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Lutein protects dopaminergic neurons against MPTP-induced apoptotic death and motor dysfunction by ameliorating mitochondrial disruption and oxidative stress.
Nutr Neurosci. 2016 Jul; 19(6):237-46.NN

Abstract

OBJECTIVE

Mitochondrial dysfunction and oxidative stress-mediated apoptosis plays an important role in various neurodegenerative diseases including Huntington's disease, Parkinson's disease (PD) and Alzheimer's disease (AD). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), the most widely used neurotoxin mimics the symptoms of PD by inhibiting mitochondrial complex I that stimulates excessive intracellular reactive oxygen species (ROS) and finally leads to mitochondrial-dependent apoptosis. Lutein, a carotenoid of xanthophyll family, is found abundantly in leafy green vegetables such as spinach, kale and in egg yolk, animal fat and human eye retinal macula. Increasing evidence indicates that lutein has offers benefits against neuronal damages during diabetic retinopathy, ischemia and AD by virtue of its mitochondrial protective, antioxidant and anti-apoptotic properties.

METHODS

Male C57BL/6 mice (23-26 g) were randomized and grouped in to Control, MPTP, and Lutein treated groups.

RESULTS

Lutein significantly reversed the loss of nigral dopaminergic neurons by increasing the striatal dopamine level in mice. Moreover, lutein-ameliorated MPTP induced mitochondrial dysfunction, oxidative stress and motor abnormalities. In addition, lutein repressed the MPTP-induced neuronal damage/apoptosis by inhibiting the activation of pro-apoptotic markers (Bax, caspases-3, 8 and 9) and enhancing anti-apoptotic marker (Bcl-2) expressions.

DISCUSSION

Our current results revealed that lutein possessed protection on dopaminergic neurons by enhancing antioxidant defense and diminishing mitochondrial dysfunction and apoptotic death, suggesting the potential benefits of lutein for PD treatment.

Links

Publisher Full Text (DOI)

Authors+Show Affiliations

Nataraj J
a Department of Biochemistry and Biotechnology, Faculty of Science , Annamalai University , Annamalai Nagar 608 002 , Tamilnadu , India.
Manivasagam T
a Department of Biochemistry and Biotechnology, Faculty of Science , Annamalai University , Annamalai Nagar 608 002 , Tamilnadu , India.
Thenmozhi AJ
a Department of Biochemistry and Biotechnology, Faculty of Science , Annamalai University , Annamalai Nagar 608 002 , Tamilnadu , India.
Essa MM
b Department of Food Science and Nutrition , CAMS, Sultan Qaboos University , Muscat , Oman.

MeSH

AnimalsAntiparkinson AgentsApoptosisApoptosis Regulatory ProteinsBehavior, AnimalBiomarkersDietary SupplementsDopamineDopaminergic NeuronsLuteinMPTP PoisoningMaleMice, Inbred C57BLMitochondriaMotor ActivityNerve Tissue ProteinsNeuroprotective AgentsOxidative StressParkinson DiseaseRandom AllocationSubstantia Nigra

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

25730317

Citation

Nataraj, Jagatheesan, et al. "Lutein Protects Dopaminergic Neurons Against MPTP-induced Apoptotic Death and Motor Dysfunction By Ameliorating Mitochondrial Disruption and Oxidative Stress." Nutritional Neuroscience, vol. 19, no. 6, 2016, pp. 237-46.
Nataraj J, Manivasagam T, Thenmozhi AJ, et al. Lutein protects dopaminergic neurons against MPTP-induced apoptotic death and motor dysfunction by ameliorating mitochondrial disruption and oxidative stress. Nutr Neurosci. 2016;19(6):237-46.
Nataraj, J., Manivasagam, T., Thenmozhi, A. J., & Essa, M. M. (2016). Lutein protects dopaminergic neurons against MPTP-induced apoptotic death and motor dysfunction by ameliorating mitochondrial disruption and oxidative stress. Nutritional Neuroscience, 19(6), 237-46. https://doi.org/10.1179/1476830515Y.0000000010
Nataraj J, et al. Lutein Protects Dopaminergic Neurons Against MPTP-induced Apoptotic Death and Motor Dysfunction By Ameliorating Mitochondrial Disruption and Oxidative Stress. Nutr Neurosci. 2016;19(6):237-46. PubMed PMID: 25730317.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lutein protects dopaminergic neurons against MPTP-induced apoptotic death and motor dysfunction by ameliorating mitochondrial disruption and oxidative stress. AU - Nataraj,Jagatheesan, AU - Manivasagam,Thamilarasan, AU - Thenmozhi,Arokiasamy Justin, AU - Essa,Musthafa Mohammed, Y1 - 2015/03/02/ PY - 2015/3/3/entrez PY - 2015/3/3/pubmed PY - 2017/3/11/medline KW - Apoptosis and lutein KW - Mitochondrial dysfunction KW - Oxidative stress KW - Parkinson's disease SP - 237 EP - 46 JF - Nutritional neuroscience JO - Nutr Neurosci VL - 19 IS - 6 N2 - OBJECTIVE: Mitochondrial dysfunction and oxidative stress-mediated apoptosis plays an important role in various neurodegenerative diseases including Huntington's disease, Parkinson's disease (PD) and Alzheimer's disease (AD). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), the most widely used neurotoxin mimics the symptoms of PD by inhibiting mitochondrial complex I that stimulates excessive intracellular reactive oxygen species (ROS) and finally leads to mitochondrial-dependent apoptosis. Lutein, a carotenoid of xanthophyll family, is found abundantly in leafy green vegetables such as spinach, kale and in egg yolk, animal fat and human eye retinal macula. Increasing evidence indicates that lutein has offers benefits against neuronal damages during diabetic retinopathy, ischemia and AD by virtue of its mitochondrial protective, antioxidant and anti-apoptotic properties. METHODS: Male C57BL/6 mice (23-26 g) were randomized and grouped in to Control, MPTP, and Lutein treated groups. RESULTS: Lutein significantly reversed the loss of nigral dopaminergic neurons by increasing the striatal dopamine level in mice. Moreover, lutein-ameliorated MPTP induced mitochondrial dysfunction, oxidative stress and motor abnormalities. In addition, lutein repressed the MPTP-induced neuronal damage/apoptosis by inhibiting the activation of pro-apoptotic markers (Bax, caspases-3, 8 and 9) and enhancing anti-apoptotic marker (Bcl-2) expressions. DISCUSSION: Our current results revealed that lutein possessed protection on dopaminergic neurons by enhancing antioxidant defense and diminishing mitochondrial dysfunction and apoptotic death, suggesting the potential benefits of lutein for PD treatment. SN - 1476-8305 UR - https://www.unboundmedicine.com/medline/citation/25730317/Lutein_protects_dopaminergic_neurons_against_MPTP_induced_apoptotic_death_and_motor_dysfunction_by_ameliorating_mitochondrial_disruption_and_oxidative_stress_ DB - PRIME DP - Unbound Medicine ER -