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Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations
Vitamin B(12) deficiency causes significant changes in cellular metabolism leading to various clinical symptoms, such as hematological, psychiatric, and neurological disorders. We hypothesize that skin pigmentation disorders may be a diagnostically important manifestation of vitamin B(12) deficiency...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163934/ https://www.ncbi.nlm.nih.gov/pubmed/30235895 http://dx.doi.org/10.3390/ijms19092845 |
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author | Rzepka, Zuzanna Respondek, Michalina Rok, Jakub Beberok, Artur ó Proinsias, Keith Gryko, Dorota Wrześniok, Dorota |
author_facet | Rzepka, Zuzanna Respondek, Michalina Rok, Jakub Beberok, Artur ó Proinsias, Keith Gryko, Dorota Wrześniok, Dorota |
author_sort | Rzepka, Zuzanna |
collection | PubMed |
description | Vitamin B(12) deficiency causes significant changes in cellular metabolism leading to various clinical symptoms, such as hematological, psychiatric, and neurological disorders. We hypothesize that skin pigmentation disorders may be a diagnostically important manifestation of vitamin B(12) deficiency, however the cellular and molecular mechanisms underlying these effects remain unknown. The aim of this study was to examine the effect of vitamin B(12) deficiency on melanocytes homeostasis. Hypocobalaminemia in vitro model was developed by treating epidermal melanocytes with synthesized vitamin B(12) antagonist—hydroxycobalamin(c-lactam). The cells were examined using immunoenzymatic, spectrophotometric, and fluorimetric assays as well as image cytometry. Significant melanogenesis stimulation—the increase of relative melanin content and tyrosinase activity up to 131% and 135%, respectively—has been indicated. Cobalamin-deficient cells displayed the elevation (by 120%) in reactive oxygen species level. Moreover, the redox status imbalance was stated. The study provided a scientific evidence for melanocytes homeostasis disturbance under hypocobalaminemia, thus indicating a significant element of the hyperpigmentation mechanism due to vitamin B(12) deficiency. Furthermore, the implication between pigmentary and hematological and/or neuropsychiatric symptoms in cobalamin-deficient patients may be an important issue. |
format | Online Article Text |
id | pubmed-6163934 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-61639342018-10-10 Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations Rzepka, Zuzanna Respondek, Michalina Rok, Jakub Beberok, Artur ó Proinsias, Keith Gryko, Dorota Wrześniok, Dorota Int J Mol Sci Article Vitamin B(12) deficiency causes significant changes in cellular metabolism leading to various clinical symptoms, such as hematological, psychiatric, and neurological disorders. We hypothesize that skin pigmentation disorders may be a diagnostically important manifestation of vitamin B(12) deficiency, however the cellular and molecular mechanisms underlying these effects remain unknown. The aim of this study was to examine the effect of vitamin B(12) deficiency on melanocytes homeostasis. Hypocobalaminemia in vitro model was developed by treating epidermal melanocytes with synthesized vitamin B(12) antagonist—hydroxycobalamin(c-lactam). The cells were examined using immunoenzymatic, spectrophotometric, and fluorimetric assays as well as image cytometry. Significant melanogenesis stimulation—the increase of relative melanin content and tyrosinase activity up to 131% and 135%, respectively—has been indicated. Cobalamin-deficient cells displayed the elevation (by 120%) in reactive oxygen species level. Moreover, the redox status imbalance was stated. The study provided a scientific evidence for melanocytes homeostasis disturbance under hypocobalaminemia, thus indicating a significant element of the hyperpigmentation mechanism due to vitamin B(12) deficiency. Furthermore, the implication between pigmentary and hematological and/or neuropsychiatric symptoms in cobalamin-deficient patients may be an important issue. MDPI 2018-09-19 /pmc/articles/PMC6163934/ /pubmed/30235895 http://dx.doi.org/10.3390/ijms19092845 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Rzepka, Zuzanna Respondek, Michalina Rok, Jakub Beberok, Artur ó Proinsias, Keith Gryko, Dorota Wrześniok, Dorota Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations |
title | Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations |
title_full | Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations |
title_fullStr | Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations |
title_full_unstemmed | Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations |
title_short | Vitamin B(12) Deficiency Induces Imbalance in Melanocytes Homeostasis—A Cellular Basis of Hypocobalaminemia Pigmentary Manifestations |
title_sort | vitamin b(12) deficiency induces imbalance in melanocytes homeostasis—a cellular basis of hypocobalaminemia pigmentary manifestations |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163934/ https://www.ncbi.nlm.nih.gov/pubmed/30235895 http://dx.doi.org/10.3390/ijms19092845 |
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