Search

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous contaminants that can be responsible for a variety of deleterious effects on organisms. These adverse outcomes are relatively well studied, but at concentrations rarely found in the environment. Among the documented effects of sublethal acute PAH exposure are reductions in osmoregulatory capacity and immune function, and changes in the function of critical metabolic organs such as the liver. Gulf toadfish (Opsanus beta) were exposed to control seawater (0.006 µg tPAH50 /L) or water accommodated fractions of Deepwater Horizon spill oil diluted to 3 flow-through exposure regimes (0.009, 0.059, and 2.82 µg tPAH50 /L) for 7 d, with a recovery period of equal duration. We hypothesized that these chronic exposures would induce the aryl hydrocarbon receptor (AhR)-mediated pathways and result in significant impacts on markers of osmoregulatory, immune, and metabolic function. We further hypothesized that measurable reversal of these impacts would be observed during the recovery period. Our results indicate that activation of cytochrome P 450 (CYP)1A1 was achieved during exposure and reversed during the recovery phase. The only significant deviations from controls measured were a reduction in plasma glucose in fish exposed to medium and high levels of PAH after 7 d of exposure and a reduction in plasma osmolality fish exposed to high levels of PAHs after 7 d of recovery, when CYP1A1 messenger (m)RNA levels had returned to control levels. Our study illustrates a disconnect between the activation of CYP1A1 in response to environmentally realistic PAHs concentrations and several physiological endpoints and supports the idea that the AhR might not be associated with mediating osmoregulatory, immune, and metabolic changes in Gulf toadfish. Environ Toxicol Chem 2021;40:1075-1086. © 2020 SETAC.

Serotonin selective reuptake inhibitors (SSRIs) are pollutants that influence behaviour, physiology and survival of freshwater animals. Factors influencing the sensitivity of freshwater invertebrates to these drugs must be understood in order to predict their effects on freshwater ecosystems. The toxicities of fluoxetine (Prozac), paroxetine (Paxil) and citalopram (Celexa), were tested in larval Aedes aegypti (Insecta, Diptera), Cypridopsis vidua (Crustacea, Ostracoda) and Hydra vulgaris (Cnidaria, Hydrozoa) across a broad range of ambient pH values. H. vulgaris were most sensitive, with minimal survival in the presence of drugs (1×10–5 molL–1) in all but acidic media, whereas A. aegypti larvae were least sensitive. In all species tested the drugs were toxic in neutral and alkaline media but showed minimal or no toxicity in acidic media, whereas citalopram and fluoxetine enhanced survival of C. vidua in pH 4 media. Increased toxicity in alkaline media supports the hypothesis that the ionisation states of the drugs influences their toxicity by effects on membrane permeability, whereas enhanced survival of C. vidua in acidic media in the presence of SSRIs suggests that serotonergic pathways may be involved in regulation of acid–base balance in this species.