Microplastic particles cause intestinal damage and other adverse effects in zebrafish Danio rerio and nematode Caenorhabditis elegans

Microplastics have been frequently detected in aquatic environments, and there are increasing concerns about potential effects on biota. In this study, zebrafish Danio rerio and nematode Caenorhabditis elegans were used as model organisms for microplastic exposure in freshwater pelagic (i.e. water c...

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Published inThe Science of the total environment Vol. 619-620; pp. 1 - 8
Main Authors Lei, Lili, Wu, Siyu, Lu, Shibo, Liu, Mengting, Song, Yang, Fu, Zhenhuan, Shi, Huahong, Raley-Susman, Kathleen M., He, Defu
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.04.2018
Subjects
Online AccessGet full text
ISSN0048-9697
1879-1026
1879-1026
DOI10.1016/j.scitotenv.2017.11.103

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Abstract Microplastics have been frequently detected in aquatic environments, and there are increasing concerns about potential effects on biota. In this study, zebrafish Danio rerio and nematode Caenorhabditis elegans were used as model organisms for microplastic exposure in freshwater pelagic (i.e. water column) and benthic (i.e. sediment) environments. We investigated the toxic effects of five common types of microplastics: polyamides (PA), polyethylene (PE), polypropylene (PP), polyvinyl chloride (PVC) and polystyrene (PS) particles. Results showed no or low lethality in D. rerio after exposure for 10d at 0.001–10.0mgL−1 microplastics. The PA, PE, PP and/or PVC microplastics with ~70μm size caused intestinal damage including cracking of villi and splitting of enterocytes. Exposure to 5.0mgm−2 microplastics for 2d significantly inhibited survival rates, body length and reproduction of C. elegans. Moreover, exposure to microplastics reduced calcium levels but increased expression of the glutathione S-transferase 4 enzyme in the intestine, which indicates intestinal damage and oxidative stress are major effects of microplastic exposure. Among 0.1, 1.0 and 5.0μm sizes of fluorescently labeled PS, 1.0μm particles caused the highest lethality, the maximum accumulation, the lowest Ca2+ level in the intestine and the highest expression of glutathione S-transferase 4 in nematodes. Taken together, these findings suggest that intestinal damage is a key effect of microplastics; and that the toxicity of microplastics is closely dependent on their size, rather than their composition. [Display omitted] •Toxicity was comparatively studied on five common types of microplastics (MPs).•MPs with similar size induced intestine enterocyte damages in Danio rerio.•MPs reduced Ca2+ but increased gst-4 expression in intestine of Caenorhabditis elegans.•1.0μm MPs caused stronger toxicity than 0.1 or 5.0μm MPs in Caenorhabditis elegans.•Intestine damages are key effects of pristine MPs mostly dependent on their sizes.
AbstractList Microplastics have been frequently detected in aquatic environments, and there are increasing concerns about potential effects on biota. In this study, zebrafish Danio rerio and nematode Caenorhabditis elegans were used as model organisms for microplastic exposure in freshwater pelagic (i.e. water column) and benthic (i.e. sediment) environments. We investigated the toxic effects of five common types of microplastics: polyamides (PA), polyethylene (PE), polypropylene (PP), polyvinyl chloride (PVC) and polystyrene (PS) particles. Results showed no or low lethality in D. rerio after exposure for 10d at 0.001–10.0mgL⁻¹ microplastics. The PA, PE, PP and/or PVC microplastics with ~70μm size caused intestinal damage including cracking of villi and splitting of enterocytes. Exposure to 5.0mgm⁻² microplastics for 2d significantly inhibited survival rates, body length and reproduction of C. elegans. Moreover, exposure to microplastics reduced calcium levels but increased expression of the glutathione S-transferase 4 enzyme in the intestine, which indicates intestinal damage and oxidative stress are major effects of microplastic exposure. Among 0.1, 1.0 and 5.0μm sizes of fluorescently labeled PS, 1.0μm particles caused the highest lethality, the maximum accumulation, the lowest Ca²⁺ level in the intestine and the highest expression of glutathione S-transferase 4 in nematodes. Taken together, these findings suggest that intestinal damage is a key effect of microplastics; and that the toxicity of microplastics is closely dependent on their size, rather than their composition.
Microplastics have been frequently detected in aquatic environments, and there are increasing concerns about potential effects on biota. In this study, zebrafish Danio rerio and nematode Caenorhabditis elegans were used as model organisms for microplastic exposure in freshwater pelagic (i.e. water column) and benthic (i.e. sediment) environments. We investigated the toxic effects of five common types of microplastics: polyamides (PA), polyethylene (PE), polypropylene (PP), polyvinyl chloride (PVC) and polystyrene (PS) particles. Results showed no or low lethality in D. rerio after exposure for 10d at 0.001-10.0mgL-1 microplastics. The PA, PE, PP and/or PVC microplastics with ~70μm size caused intestinal damage including cracking of villi and splitting of enterocytes. Exposure to 5.0mgm-2 microplastics for 2d significantly inhibited survival rates, body length and reproduction of C. elegans. Moreover, exposure to microplastics reduced calcium levels but increased expression of the glutathione S-transferase 4 enzyme in the intestine, which indicates intestinal damage and oxidative stress are major effects of microplastic exposure. Among 0.1, 1.0 and 5.0μm sizes of fluorescently labeled PS, 1.0μm particles caused the highest lethality, the maximum accumulation, the lowest Ca2+ level in the intestine and the highest expression of glutathione S-transferase 4 in nematodes. Taken together, these findings suggest that intestinal damage is a key effect of microplastics; and that the toxicity of microplastics is closely dependent on their size, rather than their composition.Microplastics have been frequently detected in aquatic environments, and there are increasing concerns about potential effects on biota. In this study, zebrafish Danio rerio and nematode Caenorhabditis elegans were used as model organisms for microplastic exposure in freshwater pelagic (i.e. water column) and benthic (i.e. sediment) environments. We investigated the toxic effects of five common types of microplastics: polyamides (PA), polyethylene (PE), polypropylene (PP), polyvinyl chloride (PVC) and polystyrene (PS) particles. Results showed no or low lethality in D. rerio after exposure for 10d at 0.001-10.0mgL-1 microplastics. The PA, PE, PP and/or PVC microplastics with ~70μm size caused intestinal damage including cracking of villi and splitting of enterocytes. Exposure to 5.0mgm-2 microplastics for 2d significantly inhibited survival rates, body length and reproduction of C. elegans. Moreover, exposure to microplastics reduced calcium levels but increased expression of the glutathione S-transferase 4 enzyme in the intestine, which indicates intestinal damage and oxidative stress are major effects of microplastic exposure. Among 0.1, 1.0 and 5.0μm sizes of fluorescently labeled PS, 1.0μm particles caused the highest lethality, the maximum accumulation, the lowest Ca2+ level in the intestine and the highest expression of glutathione S-transferase 4 in nematodes. Taken together, these findings suggest that intestinal damage is a key effect of microplastics; and that the toxicity of microplastics is closely dependent on their size, rather than their composition.
Microplastics have been frequently detected in aquatic environments, and there are increasing concerns about potential effects on biota. In this study, zebrafish Danio rerio and nematode Caenorhabditis elegans were used as model organisms for microplastic exposure in freshwater pelagic (i.e. water column) and benthic (i.e. sediment) environments. We investigated the toxic effects of five common types of microplastics: polyamides (PA), polyethylene (PE), polypropylene (PP), polyvinyl chloride (PVC) and polystyrene (PS) particles. Results showed no or low lethality in D. rerio after exposure for 10d at 0.001-10.0mgL microplastics. The PA, PE, PP and/or PVC microplastics with ~70μm size caused intestinal damage including cracking of villi and splitting of enterocytes. Exposure to 5.0mgm microplastics for 2d significantly inhibited survival rates, body length and reproduction of C. elegans. Moreover, exposure to microplastics reduced calcium levels but increased expression of the glutathione S-transferase 4 enzyme in the intestine, which indicates intestinal damage and oxidative stress are major effects of microplastic exposure. Among 0.1, 1.0 and 5.0μm sizes of fluorescently labeled PS, 1.0μm particles caused the highest lethality, the maximum accumulation, the lowest Ca level in the intestine and the highest expression of glutathione S-transferase 4 in nematodes. Taken together, these findings suggest that intestinal damage is a key effect of microplastics; and that the toxicity of microplastics is closely dependent on their size, rather than their composition.
Microplastics have been frequently detected in aquatic environments, and there are increasing concerns about potential effects on biota. In this study, zebrafish Danio rerio and nematode Caenorhabditis elegans were used as model organisms for microplastic exposure in freshwater pelagic (i.e. water column) and benthic (i.e. sediment) environments. We investigated the toxic effects of five common types of microplastics: polyamides (PA), polyethylene (PE), polypropylene (PP), polyvinyl chloride (PVC) and polystyrene (PS) particles. Results showed no or low lethality in D. rerio after exposure for 10d at 0.001–10.0mgL−1 microplastics. The PA, PE, PP and/or PVC microplastics with ~70μm size caused intestinal damage including cracking of villi and splitting of enterocytes. Exposure to 5.0mgm−2 microplastics for 2d significantly inhibited survival rates, body length and reproduction of C. elegans. Moreover, exposure to microplastics reduced calcium levels but increased expression of the glutathione S-transferase 4 enzyme in the intestine, which indicates intestinal damage and oxidative stress are major effects of microplastic exposure. Among 0.1, 1.0 and 5.0μm sizes of fluorescently labeled PS, 1.0μm particles caused the highest lethality, the maximum accumulation, the lowest Ca2+ level in the intestine and the highest expression of glutathione S-transferase 4 in nematodes. Taken together, these findings suggest that intestinal damage is a key effect of microplastics; and that the toxicity of microplastics is closely dependent on their size, rather than their composition. [Display omitted] •Toxicity was comparatively studied on five common types of microplastics (MPs).•MPs with similar size induced intestine enterocyte damages in Danio rerio.•MPs reduced Ca2+ but increased gst-4 expression in intestine of Caenorhabditis elegans.•1.0μm MPs caused stronger toxicity than 0.1 or 5.0μm MPs in Caenorhabditis elegans.•Intestine damages are key effects of pristine MPs mostly dependent on their sizes.
Author He, Defu
Fu, Zhenhuan
Shi, Huahong
Raley-Susman, Kathleen M.
Liu, Mengting
Wu, Siyu
Song, Yang
Lei, Lili
Lu, Shibo
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  organization: Lab of Toxicology, School of Ecological and Environmental Sciences, East China Normal University, 500# DongChuan RD, Shanghai 200241, China
– sequence: 2
  givenname: Siyu
  surname: Wu
  fullname: Wu, Siyu
  organization: Lab of Toxicology, School of Ecological and Environmental Sciences, East China Normal University, 500# DongChuan RD, Shanghai 200241, China
– sequence: 3
  givenname: Shibo
  surname: Lu
  fullname: Lu, Shibo
  organization: Lab of Toxicology, School of Ecological and Environmental Sciences, East China Normal University, 500# DongChuan RD, Shanghai 200241, China
– sequence: 4
  givenname: Mengting
  surname: Liu
  fullname: Liu, Mengting
  organization: Lab of Toxicology, School of Ecological and Environmental Sciences, East China Normal University, 500# DongChuan RD, Shanghai 200241, China
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  givenname: Yang
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  fullname: Song, Yang
  organization: Lab of Toxicology, School of Ecological and Environmental Sciences, East China Normal University, 500# DongChuan RD, Shanghai 200241, China
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  givenname: Zhenhuan
  surname: Fu
  fullname: Fu, Zhenhuan
  organization: Lab of Toxicology, School of Ecological and Environmental Sciences, East China Normal University, 500# DongChuan RD, Shanghai 200241, China
– sequence: 7
  givenname: Huahong
  surname: Shi
  fullname: Shi, Huahong
  organization: State Key Laboratory of Estuarine and Coastal Research, East China Normal University, Shanghai 200062, China
– sequence: 8
  givenname: Kathleen M.
  surname: Raley-Susman
  fullname: Raley-Susman, Kathleen M.
  organization: Department of Biology, Vassar College, Poughkeepsie, NY 12604, USA
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  givenname: Defu
  orcidid: 0000-0002-0850-0881
  surname: He
  fullname: He, Defu
  email: dfhe@des.ecnu.edu.cn
  organization: Lab of Toxicology, School of Ecological and Environmental Sciences, East China Normal University, 500# DongChuan RD, Shanghai 200241, China
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29136530$$D View this record in MEDLINE/PubMed
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Keywords Caenorhabditis elegans
Oxidative stress
Microplastics
Intestinal damages
Ecotoxicity
Danio rerio
Language English
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Snippet Microplastics have been frequently detected in aquatic environments, and there are increasing concerns about potential effects on biota. In this study,...
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SubjectTerms adverse effects
Animals
aquatic environment
body length
Caenorhabditis elegans
Calcium
cracking
Danio rerio
Ecotoxicity
enterocytes
Environmental Monitoring
freshwater
Glutathione Transferase
Intestinal damages
Intestines - injuries
Microplastics
Oxidative Stress
plastics
Plastics - adverse effects
poly(vinyl chloride)
polyamides
polypropylenes
polystyrenes
reproduction
sediments
survival rate
toxicity
villi
Water Pollutants, Chemical - adverse effects
Zebrafish
Title Microplastic particles cause intestinal damage and other adverse effects in zebrafish Danio rerio and nematode Caenorhabditis elegans
URI https://dx.doi.org/10.1016/j.scitotenv.2017.11.103
https://www.ncbi.nlm.nih.gov/pubmed/29136530
https://www.proquest.com/docview/1964703504
https://www.proquest.com/docview/2000617351
Volume 619-620
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