Exposure to environmentally relevant concentrations of cylindrospermopsin impair thyroid hormone function, osmoregulation.
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Exposure to cylindrospermopsin could lead to oxidative stress, disruption of osmoregulation, and morphological defects.
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Cylindrospermopsin affects the survival rate and overall health of zebrafish embryos, and may impact the fish population.
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Parameters affected by CYN exposure may be used as potential biomarkers for screening the presence of cyanotoxins in the water.
Abstract
Cyanotoxins are among common contaminants that can impair human, animal, and environmental health. Cylindrospermopsin (CYN) is an abundant form of cyanotoxins elevated following algal bloom in the water worldwide. Previous studies have described CYN effects on several organs in mammals. However, little is known about its toxicity mechanisms in other vertebrates. This study aims to characterize the developmental effects of CYN using zebrafish larvae as an aquatic model organism. A wide range of CYN concentrations (0–2000 μg/L) was tested using a morphometric approach for survival, hatching, various growth and developmental abnormalities. We also investigated the expression of genes related to oxidative stress, osmoregulation, and thyroid function. Exposure to CYN resulted in decreased growth, increased developmental abnormalities such as pericardial and yolk sac edema as well as swim bladder absence. In addition, CYN increased tr1a, and decreased dio1 and dio3 transcript levels which are involved in thyroid-mediated function. It also increased transcript levels related to oxidative stress, including hsp70, ahr1a, cyp1a, gpx and cat. Lastly, CYN exposure increased aqp3a and decreased dab2, which are involved in osmoregulation with a threshold of 10 μg/L. The present study demonstrates multiple effects of exposure to environmentally relevant CYN concentrations in zebrafish embryos.
