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1.
PeerJ ; 9: e11814, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34395076

RESUMEN

The vulnerability of a fish stock to becoming overfished is dependent upon biological traits that influence productivity and external factors that determine susceptibility or exposure to fishing effort. While a suite of life history traits are traditionally incorporated into management efforts due to their direct association with vulnerability to overfishing, spawning behavioral traits are seldom considered. We synthesized the existing biological and fisheries information of 28 fish stocks in the U.S. Gulf of Mexico to investigate relationships between life history traits, spawning behavioral traits, management regulations, and vulnerability to fishing during the spawning season. Our results showed that spawning behavioral traits were not correlated with life history traits but improved identification of species that have been historically overfished. Species varied widely in their intrinsic vulnerability to fishing during spawning in association with a broad range of behavioral strategies. Extrinsic vulnerability was high for nearly all species due to exposure to fishing during the spawning season and few management measures in place to protect spawning fish. Similarly, several species with the highest vulnerability scores were historically overfished in association with spawning aggregations. The most vulnerable species included several stocks that have not been assessed and should be prioritized for further research and monitoring. Collectively, the results of this study illustrate that spawning behavior is a distinct aspect of fish ecology that is important to consider for predictions of vulnerability and resilience to fisheries exploitation.

2.
PeerJ ; 6: e5582, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-30245931

RESUMEN

Estimating the growth of fishes is critical to understanding their life history and conducting fisheries assessments. It is imperative to sufficiently sample each size and age class of fishes to construct models that accurately reflect biological growth patterns, but this may be a challenging endeavor for highly-exploited species in which older fish are rare. Here, we use the Gulf Corvina (Cynoscion othonopterus), a vulnerable marine fish that has been persistently overfished for two decades, as a model species to compare the performance of several growth models. We fit the von Bertalanffy, Gompertz, logistic, Schnute, and Schnute-Richards growth models to length-at-age data by nonlinear least squares regression and used simple indicators to reveal biased data and ensure our results were biologically feasible. We then explored the consequences of selecting a biased growth model with a per-recruit model that estimated female spawning-stock-biomass-per-recruit and yield-per-recruit. Based on statistics alone, we found that the Schnute-Richards model described our data best. However, it was evident that our data were biased by a bimodal distribution of samples and underrepresentation of large, old individuals, and we found the Schnute-Richards model output to be biologically implausible. By simulating an equal distribution of samples across all age classes, we found that sample distribution distinctly influenced model output for all growth models tested. Consequently, we determined that the growth pattern of the Gulf Corvina was best described by the von Bertalanffy growth model, which was the most robust to biased data, comparable across studies, and statistically comparable to the Schnute-Richards model. Growth model selection had important consequences for assessment, as the per-recruit model employing the Schnute-Richards model fit to raw data predicted the stock to be in a much healthier state than per-recruit models employing other growth models. Our results serve as a reminder of the importance of complete sampling of all size and age classes when possible and transparent identification of biased data when complete sampling is not possible.

3.
Aquat Toxicol ; 201: 66-72, 2018 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-29879596

RESUMEN

Phenols are classified as polar narcotics, which are thought to cause toxicity by non-specific mechanisms, possibly by disrupting membrane structure and function. Here we test three phenolic chemicals, phenol, 2,4-dichlorphenol and pentachlorophenol on embryo development, heartbeat rate and mitochondrial respiration in fathead minnow (Pimephales promelas). While these chemicals have been used on isolated mitochondria, they have not yet been used to verify respiration in intact embryos. Mitochondrial respiration in intact embryos was measured after optimizing the Seahorse XFe24 Extracellular Flux Analyzer. Heartbeat rate and mitochondrial respiration patterns of fathead minnow embryos at different developmental stages were also characterized. Exposures of embryos at developmental stage 20 occurred for 24 h with five concentrations of each phenolic compound ranging from 0.85 to 255 µM for phenol, 0.49 to 147 µM for 2,4-dichlorophenol and 0.3 to 90 µM for pentachlorophenol. Exposure to phenol at the concentrations tested had no effects on development, heartbeat or mitochondrial respiration. However, both 2,4-dichlorophenol and pentachlorophenol showed dose-dependent effects on development, heartbeat rate, and mitochondrial respiration, with the effects occurring at lower concentrations of pentachlorophenol, compared to 2,4-dichlorophenol, highlighting the higher toxicity of the more chlorinated phenols. Both 2,4-dichlorophenol and pentachlorophenol decreased basal mitochondrial respiration of embryos and ATP production. These results indicate that higher chlorinated phenolic chemicals cause developmental toxicity in fathead minnow embryos by decreasing mitochondrial respiration and heartbeat rate.


Asunto(s)
Cyprinidae/embriología , Embrión no Mamífero/efectos de los fármacos , Fenoles/toxicidad , Contaminantes Químicos del Agua/toxicidad , Animales , Respiración de la Célula/efectos de los fármacos , Desarrollo Embrionario/efectos de los fármacos , Frecuencia Cardíaca/efectos de los fármacos , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo
4.
Artículo en Inglés | MEDLINE | ID: mdl-29625345

RESUMEN

Chemical contaminants present in the environment can affect mitochondrial bioenergetics in aquatic organisms and can have substantial effects on individual fitness. As early life stages of fish are particularly vulnerable to environmental contaminants, they are ideal models for examining the relationship between impaired mitochondrial bioenergetics (ATP-dependent respiration, basal oxidative respiration) and apical endpoints such as growth. Here, early life stages of the fathead minnow (Pimephales promelas), an ecologically relevant North American species, were used to investigate the relationship between mitochondrial bioenergetics and growth following perturbation with model mitochondrial toxicants 2,4-dinitrophenol and octylamine. Fathead minnows were exposed to 2,4-dinitrophenol and octylamine at 3 concentrations for 24 h and endpoints related to mitochondrial bioenergetics were measured with the Agilent Seahorse XFe24 Bioanalyzer. In order to link changes in mitochondrial bioenergetics to growth, fathead minnows were exposed to the same chemical contaminants for 7-14 days and growth was measured by measuring total length on a weekly basis. There was a significant correlation between decrease in average length at 14 days and basal respiration (r = 0.997, p = 0.050, n = 3), as well as maximal respiration (r = 0.998, p-value = 0.043, n = 3) for embryos exposed to 2,4 dinitrophenol. For octylamine, ATP production was highly correlated with average length at 7 days (p-value = 0.1) and spare respiratory capacity and average length at 14 days were highly correlated (p-value = 0.1). These data improve understanding of how mitochondrial toxicants impair growth in fish larvae and may be useful for developing an adverse outcome pathway for growth.


Asunto(s)
2,4-Dinitrofenol/toxicidad , Aminas/toxicidad , Cyprinidae/fisiología , Desarrollo Embrionario/efectos de los fármacos , Larva/efectos de los fármacos , Mitocondrias/efectos de los fármacos , Contaminantes Químicos del Agua/toxicidad , Adenosina Trifosfato/metabolismo , Animales , Acuicultura , Tamaño Corporal/efectos de los fármacos , Análisis por Conglomerados , Cyprinidae/embriología , Cyprinidae/crecimiento & desarrollo , Transporte de Electrón/efectos de los fármacos , Embrión no Mamífero/efectos de los fármacos , Embrión no Mamífero/fisiología , Metabolismo Energético/efectos de los fármacos , Concentración de Iones de Hidrógeno , Larva/crecimiento & desarrollo , Larva/fisiología , Mitocondrias/enzimología , Mitocondrias/metabolismo , Concentración Osmolar , Consumo de Oxígeno/efectos de los fármacos , Reproducibilidad de los Resultados , Pruebas de Toxicidad Aguda
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