ArticleEcotoxicology (London, England)2014
Antioxidant and neurotoxicity markers in the model organism Enchytraeus albidus (Oligochaeta): mechanisms of response to atrazine, dimethoate and carbendazim.
Article in Ecotoxicology (London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Article
- Dimethoate induces genotoxicity as a result of oxidative stress: in vivo and in vitro studies.Environmental science and pollution research international · 2021Review
- Inhibition and recovery of biomarkers of earthworm Eisenia fetida after exposure to thiacloprid.Environmental science and pollution research international · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
The present study aimed to investigate the effects of dimethoate, atrazine and carbendazim on the antioxidant defences and neuronal function of the soil organism Enchytraeus albidus. Effects were studied at concentrations known to affect their reproduction (EC20, EC50 and EC90) and along time (2, 4, 8, 14 and 21 days). In general, responses were more pronounced at periods of exposure longer than 8 days and at the highest concentrations. Multivariate statistics (RDA-PRC) clearly displayed that exposure duration had an effect itself, biomarkers' responses showed interaction for all pesticides and catalase scored consistently high, indicating its relevancy in the group of measured markers. Univariate analysis indicated oxidative stress for all pesticides and atrazine induced oxidative damage in lipids. Atrazine seems to be effectively metabolized by GST of the biotransformation system, as its activity significantly increased after exposure to this pesticide. Dimethoate caused ChE inhibition, indicating an impairment of the neuronal function. Carbendazim impaired the antioxidant system, but no oxidative damage was observed, along with any effects on the ChE activity. The integrated biomarker response analysis was performed but we suggest modifications due to limiting artefacts.
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Registered trials
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