Vitamin E Supplementation Reduces Cellular Loss in the Brain of a Premature Aging Mouse Model

G La Fata; N van Vliet; S Barnhoorn; R M C Brandt; S Etheve; E Chenal; C Grunenwald; N Seifert; P Weber; J H J Hoeijmakers; M H Mohajeri; W P Vermeij

doi:10.14283/jpad.2017.30

Vitamin E Supplementation Reduces Cellular Loss in the Brain of a Premature Aging Mouse Model

G La Fata, N van Vliet, S Barnhoorn, R M C Brandt, S Etheve, E Chenal, C Grunenwald, N Seifert, P Weber, J H J Hoeijmakers, M H Mohajeri, W P Vermeij

Research output: Contribution to journal › Article › peer-review

22 Citations (Scopus)

Abstract

BACKGROUND: Aging is a highly complex biological process driven by multiple factors. Its progression can partially be influenced by nutritional interventions. Vitamin E is a lipid-soluble anti-oxidant that is investigated as nutritional supplement for its ability to prevent or delay the onset of specific aging pathologies, including neurodegenerative disorders.

PURPOSE: We aimed here to investigate the effect of vitamin E during aging progression in a well characterized mouse model for premature aging.

METHOD: Xpg-/- animals received diets with low (~2.5 mg/kg feed), medium (75 mg/kg feed) or high (375 mg/kg feed) vitamin E concentration and their phenotype was monitored during aging progression. Vitamin E content was analyzed in the feed, for stability reasons, and in mouse plasma, brain, and liver, for effectiveness of the treatment. Subsequent age-related changes were monitored for improvement by increased vitamin E or worsening by depletion in both liver and nervous system, organs sensitive to oxidative stress.

RESULTS: Mice supplemented with high levels of vitamin E showed a delayed onset of age-related body weight decline and appearance of tremors when compared to mice with a low dietary vitamin E intake. DNA damage resulting in liver abnormalities such as changes in polyploidy, was considerably prevented by elevated amounts of vitamin E. Additionally, immunohistochemical analyses revealed that high intake of vitamin E, when compared with low and medium levels of vitamin E in the diet, reduces the number of p53-positive cells throughout the brain, indicative of a lower number of cells dying due to DNA damage accumulated over time.

CONCLUSIONS: Our data underline a neuroprotective role of vitamin E in the premature aging animal model used in this study, likely via a reduction of oxidative stress, and implies the importance of improved nutrition to sustain health.

Original language	English
Pages (from-to)	226-235
Number of pages	10
Journal	The journal of prevention of Alzheimer's disease
Volume	4
Issue number	4
DOIs	https://doi.org/10.14283/jpad.2017.30
Publication status	Published - 2017
Externally published	Yes

Keywords

Aging, Premature/diet therapy
Animals
Body Weight
Brain/metabolism
Cell Death/physiology
DNA-Binding Proteins/deficiency
Dietary Supplements
Disease Models, Animal
Eating
Endonucleases/deficiency
Liver/metabolism
Mice, Inbred C57BL
Mice, Knockout
Nuclear Proteins/deficiency
Oxidative Stress/physiology
Random Allocation
Time Factors
Transcription Factors/deficiency
Tremor/diet therapy
Vitamin E/administration & dosage

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10.14283/jpad.2017.30

Cite this

La Fata, G., van Vliet, N., Barnhoorn, S., Brandt, R. M. C., Etheve, S., Chenal, E., Grunenwald, C., Seifert, N., Weber, P., Hoeijmakers, J. H. J., Mohajeri, M. H., & Vermeij, W. P. (2017). Vitamin E Supplementation Reduces Cellular Loss in the Brain of a Premature Aging Mouse Model. The journal of prevention of Alzheimer's disease, 4(4), 226-235. https://doi.org/10.14283/jpad.2017.30

@article{6f6e1f10bffc4ab9862023b51f4346a8,

title = "Vitamin E Supplementation Reduces Cellular Loss in the Brain of a Premature Aging Mouse Model",

abstract = "BACKGROUND: Aging is a highly complex biological process driven by multiple factors. Its progression can partially be influenced by nutritional interventions. Vitamin E is a lipid-soluble anti-oxidant that is investigated as nutritional supplement for its ability to prevent or delay the onset of specific aging pathologies, including neurodegenerative disorders.PURPOSE: We aimed here to investigate the effect of vitamin E during aging progression in a well characterized mouse model for premature aging.METHOD: Xpg-/- animals received diets with low (~2.5 mg/kg feed), medium (75 mg/kg feed) or high (375 mg/kg feed) vitamin E concentration and their phenotype was monitored during aging progression. Vitamin E content was analyzed in the feed, for stability reasons, and in mouse plasma, brain, and liver, for effectiveness of the treatment. Subsequent age-related changes were monitored for improvement by increased vitamin E or worsening by depletion in both liver and nervous system, organs sensitive to oxidative stress.RESULTS: Mice supplemented with high levels of vitamin E showed a delayed onset of age-related body weight decline and appearance of tremors when compared to mice with a low dietary vitamin E intake. DNA damage resulting in liver abnormalities such as changes in polyploidy, was considerably prevented by elevated amounts of vitamin E. Additionally, immunohistochemical analyses revealed that high intake of vitamin E, when compared with low and medium levels of vitamin E in the diet, reduces the number of p53-positive cells throughout the brain, indicative of a lower number of cells dying due to DNA damage accumulated over time.CONCLUSIONS: Our data underline a neuroprotective role of vitamin E in the premature aging animal model used in this study, likely via a reduction of oxidative stress, and implies the importance of improved nutrition to sustain health.",

keywords = "Aging, Premature/diet therapy, Animals, Body Weight, Brain/metabolism, Cell Death/physiology, DNA-Binding Proteins/deficiency, Dietary Supplements, Disease Models, Animal, Eating, Endonucleases/deficiency, Liver/metabolism, Mice, Inbred C57BL, Mice, Knockout, Nuclear Proteins/deficiency, Oxidative Stress/physiology, Random Allocation, Time Factors, Transcription Factors/deficiency, Tremor/diet therapy, Vitamin E/administration & dosage",

author = "{La Fata}, G and {van Vliet}, N and S Barnhoorn and Brandt, {R M C} and S Etheve and E Chenal and C Grunenwald and N Seifert and P Weber and Hoeijmakers, {J H J} and Mohajeri, {M H} and Vermeij, {W P}",

year = "2017",

doi = "10.14283/jpad.2017.30",

language = "English",

volume = "4",

pages = "226--235",

journal = "The journal of prevention of Alzheimer's disease",

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publisher = "Serdi-Editions",

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La Fata, G, van Vliet, N, Barnhoorn, S, Brandt, RMC, Etheve, S, Chenal, E, Grunenwald, C, Seifert, N, Weber, P, Hoeijmakers, JHJ, Mohajeri, MH & Vermeij, WP 2017, 'Vitamin E Supplementation Reduces Cellular Loss in the Brain of a Premature Aging Mouse Model', The journal of prevention of Alzheimer's disease, vol. 4, no. 4, pp. 226-235. https://doi.org/10.14283/jpad.2017.30

TY - JOUR

T1 - Vitamin E Supplementation Reduces Cellular Loss in the Brain of a Premature Aging Mouse Model

AU - La Fata, G

AU - van Vliet, N

AU - Barnhoorn, S

AU - Brandt, R M C

AU - Etheve, S

AU - Chenal, E

AU - Grunenwald, C

AU - Seifert, N

AU - Weber, P

AU - Hoeijmakers, J H J

AU - Mohajeri, M H

AU - Vermeij, W P

PY - 2017

Y1 - 2017

N2 - BACKGROUND: Aging is a highly complex biological process driven by multiple factors. Its progression can partially be influenced by nutritional interventions. Vitamin E is a lipid-soluble anti-oxidant that is investigated as nutritional supplement for its ability to prevent or delay the onset of specific aging pathologies, including neurodegenerative disorders.PURPOSE: We aimed here to investigate the effect of vitamin E during aging progression in a well characterized mouse model for premature aging.METHOD: Xpg-/- animals received diets with low (~2.5 mg/kg feed), medium (75 mg/kg feed) or high (375 mg/kg feed) vitamin E concentration and their phenotype was monitored during aging progression. Vitamin E content was analyzed in the feed, for stability reasons, and in mouse plasma, brain, and liver, for effectiveness of the treatment. Subsequent age-related changes were monitored for improvement by increased vitamin E or worsening by depletion in both liver and nervous system, organs sensitive to oxidative stress.RESULTS: Mice supplemented with high levels of vitamin E showed a delayed onset of age-related body weight decline and appearance of tremors when compared to mice with a low dietary vitamin E intake. DNA damage resulting in liver abnormalities such as changes in polyploidy, was considerably prevented by elevated amounts of vitamin E. Additionally, immunohistochemical analyses revealed that high intake of vitamin E, when compared with low and medium levels of vitamin E in the diet, reduces the number of p53-positive cells throughout the brain, indicative of a lower number of cells dying due to DNA damage accumulated over time.CONCLUSIONS: Our data underline a neuroprotective role of vitamin E in the premature aging animal model used in this study, likely via a reduction of oxidative stress, and implies the importance of improved nutrition to sustain health.

AB - BACKGROUND: Aging is a highly complex biological process driven by multiple factors. Its progression can partially be influenced by nutritional interventions. Vitamin E is a lipid-soluble anti-oxidant that is investigated as nutritional supplement for its ability to prevent or delay the onset of specific aging pathologies, including neurodegenerative disorders.PURPOSE: We aimed here to investigate the effect of vitamin E during aging progression in a well characterized mouse model for premature aging.METHOD: Xpg-/- animals received diets with low (~2.5 mg/kg feed), medium (75 mg/kg feed) or high (375 mg/kg feed) vitamin E concentration and their phenotype was monitored during aging progression. Vitamin E content was analyzed in the feed, for stability reasons, and in mouse plasma, brain, and liver, for effectiveness of the treatment. Subsequent age-related changes were monitored for improvement by increased vitamin E or worsening by depletion in both liver and nervous system, organs sensitive to oxidative stress.RESULTS: Mice supplemented with high levels of vitamin E showed a delayed onset of age-related body weight decline and appearance of tremors when compared to mice with a low dietary vitamin E intake. DNA damage resulting in liver abnormalities such as changes in polyploidy, was considerably prevented by elevated amounts of vitamin E. Additionally, immunohistochemical analyses revealed that high intake of vitamin E, when compared with low and medium levels of vitamin E in the diet, reduces the number of p53-positive cells throughout the brain, indicative of a lower number of cells dying due to DNA damage accumulated over time.CONCLUSIONS: Our data underline a neuroprotective role of vitamin E in the premature aging animal model used in this study, likely via a reduction of oxidative stress, and implies the importance of improved nutrition to sustain health.

KW - Aging, Premature/diet therapy

KW - Animals

KW - Body Weight

KW - Brain/metabolism

KW - Cell Death/physiology

KW - DNA-Binding Proteins/deficiency

KW - Dietary Supplements

KW - Disease Models, Animal

KW - Eating

KW - Endonucleases/deficiency

KW - Liver/metabolism

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Nuclear Proteins/deficiency

KW - Oxidative Stress/physiology

KW - Random Allocation

KW - Time Factors

KW - Transcription Factors/deficiency

KW - Tremor/diet therapy

KW - Vitamin E/administration & dosage

U2 - 10.14283/jpad.2017.30

DO - 10.14283/jpad.2017.30

M3 - Article

C2 - 29181487

SN - 2274-5807

VL - 4

SP - 226

EP - 235

JO - The journal of prevention of Alzheimer's disease

JF - The journal of prevention of Alzheimer's disease

IS - 4

ER -

Vitamin E Supplementation Reduces Cellular Loss in the Brain of a Premature Aging Mouse Model

Abstract

Keywords

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