Effects of weathered polyethylene microplastic ingestion on sexual maturation, fecundity and egg quality in maturing broodstock Atlantic cod Gadus morhua.

Microplastics (MPs) have become a global issue as they are omnipresent in the ocean. Fish ingesting MPs through feed could be affected in their physiological function, e.g., disrupted enzyme production and function, reduction of feeding and reproductive failure. This study assessed the effects of feed containing naturally weathered MPs from the Oslofjord (Norway) on the reproductive physiology of Atlantic cod (Gadus morhua). Farmed cod broodstock were fed either control (C-diet) or feeds containing 1% microplastic (MP-diet) starting nine months prior to spawning, from June until May. No major differences were found between diet groups in overall biometrics or gonad histology. Sex steroid levels (testosterone, 11-ketotestosterone and 17ß-estradiol) resulted in expected profiles increasing over time without any significant differences between treatments. Gene expression levels of the steroidogenic enzyme 20ß-hydroxysteroid dehydrogenase (20ß-hsd) and vitellogenin1 (vtg1) showed significant differences between dietary treatments with lower expression in the control group. This can be a direct effect of MPs, but endocrine disrupting effects of potentially leachable plastic additives cannot be completely ruled out. Thus, these enzymes could be indicators of exposure to contaminants that disrupt sexual maturation by affecting the production of primarily maturation-inducing steroid. Although the concentration of MPs employed in this study may not be high enough to elicit any observable short-term biological effects, the observed gene expression suggests that long-term consequences should be considered caused by an expected increase of MPs in marine environments.

Transcriptome profiling reveals exposure to predicted end-of-century ocean acidification as a stealth stressor for Atlantic cod larvae.

Ocean acidification (OA), a direct consequence of increasing atmospheric CO2 concentration dissolving in ocean waters, is impacting many fish species. Little is known about the molecular mechanisms underlying the observed physiological impacts in fish. We used RNAseq to characterize the transcriptome of 3 different larval stages of Atlantic cod (Gadus morhua) exposed to simulated OA at levels (1179 µatm CO2) representing end-of-century predictions compared to controls (503 µatm CO2), which were shown to induce tissue damage and elevated mortality in G. morhua. Only few genes were differentially expressed in 6 and 13 days-post-hatching (dph) (3 and 16 genes, respectively), during a period when maximal mortality as a response to elevated pCO2 occurred. At 36 dph, 1413 genes were differentially expressed, most likely caused by developmental asynchrony between the treatment groups, with individuals under OA growing faster. A target gene analysis revealed only few genes of the universal and well-defined cellular stress response to be differentially expressed. We thus suggest that predicted ocean acidification levels constitute a "stealth stress" for early Atlantic cod larvae, with a rapid breakdown of cellular homeostasis leading to organismal death that was missed even with an 8-fold replication implemented in this study.

Effects of parental acclimation and energy limitation in response to high CO2 exposure in Atlantic cod.

Ocean acidification (OA), the dissolution of excess anthropogenic carbon dioxide in ocean waters, is a potential stressor to many marine fish species. Whether species have the potential to acclimate and adapt to changes in the seawater carbonate chemistry is still largely unanswered. Simulation experiments across several generations are challenging for large commercially exploited species because of their long generation times. For Atlantic cod (Gadus morhua), we present first data on the effects of parental acclimation to elevated aquatic CO2 on larval survival, a fundamental parameter determining population recruitment. The parental generation in this study was exposed to either ambient or elevated aquatic CO2 levels simulating end-of-century OA levels (~1100 µatm CO2) for six weeks prior to spawning. Upon fully reciprocal exposure of the F1 generation, we quantified larval survival, combined with two larval feeding regimes in order to investigate the potential effect of energy limitation. We found a significant reduction in larval survival at elevated CO2 that was partly compensated by parental acclimation to the same CO2 exposure. Such compensation was only observed in the treatment with high food availability. This complex 3-way interaction indicates that surplus metabolic resources need to be available to allow a transgenerational alleviation response to ocean acidification.