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Animals routinely encounter environmental (e.g., high temperatures and hypoxia) as well as physiological perturbations (e.g., exercise and digestion) that may threaten homeostasis. However, comparing the relative threat or "disruptiveness" imposed by different stressors is difficult, as stressors vary in their mechanisms, effects, and timescales. We exploited the fact that several acute stressors can induce the loss of equilibrium (LOE) in fish to (i) compare the metabolic recovery profiles of three environmentally relevant stressors and (ii) test the concept that LOE could be used as a physiological calibration for the intensity of different stressors. We focused on Etheostoma caeruleum, a species that routinely copes with environmental fluctuations in temperature and oxygen and that relies on burst swimming to relocate and avoid predators, as our model. Using stop‐flow (intermittent) respirometry, we tracked the oxygen consumption rate (MO2) as E. caeruleum recovered from LOE induced by hypoxia (PO2 at LOE), warming (critical thermal maximum, CTmax), or exhaustive exercise. Regardless of the stressor used, E. caeruleum recovered rapidly, returning to routine MO2 within ~3 h. Fish recovering from hypoxia and warming had similar maximum MO2, aerobic scopes, recovery time, and total excess post‐hypoxia or post‐warming oxygen consumption. Though exhaustive exercise induced a greater maximum MO2 and corresponding higher aerobic scope than warming or hypoxia, its recovery profile was otherwise similar to the other stressors, suggesting that "calibration" to a physiological state such as LOE may be a viable conceptual approach for investigators interested in questions related to multiple stressors, cross tolerance, and how animals cope with challenges to homeostasis. [ABSTRACT FROM AUTHOR]

Wastewater treatment plant (WWTP) effluent often releases pharmaceuticals like venlafaxine (a serotonin–norephinephrine reuptake inhibitor antidepressant) to freshwater ecosystems at levels causing adverse metabolic effects on fish. Changes to fish metabolism can be regulated by epigenetic mechanisms like microRNA (small RNA molecules that regulate mRNA translation), including regulating mitochondrial mRNAs. Nuclear‐encoded microRNAs regulate mitochondrial gene expression in mammals, and have predicted effects in fish. We aimed to identify whether venlafaxine exposure changed mitochondrial respiration and resulted in differentially abundant mitochondrial microRNA (mitomiRs) in zebrafish brains. In vitro exposure of brain homogenate to below environmentally relevant concentrations of venlafaxine (<1 µg/L) caused a decrease in mitochondrial respiration, although this was not driven by changes to mitochondrial Complex I or II function. To identify whether these effects occur in vivo, zebrafish were exposed to 1 µg/L venlafaxine for 0, 1, 6, 12, 24, and 96 h. In vivo, venlafaxine exposure had no significant effects on brain mitochondrial respiration; however, select mitomiRs (dre‐miR‐301a‐5p, dre‐miR‐301b‐3p, and dre‐miR‐301c‐3p) were also measured, because they were bioinformatically predicted to regulate mitochondrial cytochrome c oxidase subunit I (COI) abundance. These mitomiRs were differentially regulated based on venlafaxine exposure (with miR‐301c‐3p abundance differing during the day and miR‐301b‐3p being lower in exposed fish at night), and with respect to sex and time sampled. Overall, the results demonstrated that in vitro venlafaxine exposure to zebrafish brain caused a decrease in mitochondrial respiration, but these effects were not seen after acute in vivo exposure. Results may have differed because in vivo exposure allows for fish to mitigate effects through mechanisms that could include mitomiR regulation, and because fish were only acutely exposed. Environ Toxicol Chem 2024;43:1569–1582. © 2024 The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals LLC on behalf of SETAC. [ABSTRACT FROM AUTHOR]

Anthropogenic stressors such as agriculture and urbanization can increase river turbidity, which can negatively impact fish gill morphology and growth due to reduced oxygen in the benthic environment. We assessed the gill morphology, field metabolic rate (FMR), and two hypoxia tolerance metrics (oxygen partial pressure at loss of equilibrium, PO2 at LOE, and critical oxygen tension, Pcrit) of eastern sand darter (Ammocrypta pellucida), a small benthic fish listed as threatened under the Species at Risk Act in Canada, from rivers in southern Ontario. Field trials were conducted streamside in the Grand River (August 2019; mean NTU 8) and in the comparatively more turbid Thames River (August 2020; mean NTU 94) to test the effect of turbidity on each physiological endpoint. Gills were collected from incidental mortalities and museum specimens, and were assessed using hematoxylin and eosin and immunofluorescent staining. The between‐river comparison indicated that turbidity significantly increased interlamellar space and filament width but had no significant influence on other gill morphometrics or FMR. Turbidity significantly increased PO2 at LOE (i.e., fish had a lower hypoxia tolerance) but did not significantly impact Pcrit. Therefore, although turbidity influences hypoxia tolerance through LOE, turbidity levels were not sufficiently high in the study rivers to contribute to measurable changes in gill morphology or metabolism in the wild. Determining whether changes in gill morphology or metabolism occur under higherturbidity levels would help resolve the ecological importance of turbidity on species physiology in urban and agricultural ecosystems. [ABSTRACT FROM AUTHOR]

Micro ribonucleic acids (miRNAs) are recently discovered small regulatory molecules that control messenger RNA (mRNA) translation in plants and animals and have been implicated in a variety of hormone-related physiological pathways. Estrogens, thyroid hormones, and gonadotropins are all known to act on miRNA abundance to cause major shifts in cellular activity, physiology, and homeostatic control mechanisms. Research on cancer biology has also recently considered miRNA as therapeutic targets, because the deregulation of specific miRNAs in various tissues has been correlated with tumorigenesis and other carcinogenic responses. Because many pharmaceuticals are considered to be endocrine-disrupting chemicals (EDCs), their effects on miRNAs may be important to our understanding of basic physiological control and phenotypic outcomes of wildlife exposed to EDCs. Presented is a brief overview of the synthesis, control, and action of miRNAs, focusing on endocrine systems. The antidepressant fluoxetine will be used as an example for miRNA studies in aquatic species, one of the few examples in ecotoxicology. Given the mounting evidence that miRNAs are regulated by hormones, a clear need exists to investigate the potential for environmental EDCs to deregulate miRNA expression and action. Environ Toxicol Chem 2016;35:788-793. © 2015 SETAC [ABSTRACT FROM AUTHOR]

Both exercise training and cold acclimatization induce muscle remodelling in vertebrates, producing a more aerobic phenotype. In ectothermic species exercise training and cold-acclimatization represent distinct stimuli. It is currently unclear if these stimuli act through a common mechanism or if different mechanisms lead to a common phenotype. The goal of this study was to survey responses that represent potential mechanisms responsible for contraction- and temperature-induced muscle remodelling, using an ectothermic vertebrate. Separate groups of adult zebrafish ( Danio rerio) were either swim trained or cold acclimatized for 4 weeks. We found that the mitochondrial marker enzyme citrate synthase (CS) was increased by 1.5× in cold and by 1.3× with exercise ( P < 0.05). Cytochrome c oxidase (COx) was increased by 1.2× following exercise training ( P < 0.05) and 1.2× ( P= 0.07) with cold acclimatization. However, only cold acclimatization increased β-hydroxyacyl-CoA dehydrogenase (HOAD) compared to exercise-trained (by 1.3×) and pyruvate kinase (PK) relative to control zebrafish. We assessed the whole-animal performance outcomes of these treatments. Maximum absolute sustained swimming speed ( Ucrit) was increased in the exercise trained group but not in the cold acclimatized group. Real-time PCR analysis indicated that increases in CS are primarily transcriptionally regulated with exercise but not with cold treatments. Both treatments showed increases in nuclear respiratory factor (NRF)-1 mRNA which was increased by 2.3× in cold-acclimatized and 4× in exercise-trained zebrafish above controls. In contrast, peroxisome proliferator-activated receptor (PPAR)-α mRNA levels were decreased in both experimental groups while PPAR-β1 declined in exercise training only. Moreover, PPAR-γ coactivator (PGC)-1α mRNA was not changed by either treatment. In zebrafish, both temperature and exercise produce a more aerobic phenotype, but there are stimulus-dependent responses (i.e. HOAD and PK activities). While similar changes in NRF-1 mRNA suggest that common responses might underlie aerobic muscle remodelling there are distinct changes (i.e. CS and PPAR-β1 mRNA) that contribute to specific temperature- and exercise-induced phenotypes. [ABSTRACT FROM AUTHOR]