In ovo exposure to selenomethionine via maternal transfer increases developmental toxicities and impairs swim performance in F1 generation zebrafish (Danio rerio)

•Entire life-cycle F1 generation zebrafish exposed in ovo to SeMet were investigated.•Dose- and time-dependent increases in embryo mortality and larval deformities.•Surviving offspring were raised until adulthood with no further SeMet exposure.•Swimming performance and swim motion were impaired in a...

Full description

Saved in:
Bibliographic Details
Published inAquatic toxicology Vol. 152; pp. 20 - 29
Main Authors Thomas, Jith K., Janz, David M.
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier B.V 01.07.2014
Elsevier
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:•Entire life-cycle F1 generation zebrafish exposed in ovo to SeMet were investigated.•Dose- and time-dependent increases in embryo mortality and larval deformities.•Surviving offspring were raised until adulthood with no further SeMet exposure.•Swimming performance and swim motion were impaired in adults exposed in ovo.•No transgenerational effects were observed in F2 generation offspring. Selenomethionine (SeMet) is the major form of organoselenium present in food. Adult female fish can accumulate greater concentrations of SeMet from food in aquatic ecosystems contaminated with selenium (Se), and maternal transfer to eggs increases the incidence of developmental toxicities and mortality in F1 generation larval fish. The present study was designed to investigate both immediate and persistent adverse effects of graded exposure to SeMet via in ovo maternal transfer to F1 generation zebrafish (Danio rerio). Adult zebrafish were fed either control food (1.3μg Se/g, dry mass or d.m.) or food spiked with increasing concentrations of Se (3.7, 9.6 or 26.6μg Se/g, d.m.) in the form of SeMet for 60d at 5% body mass/d ration, and an additional 30–40d with equal rations (2.5%) of control or SeMet-spiked diets and clean chironomids. Concentrations of Se in eggs of adult zebrafish fed 1.3, 3.7, 9.6 or 26.6μg Se/g d.m. were 2.1, 6.0, 9.6 and 21.9μg Se/g d.m., respectively. Exposure to SeMet via in ovo maternal transfer increased larval zebrafish mortalities in a concentration- and time-dependent fashion. In order to investigate persistent adverse effects of in ovo exposure to excess Se, we determined swim performance (Ucrit), tailbeat amplitude and frequency, energy stores (whole body triglycerides and glycogen), and a marker of the physiological stress response (whole body cortisol) of F1 generation zebrafish at 140 days post-fertilization (dpf), and reproductive performance at 180dpf. Reduced Ucrit was observed in F1 generation adult zebrafish exposed to ≥6.0μg Se/g d.m. Concentrations of whole body glycogen in the 6.0μg Se/g d.m. exposed group were significantly lower than the controls. However, no differences were found in concentrations of whole body triglycerides or cortisol in adult zebrafish. Mortalities and developmental toxicities in offspring (F2 generation) of F1 generation adult zebrafish exposed to excess Se via in ovo maternal transfer were comparable to the controls. Overall, the results of this study suggest that exposure to greater concentrations of SeMet via in ovo maternal transfer can significantly impact the survivability of F1 generation fish, which could impact recruitment of wild fish inhabiting Se-contaminated aquatic ecosystems.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0166-445X
1879-1514
DOI:10.1016/j.aquatox.2014.03.022