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6 results on '"Brandt, R. M. C."'

1. Restricted diet delays accelerated ageing and genomic stress in DNA-repair-deficient mice

Author

Vermeij, W. P., Doll, M. E. T., Reiling, E., Jaarsma, D., Payan-Gomez, C., Bombardieri, C. R., Wu, H., Roks, A. J. M., Botter, S. M., van der Eerden, B. C., Youssef, S. A., Kuiper, R. V., Nagarajah, B., van Oostrom, C. T., Brandt, R. M. C., Barnhoorn, S., Imholz, S., Pennings, J. L. A., de Bruin, A., Gyenis, ., Pothof, J., Vijg, J., van Steeg, H., and Hoeijmakers, J. H. J.

Subjects
DNA damage -- Prevention, Aging (Biology) -- Health aspects -- Genetic aspects, Diet -- Methods -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): W. P. Vermeij [1]; M. E. T. Doll (corresponding author) [2]; E. Reiling [1, 2]; D. Jaarsma [3]; C. Payan-Gomez [1, 4]; C. R. Bombardieri [1]; H. Wu [5]; [...]

Published
2016
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2. Vitamin E Supplementation Reduces Cellular Loss in the Brain of a Premature Aging Mouse Model

Author

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., 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., and Vermeij, W. P.

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 (similar to 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.

Published
2017

3. Restricted diet delays accelerated ageing and genomic stress in DNA-repair-deficient mice

Author

Regenerative Medicine, Stem Cells & Cancer, dPB RMSC, LS onderwijskwaliteit, LS Pathobiologie, Dep Biomolecular Health Sciences, Vermeij, W P, Dollé, M E T, Reiling, E, Jaarsma, D, Payan-Gomez, C, Bombardieri, C R, Wu, H, Roks, A J M, Botter, S M, van der Eerden, B C, Youssef, S A, Kuiper, R V, Nagarajah, B, van Oostrom, C T, Brandt, R M C, Barnhoorn, S, Imholz, S, Pennings, J L A, de Bruin, A, Gyenis, Á, Pothof, J, Vijg, J, van Steeg, H, Hoeijmakers, J H J, Regenerative Medicine, Stem Cells & Cancer, dPB RMSC, LS onderwijskwaliteit, LS Pathobiologie, Dep Biomolecular Health Sciences, Vermeij, W P, Dollé, M E T, Reiling, E, Jaarsma, D, Payan-Gomez, C, Bombardieri, C R, Wu, H, Roks, A J M, Botter, S M, van der Eerden, B C, Youssef, S A, Kuiper, R V, Nagarajah, B, van Oostrom, C T, Brandt, R M C, Barnhoorn, S, Imholz, S, Pennings, J L A, de Bruin, A, Gyenis, Á, Pothof, J, Vijg, J, van Steeg, H, and Hoeijmakers, J H J

Published
2016

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

Author

La Fata G, van Vliet N, Barnhoorn S, Brandt RMC, Etheve S, Chenal E, Grunenwald C, Seifert N, Weber P, Hoeijmakers JHJ, Mohajeri MH, and Vermeij WP

Subjects
Aging, Premature metabolism, Animals, Body Weight, Brain metabolism, DNA-Binding Proteins deficiency, DNA-Binding Proteins genetics, Disease Models, Animal, Eating, Endonucleases deficiency, Endonucleases genetics, Liver metabolism, Liver pathology, Mice, Inbred C57BL, Mice, Knockout, Nuclear Proteins deficiency, Nuclear Proteins genetics, Oxidative Stress physiology, Random Allocation, Time Factors, Transcription Factors deficiency, Transcription Factors genetics, Tremor diet therapy, Tremor metabolism, Tremor pathology, Vitamin E metabolism, Aging, Premature diet therapy, Aging, Premature pathology, Brain pathology, Cell Death physiology, Dietary Supplements, Vitamin E administration & dosage
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., Competing Interests: G.L.F, S.E., E.C., C.G., N.S., P.W., and M.H.M. are employees of DSM Nutritional Products. All other authors declare no conflict of interests.

Published
2017
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