Diet quality and NSAIDs promote changes in formation of prostaglandins by an aquatic invertebrate. (October 2020)

• Record Type: Journal Article
• Authors: López-Doval, J.C.; Serra-Compte, A.; Rodríguez-Mozaz, S.; Barceló, D.; Sabater, S.
• Is Part Of: Chemosphere. Volume 257(2020)
• Publication Date: 2020-10
• Subjects: Hydropsyche sp. -- Arachidonic acid -- Metabolomics -- Multiple stressors -- Lipid metabolism; Pollution -- Periodicals; Pollution -- Physiological effect -- Periodicals; Environmental sciences -- Periodicals; Atmospheric chemistry -- Periodicals; 551.511
• DOI: 10.1016/j.chemosphere.2020.126892
• Languages: English
• ISSNs: 0045-6535

Abstract

Abstract: We used the freshwater insect Hydropsyche sp. to investigate the impact of diets lacking arachidonic acid (ARA) and an environmentally relevant mixture of NSAIDs (Ibuprofen, Ketoprofen, Diclofenac and Naproxen at a nominal concentration of all compounds together 16.75 μg L −1 ) on their metabolism of ARA and prostaglandins (PGs). The organisms were exposed for 16 days to four different treatments: a reference (FF), a diet lacking ARA (O), to NSAIDs in water (FFN) and to the combination of the two factors (ON). Mortality, biomass and bioconcentration of pharmaceuticals were investigated. The ARA and PGs levels in the organisms were monitored by utilising a targeted metabolomics approach. NSAIDs or dietary constraints did not produce significant differences in biomass or mortality of Hydropsyche sp. among treatments. In organisms exposed to NSAIDs, all pharmaceuticals were detected, except for Ketoprofen. Metabolomic approach determined the presence of PGH2, PGE1 and PGD1 . Levels of ARA diminished significantly in those organisms in treatment ON. The levels of PGs responded negatively to the absence of ARA in diet: PGH2 diminished significantly with respect to the reference in treatment O while PGE1 diminished significantly in treatment ON. Regarding the effects of NSAIDs on ARA metabolism, our results suggest that it was sensitive to NSAIDs, but effects were weak and did not imply a general decrease in the PGs. We confirmed that ARA was the main substrate for the synthesis of PGs in Hydropsyche sp, their absence or poor levels of ARA in diet, produced changes in the PG levels. Highlights: Hydropsyche sp. was not able to synthesize ARA from other dietary fatty acids. PGs levels in Hydropsyche sp. are dependent on the levels of ARA in the diet. NSAIDs produce weak modifications on PGs levels. Ketoprofen did not bioconcentratate in Hydropsyche sp. Ecological implications of these results are possible, but further research is necessary.