdez et al (23) reported 60% decrease in locomotive activity in the open eld test in rotenone-treated rats. von Wrangel et al, (24) reported that rotenone-treated rats showed signi cant impairment in Rotarod and signi cant decline in tyrosine hydroxylase in the striatum.…”

Section: Discussionmentioning

confidence: 78%

Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated rats

Monir

Mahmoud

Galal

et al. 2020

Preprint

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Background: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive loss of nigrostriatal dopaminergic neurons leading to dopamine depletion and problems of movement, emotions and cognition. While the pathogenesis of PD is not clear, damage of dopaminergic neurons by oxygen-derived free radicals is considered an important contributing mechanism.This study aimed to evaluate the role of treadmill exercise in male Wister rats as a single treatment and as an aid-therapy with L-dopa for rotenone-induced PD. To study the role of NRF2-ARE pathway as a mechanism involved in exercise associated improvement in rotenone rat model of PD.Method: Animals were divided into 5 groups, (Control, rotenone, rotenone\exercise, rotenone\L-dopa, and rotenone\exercise\L-dopa (combination) groups). After the PD induction, rats in the rotenone\exercise and combination groups were daily treadmill exercised for 4 weeks.Results: Treadmill exercise significantly improved behavioral and motor aspects of rotenone model of PD. When treadmill exercise introduced as a single intervention, it amended most behavioral aspects of PD, gait fully corrected, short-term memory, and motor coordination. Where L-dopa corrected locomotor activity and motor co-ordination but failed to improve short-term memory and only partially corrected the gait of rotenone-treated rats. When treadmill exercise was combined with L-dopa, all features of PD were corrected. It was found that exercise upregulated some of its associative genes to NRF2 pathways such as TFAM, NRF2, Noq.1 mRNA expression.Conclusion: This study suggests that forced exercise improved parkinsonian like features by activating NRF2 pathway.

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Section: Discussionmentioning

confidence: 78%

Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated rats

Monir

Mahmoud

Galal

et al. 2020

Preprint

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“…NM-laden cells displayed high levels of oxidative stress and disturbed mitochondrial respiration, which may be responsible for the substantial cell death observed in this study [169]. Furthermore, complex I inhibition and mitochondria-induced ROS are suggested to account for the majority of neuron cell loss in PD as dopaminergic neurons are particularly susceptible to oxidative stress (Table 1) [68,170,171]. It was found that mitochondrial function and complex I activity was interrupted in the striatum and cortex of the rats with PD induced by rotenone treatment (Figure 3B) [68].…”

Section: Inflammaging In Neurodegenerative Diseasesmentioning

confidence: 98%

“…Furthermore, complex I inhibition and mitochondria-induced ROS are suggested to account for the majority of neuron cell loss in PD as dopaminergic neurons are particularly susceptible to oxidative stress (Table 1) [68,170,171]. It was found that mitochondrial function and complex I activity was interrupted in the striatum and cortex of the rats with PD induced by rotenone treatment (Figure 3B) [68]. Elevation in ROS levels can lead to oxidation of lipid, protein, and DNA, as well as induce neuron cell apoptosis [62].…”

Section: Inflammaging In Neurodegenerative Diseasesmentioning

confidence: 99%

Inflammaging and Oxidative Stress in Human Diseases: From Molecular Mechanisms to Novel Treatments

Zuo

Stetskiv

et al. 2019

IJMS

294

161

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It has been proposed that a chronic state of inflammation correlated with aging known as inflammaging, is implicated in multiple disease states commonly observed in the elderly population. Inflammaging is associated with over-abundance of reactive oxygen species in the cell, which can lead to oxidation and damage of cellular components, increased inflammation, and activation of cell death pathways. This review focuses on inflammaging and its contribution to various age-related diseases such as cardiovascular disease, cancer, neurodegenerative diseases, chronic obstructive pulmonary disease, diabetes, and rheumatoid arthritis. Recently published mechanistic details of the roles of reactive oxygen species in inflammaging and various diseases will also be discussed. Advancements in potential treatments to ameliorate inflammaging, oxidative stress, and consequently, reduce the morbidity of multiple disease states will be explored.

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“…Complex I, also known as NADH oxidoreductase of the electron transport chain (ETC) transfers electrons from NADH to ubiquinone and so plays a key role in oxidative phosphorylation. Complex I is vulnerable to oxidative damage, and its inhibition is also strongly associated with the generation of ROS such as superoxide and hydrogen peroxide presenting a positive feedback loop [ 8 , 9 , 10 ]. Currently, neurotoxins that target complex I like 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone are used to induce parkinsonism in both in vitro and in vivo models for research, and treatment with these drugs is known to induce oxidative stress [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

Dietary Antioxidants and Parkinson’s Disease

Park

Ellis

2020

Antioxidants

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Parkinson’s disease (PD) is a neurodegenerative disorder caused by the depletion of dopaminergic neurons in the basal ganglia, the movement center of the brain. Approximately 60,000 people are diagnosed with PD in the United States each year. Although the direct cause of PD can vary, accumulation of oxidative stress-induced neuronal damage due to increased production of reactive oxygen species (ROS) or impaired intracellular antioxidant defenses invariably occurs at the cellular levels. Pharmaceuticals such as dopaminergic prodrugs and agonists can alleviate some of the symptoms of PD. Currently, however, there is no treatment to halt the progression of PD pathology. Due to the nature of PD, a long and progressive neurodegenerative process, strategies to prevent or delay PD pathology may be well suited to lifestyle changes like dietary modification with antioxidant-rich foods to improve intracellular redox homeostasis. In this review, we discuss cellular and genetic factors that increase oxidative stress in PD. We also discuss neuroprotective roles of dietary antioxidants including vitamin C, vitamin E, carotenoids, selenium, and polyphenols along with their potential mechanisms to alleviate PD pathology.

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Complex I syndrome in striatum and frontal cortex in a rat model of Parkinson disease

Cited by 22 publications

References 61 publications

Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated rats

Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated rats

Inflammaging and Oxidative Stress in Human Diseases: From Molecular Mechanisms to Novel Treatments

Dietary Antioxidants and Parkinson’s Disease

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