ArticleEnvironmental science and pollution research international2018
Acute and chronic toxicity effects of acrylonitrile to the juvenile marine flounder Paralichthys olivaceus.
Article in Environmental science and pollution research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 11 citations in OpenAlex.
- Acrylonitrile Derivatives againstPharmaceuticals (Basel, Switzerland) · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acrylonitrile (ACN) spills in marine environment have the potential to cause ecological hazards and consequences, but currently little is known about the disruptive effects of ACN on marine organisms. In the present study, we investigated the lethal and sublethal effects of ACN on juvenile flounder Paralichthys olivaceus. The results showed that the 96-h LC50 of ACN to P. olivaceus juveniles was 6.07 mg/L. The fish were then exposed to different sublethal concentrations (0.1, 0.2, and 0.4 mg/L) of ACN for 28 days and then transferred to clean seawater and keep in clean seawater for 14 days to simulate the conditions of a spill incident. Biomarkers (EROD, GST, SOD, AChE activity, and levels of LPO and DNA alkaline unwinding) were tested in liver and brain. The weight gain rates and specific growth rate of juvenile marine flounder exposed to ACN (≥ 0.1 mg/L) for 28 days decreased significantly, indicating that ACN had an inhibitory effect on juvenile growth. Deformity of fish tails was observed on individuals exposed to the highest concentration (0.4 mg/L ACN) for 14 days, and the malformation rate was 38% after 28-day exposure. The present study provides the first evidence that ACN causes inhibition of AChE activity in fish brain. Furthermore, the results showed that ACN can significantly inhibit SOD activity and cause lipid peroxidation and DNA damage in fish brain. The results indicated that brain is more sensitive to ACN toxicity compared to liver and provides a suitable tissue for biomonitoring. The biomarkers measured during the depuration period showed that the effects caused by ACN were reversible when the exposure concentration was lower than 0.4 mg/L. These results highlight the adverse effects of ACN in brain of fish, which should be considered in environmental risk assessment. Biomarkers including AChE activity, LPO, and DNA damage of brain tissue should be included in fish bioassays for toxic effect assessment of ACN spills.
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