4.7 Article

Impairment of oocyte maturation as a mechanism of decreased fecundity in Japanese medaka (Oryzias latipes) exposed to the brominated flame retardant, 1,2,5,6-tetrabromocyclooctane (TBCO)

Journal

AQUATIC TOXICOLOGY
Volume 263, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.aquatox.2023.106695

Keywords

Endocrine disruption; Oogenesis; Fecundity; Maturation inducing hormone; Vitellogenin

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Inhibition of oocyte maturation is a mechanism by which chemical stressors can impair fecundity of female fishes. The study aimed to develop an assay to evaluate oocyte maturation disruption by chemical stressors in Japanese medaka. Results showed that TBCO inhibited oocyte maturation and decreased fecundity in Japanese medaka, and in vitro assays of oocyte maturation might be predictive of fecundity in this species.
Inhibition of oocyte maturation is an understudied mechanism by which chemical stressors can impair fecundity of female fishes. The primary objective of the present study was to develop an assay to assess oocyte maturation disruption by chemical stressors in Japanese medaka (Oryzias latipes). First, an in vitro assay to assess maturation inducing hormone (MIH)-stimulated oocyte maturation in zebrafish was validated for use with Japanese medaka. Next, using the brominated flame retardant, 1,2,5,6-tetrabromocyclooctane (TBCO), which previously was shown to decrease fecundity of Japanese medaka and inhibit oocyte maturation in zebrafish, effects on oocyte maturation were quantified using in vitro and in vivo exposure. Adaptation of the protocol for in vitro MIHstimulated maturation of stage IV oocytes from zebrafish was successful in inducing greater than 80% of stage IX oocytes from female Japanese medaka to mature. To assess effects of in vitro exposure, stage IX oocytes were exposed to 0, 2, 20, and 200 mu g/L of TBCO, followed by exposure to MIH. The in vitro exposure caused a significant decrease in maturation of oocytes exposed to 20 and 200 mu g/L of TBCO. To assess effects of TBCO on fecundity and oocyte maturation following in vivo exposure, sexually mature fish were fed a control, 100 mu g/g, or 1000 mu g/g concentration of TBCO-spiked fish food for 21 days, where fecundity was measured daily, and following the exposure, stage IX oocytes were excised to assess MIH-stimulated maturation. Fecundity and oocyte maturation were significantly decreased at either concentration of TBCO. Plasma concentrations of 178-estradiol (E2) and hepatic abundances of transcripts of vitellogenin (vtgI and vtgII) were quantified, but there were no significant differences between treatments. Results suggest that inhibition of oocyte maturation is a mechanism by which TBCO decreases fecundity, and that in vitro assays of oocyte maturation might be predictive of fecundity in this species.

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