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Vitamin C Protects Porcine Oocytes From Microcystin-LR Toxicity During Maturation

Microcystin-leucine arginine (MC-LR) is the most toxic cyanotoxin found in water bodies. Microcystins are produced as secondary products of cyanobacteria metabolism. They have a stable structure, and can bioaccumulate in living organisms. Humans and livestock who drink fresh water containing MC-LR c...

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Autores principales: Zhang, Xue, Zhou, Changyin, Li, Weijian, Li, Juan, Wu, Wangjun, Tao, Jingli, Liu, Honglin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7578366/
https://www.ncbi.nlm.nih.gov/pubmed/33134299
http://dx.doi.org/10.3389/fcell.2020.582715
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author Zhang, Xue
Zhou, Changyin
Li, Weijian
Li, Juan
Wu, Wangjun
Tao, Jingli
Liu, Honglin
author_facet Zhang, Xue
Zhou, Changyin
Li, Weijian
Li, Juan
Wu, Wangjun
Tao, Jingli
Liu, Honglin
author_sort Zhang, Xue
collection PubMed
description Microcystin-leucine arginine (MC-LR) is the most toxic cyanotoxin found in water bodies. Microcystins are produced as secondary products of cyanobacteria metabolism. They have a stable structure, and can bioaccumulate in living organisms. Humans and livestock who drink fresh water containing MC-LR can be poisoned. However, few studies have reported the effects of MC-LR exposure on livestock or human reproduction. In this study, we used porcine oocytes as a model to explore the effects of MC-LR on oocyte maturation, and studied the impact of vitamin C (VC) administration on MC-LR-induced meiosis defects. Exposure to MC-LR significantly restricted cumulus cell expansion and decreased first polar body extrusion. Further studies showed that MC-LR exposure led to meiosis arrest by disturbing cytoskeleton dynamics with MC-LR exposed oocytes displaying aberrant spindle organization, low levels of acetylate α-tubulin, and disturbed actin polymerization. Additionally, MC-LR exposure impaired cytoplasmic maturation by inducing mitochondria dysfunction. Moreover, MC-LR also produced abnormal epigenetic modifications, and induced high levels of oxidative stress, caused DNA damage and early apoptosis. The administration of VC provided partial protection from all of the defects observed in oocytes exposed to MC-LR. These results demonstrate that MC-LR has a toxic effect on oocyte meiosis through mitochondrial dysfunction-induced ROS, DNA damage and early apoptosis. Supplementation of VC is able to protect against MC-LR-induced oocyte damage and represents a potential therapeutic strategy to improve the quality of MC-LR-exposed oocytes.
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spelling pubmed-75783662020-10-30 Vitamin C Protects Porcine Oocytes From Microcystin-LR Toxicity During Maturation Zhang, Xue Zhou, Changyin Li, Weijian Li, Juan Wu, Wangjun Tao, Jingli Liu, Honglin Front Cell Dev Biol Cell and Developmental Biology Microcystin-leucine arginine (MC-LR) is the most toxic cyanotoxin found in water bodies. Microcystins are produced as secondary products of cyanobacteria metabolism. They have a stable structure, and can bioaccumulate in living organisms. Humans and livestock who drink fresh water containing MC-LR can be poisoned. However, few studies have reported the effects of MC-LR exposure on livestock or human reproduction. In this study, we used porcine oocytes as a model to explore the effects of MC-LR on oocyte maturation, and studied the impact of vitamin C (VC) administration on MC-LR-induced meiosis defects. Exposure to MC-LR significantly restricted cumulus cell expansion and decreased first polar body extrusion. Further studies showed that MC-LR exposure led to meiosis arrest by disturbing cytoskeleton dynamics with MC-LR exposed oocytes displaying aberrant spindle organization, low levels of acetylate α-tubulin, and disturbed actin polymerization. Additionally, MC-LR exposure impaired cytoplasmic maturation by inducing mitochondria dysfunction. Moreover, MC-LR also produced abnormal epigenetic modifications, and induced high levels of oxidative stress, caused DNA damage and early apoptosis. The administration of VC provided partial protection from all of the defects observed in oocytes exposed to MC-LR. These results demonstrate that MC-LR has a toxic effect on oocyte meiosis through mitochondrial dysfunction-induced ROS, DNA damage and early apoptosis. Supplementation of VC is able to protect against MC-LR-induced oocyte damage and represents a potential therapeutic strategy to improve the quality of MC-LR-exposed oocytes. Frontiers Media S.A. 2020-10-08 /pmc/articles/PMC7578366/ /pubmed/33134299 http://dx.doi.org/10.3389/fcell.2020.582715 Text en Copyright © 2020 Zhang, Zhou, Li, Li, Wu, Tao and Liu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cell and Developmental Biology
Zhang, Xue
Zhou, Changyin
Li, Weijian
Li, Juan
Wu, Wangjun
Tao, Jingli
Liu, Honglin
Vitamin C Protects Porcine Oocytes From Microcystin-LR Toxicity During Maturation
title Vitamin C Protects Porcine Oocytes From Microcystin-LR Toxicity During Maturation
title_full Vitamin C Protects Porcine Oocytes From Microcystin-LR Toxicity During Maturation
title_fullStr Vitamin C Protects Porcine Oocytes From Microcystin-LR Toxicity During Maturation
title_full_unstemmed Vitamin C Protects Porcine Oocytes From Microcystin-LR Toxicity During Maturation
title_short Vitamin C Protects Porcine Oocytes From Microcystin-LR Toxicity During Maturation
title_sort vitamin c protects porcine oocytes from microcystin-lr toxicity during maturation
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7578366/
https://www.ncbi.nlm.nih.gov/pubmed/33134299
http://dx.doi.org/10.3389/fcell.2020.582715
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