Aclonifen is a diphenyl ether herbicide being included in the list of priority substances. Nevertheless, the data related to its sublethal effects on fish are limited. Therefore, the present study has been carried out to investigate the toxic effects of aclonifen in juvenile following 24, 48, 72 and 96 hours of application to sublethal concentrations of 12.7, 63.5 and 127 μg/L. The application resulted in altered blood biochemistry appearing as hyperglycemia, decreased cholesterol and induced activities of transaminases of ALT and AST. The inhibition of AChE in brain, gill and liver was unimportant revealing its weak potential as anticholinesterase. The induction recorded for SOD, CAT, GPx and GST activities was accompanied with sustained elevation in TBARS and PC levels. It demonstrates both the pro-oxidant potential of aclonifen and oxidation of lipid and proteins resulting in the loss of membrane integrity and protein function. Hyperglycemic condition and decreased protein levels in gill and liver might be proposed as general adaptive responses to compensate increased energy demand. The integrative assessment of multi-biomarker responses shows concentration and duration related rise in calculated indexes. CAT, PC and SOD achieved the maximum scores for brain, gill and liver, respectively. Considering the results, oxidative stress inducing potential and weak anticholinesterase activity along with its disturbing impact on blood biochemistry were evidenced. Moreover, adverse affects observed after short term application on , present the potential risk aclonifen may cause at population level in aquatic ecosystems emphasizing the importance of pesticide regulations to avoid adverse impacts on non-target species.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705079 | PMC |
http://dx.doi.org/10.1093/toxres/tfae229 | DOI Listing |
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