Parental dietary seleno-L-methionine exposure and resultant offspring developmental toxicity

Abstract

Selenium (Se) leaches into water from agricultural soils and from storage sites for coal fly ash. Se toxicity causes population and community level effects in fishes and birds. We used the laboratory aquarium model fish, Japanese medaka (Oryzias latipes), an asynchronous breeder, to determine aspects of uptake in adults and resultant developmental toxicity in their offspring. The superior imaging properties of the model enabled detailed descriptions of phenotypic alterations not commonly reported in the existing Se literature. Adult males and females in treatment groups were exposed, separately and together, to a dry diet spiked with 0, 12.5, 25, or 50 µg/g (dry weight) seleno-L-methionine (SeMet) for 6 days, and their embryo progeny collected for 5 days, maintained under controlled conditions and observed daily for hatchability, mortality and/or developmental toxicity. Sites of alteration included: craniofacial, pericardium and abdomen (Pc/Ab), notochord, gall bladder, spleen, blood, and swim bladder. Next, adult tissue Se concentrations (liver, skeletal muscle, ovary and testis) were determined and compared in treatment groups of bred and unbred individuals. No significant difference was found across treatment groups at the various SeMet concentrations; and, subsequent analysis compared exposed vs. control in each of the treatment groups at 10 dpf. Increased embryo mortality was observed in all treatment groups, compared to controls, and embryos had a decreased hatching rate when both parents were exposed. Exposure resulted in significantly more total altered phenotypes than controls. When altered phenotypes following exposure of both parents were higher than maternal only exposure, a male role was suggested. The comparisons between treatment groups revealed that particular types of phenotypic change may be driven by the sex of the exposed parent. Additionally, breeding reduced Se concentrations in some adult tissues, specifically the liver of exposed females and skeletal muscle of exposed males. Detailed phenotypic analysis of progeny from SeMet exposed parents should inform investigations of later life stages in an effort to determine consequences of early life exposure.

Embryo Microinjection of Selenomethionine Reduces Hatchability and Modifies Oxidant Responsive Gene Expression in Zebrafish

“…Similar toxicity (i.e. pericardial edema) has been reported in a number of developmental Se exposure studies 2 38 40 41 , and Se-induced activation of the AhR2 signalling pathway may be involved in such toxicity. Both nrf2a and nrf2b have been demonstrated to participate in cross-talk with ahr2 in zebrafish 15 .…”

Selenium Ecotoxicology in Freshwater Lakes Receiving Coal Combustion Residual Effluents: A North Carolina Example

“…The significance of this finding remains incompletely understood; selenium concentrations in fish testes are uncommonly reported in field studies and a recent analysis of such studies found that reported testes/milt concentrations are given little consideration relative to those of female fish muscle and ovary/egg tissue concentrations. 23 This issue likely reflects the prevailing theory that environmentally relevant selenium toxicity in early life stage fish occurs primarily due to selenium transfer from the maternal fish during vitellogenesis and embryonic exposure to this selenium during yolk resorption. 1 However, a recent study investigating the influence of parental selenium exposure on the occurrence of phenotypic abnormalities in F1 generation Japanese medaka ( Oryzias latipes ) reported paternal influence over some deformity categories (e.g., craniofacial) and that the highest rate of phenotypic alterations were found in the exposure group in which both maternal and paternal fish were dietarily exposed to seleno-Lmethionine.…”

Synchrotron-Based Imaging Reveals the Fate of Selenium in Striped Marsh Frog Tadpoles

“…Tadpoles have a chondrified skeleton during early premetamorphosis stages with ossification generally starting in most species during late premetamorphosis (developmental stage sampled in this experiment). Previous studies have reported spinal and craniofacial deformities in tadpoles and fish exposed to Se, which may relate to the Se accumulations in these structures. ,,− A recent study found that exposure to selenomethionine altered the expression of genes involved in the skeletogenesis of fish during early development . The study found a decreased expression of melatonin receptor ( Mtr ) in exposed fish (10–500 μM selenomethionine) and suggests that Se-induced skeletal deformities are caused by a blockage or inhibition of melatonin.…”