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Carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish

Carbofuran is a carbamate pesticide, widely used in agricultural practices to increase crop productivity. In mammals, carbofuran is known to cause several untoward effects, such as apoptosis in the hippocampal neuron, oxidative stress, loss of memory and chromosomal anomalies. Most of these effects...

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Autores principales: Khan, Alam, Fahad, Talukdar Mohammad, Akther, Tanjima, Zaman, Tanjeena, Hasan, Md Faruk, Islam Khan, Md Rafiqual, Islam, Mohammad Saiful, Kishi, Shuji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812278/
https://www.ncbi.nlm.nih.gov/pubmed/33277797
http://dx.doi.org/10.1111/jcmm.16171
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author Khan, Alam
Fahad, Talukdar Mohammad
Akther, Tanjima
Zaman, Tanjeena
Hasan, Md Faruk
Islam Khan, Md Rafiqual
Islam, Mohammad Saiful
Kishi, Shuji
author_facet Khan, Alam
Fahad, Talukdar Mohammad
Akther, Tanjima
Zaman, Tanjeena
Hasan, Md Faruk
Islam Khan, Md Rafiqual
Islam, Mohammad Saiful
Kishi, Shuji
author_sort Khan, Alam
collection PubMed
description Carbofuran is a carbamate pesticide, widely used in agricultural practices to increase crop productivity. In mammals, carbofuran is known to cause several untoward effects, such as apoptosis in the hippocampal neuron, oxidative stress, loss of memory and chromosomal anomalies. Most of these effects are implicated with cellular senescence. Therefore, the present study aimed to determine the effect of carbofuran on cellular senescence and biological ageing. Spinster homolog 1 (Spns1) is a transmembrane transporter, regulates autolysosomal biogenesis and plays a role in cellular senescence and survival. Using senescence‐associated β‐galactosidase staining, we found that carbofuran accelerates the cellular senescence in spns1 mutant zebrafish. The yolk opaqueness, a premature ageing phenotype in zebrafish embryos, was accelerated by carbofuran treatment. In the survival study, carbofuran shortened the life span of spns1 mutant zebrafish. Autophagy is the cellular lysosomal degradation, usually up‐regulated in the senescent cells. To know the impact of carbofuran exposure on autophagy progress, we established a double‐transgenic zebrafish line, harbouring EGFP‐tagged LC3‐II and mCherry‐tagged Lamp1 on spns1 mutant background, whereas we found, carbofuran exposure synergistically accelerates autolysosome formation with insufficient lysosome‐mediated degradation. Our data collectively suggest that carbofuran exposure synergistically accelerates the cellular senescence and affects biological ageing in spns1 defective animals.
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spelling pubmed-78122782021-01-22 Carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish Khan, Alam Fahad, Talukdar Mohammad Akther, Tanjima Zaman, Tanjeena Hasan, Md Faruk Islam Khan, Md Rafiqual Islam, Mohammad Saiful Kishi, Shuji J Cell Mol Med Original Articles Carbofuran is a carbamate pesticide, widely used in agricultural practices to increase crop productivity. In mammals, carbofuran is known to cause several untoward effects, such as apoptosis in the hippocampal neuron, oxidative stress, loss of memory and chromosomal anomalies. Most of these effects are implicated with cellular senescence. Therefore, the present study aimed to determine the effect of carbofuran on cellular senescence and biological ageing. Spinster homolog 1 (Spns1) is a transmembrane transporter, regulates autolysosomal biogenesis and plays a role in cellular senescence and survival. Using senescence‐associated β‐galactosidase staining, we found that carbofuran accelerates the cellular senescence in spns1 mutant zebrafish. The yolk opaqueness, a premature ageing phenotype in zebrafish embryos, was accelerated by carbofuran treatment. In the survival study, carbofuran shortened the life span of spns1 mutant zebrafish. Autophagy is the cellular lysosomal degradation, usually up‐regulated in the senescent cells. To know the impact of carbofuran exposure on autophagy progress, we established a double‐transgenic zebrafish line, harbouring EGFP‐tagged LC3‐II and mCherry‐tagged Lamp1 on spns1 mutant background, whereas we found, carbofuran exposure synergistically accelerates autolysosome formation with insufficient lysosome‐mediated degradation. Our data collectively suggest that carbofuran exposure synergistically accelerates the cellular senescence and affects biological ageing in spns1 defective animals. John Wiley and Sons Inc. 2020-12-04 2021-01 /pmc/articles/PMC7812278/ /pubmed/33277797 http://dx.doi.org/10.1111/jcmm.16171 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Khan, Alam
Fahad, Talukdar Mohammad
Akther, Tanjima
Zaman, Tanjeena
Hasan, Md Faruk
Islam Khan, Md Rafiqual
Islam, Mohammad Saiful
Kishi, Shuji
Carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish
title Carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish
title_full Carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish
title_fullStr Carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish
title_full_unstemmed Carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish
title_short Carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish
title_sort carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812278/
https://www.ncbi.nlm.nih.gov/pubmed/33277797
http://dx.doi.org/10.1111/jcmm.16171
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