Effects of low doses of glyphosate on DNA damage, cell proliferation and oxidative stress in the HepG2 cell line

Effects of low doses of glyphosate on DNA damage, cell proliferation and oxidative stress in the... We studied the toxic effects of glyphosate in vitro on HepG2 cells exposed for 4 and 24 h to low glyphosate concentrations likely to be encountered in occupational and residential exposures [the acceptable daily intake (ADI; 0.5 μg/mL), residential exposure level (REL; 2.91 μg/mL) and occupational exposure level (OEL; 3.5 μg/mL)]. The assessments were performed using biomarkers of oxidative stress, CCK-8 colorimetric assay for cell proliferation, alkaline comet assay and cytokinesis-block micronucleus (CBMN) cytome assay. The results obtained indicated effects on cell proliferation, both at 4 and 24 h. The levels of primary DNA damage after 4-h exposure were lower in treated vs. control samples, but were not significantly changed after 24 h. Using the CBMN assay, we found a significantly higher number of MN and nuclear buds at ADI and REL after 4 h and a lower number of MN after 24 h. The obtained results revealed significant oxidative damage. Four-hour exposure resulted in significant decrease at ADI [lipid peroxidation and glutathione peroxidase (GSH-Px)] and OEL [lipid peroxidation and level of total antioxidant capacity (TAC)], and 24-h exposure in significant decrease at OEL (TAC and GSH-Px). No significant effects were observed for the level of reactive oxygen species (ROS) and glutathione (GSH) for both treatment, and for 24 h for lipid peroxidation. Taken together, the elevated levels of cytogenetic damage found by the CBMN assay and the mechanisms of primary DNA damage should be further clarified, considering that the comet assay results indicate possible cross-linking or DNA adduct formation. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Environmental Science and Pollution Research Springer Journals

Effects of low doses of glyphosate on DNA damage, cell proliferation and oxidative stress in the HepG2 cell line

Environ Sci Pollut Res (2017) 24:19267–19281 DOI 10.1007/s11356-017-9438-y RESEARCH ARTICLE Effects of low doses of glyphosate on DNA damage, cell proliferation and oxidative stress in the HepG2 cell line 1 1 1 1 1,2 Vilena Kašuba & Mirta Milić & Ružica Rozgaj & Nevenka Kopjar & Marin Mladinić & 3 3 4 4 Suzana Žunec & Ana Lucić Vrdoljak & Ivan Pavičić & Ana Marija MarjanovićČermak & 5 5 1 Alica Pizent & Blanka Tariba Lovaković & Davor Želježić Received: 16 April 2017 /Accepted: 1 June 2017 /Published online: 30 June 2017 Springer-Verlag GmbH Germany 2017 Abstract We studied the toxic effects of glyphosate in vitro a lower number of MN after 24 h. The obtained results re- on HepG2 cells exposed for 4 and 24 h to low glyphosate vealed significant oxidative damage. Four-hour exposure re- concentrations likely to be encountered in occupational and sulted in significant decrease at ADI [lipid peroxidation and residential exposures [the acceptable daily intake (ADI; glutathione peroxidase (GSH-Px)] and OEL [lipid peroxida- 0.5 μg/mL), residential exposure level (REL; 2.91 μg/mL) tion and level of total antioxidant capacity (TAC)], and 24-h and occupational exposure level (OEL; 3.5 μg/mL)]. The as- exposure in significant decrease at OEL (TAC and GSH-Px). sessments were performed using biomarkers of oxidative No significant effects were observed for the level of reactive stress, CCK-8 colorimetric assay for cell proliferation, alka- oxygen species (ROS) and glutathione (GSH) for both treat- line comet assay and cytokinesis-block micronucleus ment, and for 24 h for lipid peroxidation. Taken together, the (CBMN) cytome assay. The results obtained indicated effects elevated levels of cytogenetic damage found by the CBMN on cell proliferation, both at 4 and 24 h. The levels of primary assay and the mechanisms of primary DNA damage should be DNA damage after 4-h exposure were lower in treated vs....
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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by Springer-Verlag GmbH Germany
Subject
Environment; Environment, general; Environmental Chemistry; Ecotoxicology; Environmental Health; Atmospheric Protection/Air Quality Control/Air Pollution; Waste Water Technology / Water Pollution Control / Water Management / Aquatic Pollution
ISSN
0944-1344
eISSN
1614-7499
D.O.I.
10.1007/s11356-017-9438-y
Publisher site
See Article on Publisher Site

Abstract

We studied the toxic effects of glyphosate in vitro on HepG2 cells exposed for 4 and 24 h to low glyphosate concentrations likely to be encountered in occupational and residential exposures [the acceptable daily intake (ADI; 0.5 μg/mL), residential exposure level (REL; 2.91 μg/mL) and occupational exposure level (OEL; 3.5 μg/mL)]. The assessments were performed using biomarkers of oxidative stress, CCK-8 colorimetric assay for cell proliferation, alkaline comet assay and cytokinesis-block micronucleus (CBMN) cytome assay. The results obtained indicated effects on cell proliferation, both at 4 and 24 h. The levels of primary DNA damage after 4-h exposure were lower in treated vs. control samples, but were not significantly changed after 24 h. Using the CBMN assay, we found a significantly higher number of MN and nuclear buds at ADI and REL after 4 h and a lower number of MN after 24 h. The obtained results revealed significant oxidative damage. Four-hour exposure resulted in significant decrease at ADI [lipid peroxidation and glutathione peroxidase (GSH-Px)] and OEL [lipid peroxidation and level of total antioxidant capacity (TAC)], and 24-h exposure in significant decrease at OEL (TAC and GSH-Px). No significant effects were observed for the level of reactive oxygen species (ROS) and glutathione (GSH) for both treatment, and for 24 h for lipid peroxidation. Taken together, the elevated levels of cytogenetic damage found by the CBMN assay and the mechanisms of primary DNA damage should be further clarified, considering that the comet assay results indicate possible cross-linking or DNA adduct formation.

Journal

Environmental Science and Pollution ResearchSpringer Journals

Published: Jun 30, 2017

References

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