Changes in thyroid axis responses in two ring-billed gull sub-populations differentially exposed to halogenated flame retardants

Técher, Romy; Houde, Magali; Verreault, Jonathan

doi:10.1016/j.chemosphere.2018.07.155

Cited by 9 publications

(1 citation statement)

References 36 publications

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“…The expression levels of tshβ , dio1 , dio2 , and tg in the fish brain were significantly upregulated by TCEP exposure. Because all of these genes encode molecules that positively regulate the HPT axis, their upregulation could be a feedback response to the disrupted HPT axis. ,− For instance, upregulation of tshβ might be a response at the transcriptional level to compensate for the decline of TSH in the brain. Similarly, since dio 1 and dio 2 encode deiodinases that catalyze the transformation of T4 to T3, their upregulation could be a response to the disequilibrium of T3 and T4. , Furthermore, the expressions of ttr , trα , and trβ in the zebrafish liver were also significantly altered by TCEP exposure, indicating a disrupted regulatory function of the HPT axis in the liver.…”

Section: Discussionmentioning

confidence: 99%

Tris(2-chloroethyl) Phosphate Exerts Hepatotoxic Impacts on Zebrafish by Disrupting Hypothalamic–Pituitary–Thyroid and Gut–Liver Axes

Tian

et al. 2023

Environ. Sci. Technol.

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The ubiquitous environmental presence of tris(2chloroethyl) phosphate (TCEP) poses a potential threat to animals; however, little is known about its hepatotoxicity. In this study, the effects of TCEP exposure (0.5 and 5.0 μg/L for 28 days) on liver health and the potential underlying toxification mechanisms were investigated in zebrafish. Our results demonstrated that TCEP exposure led to hepatic tissue lesions and resulted in significant alterations in liver-injury-specific markers. Moreover, TCEP-exposed fish had significantly lower levels of thyrotropin-releasing hormone and thyroid-stimulating hormone in the brain, evidently less triiodothyronine whereas more thyroxine in plasma, and markedly altered expressions of genes from the hypothalamic−pituitary−thyroid (HPT) axis in the brain or liver. In addition, a significantly higher proportion of Bacteroidetes in the gut microbiota, an elevated bacterial source endotoxin lipopolysaccharide (LPS) in the plasma, upregulated expression of LPSbinding protein and Toll-like receptor 4 in the liver, and higher levels of proinflammatory cytokines in the liver were detected in TCEP-exposed zebrafish. Furthermore, TCEP-exposed fish also suffered severe oxidative damage, possibly due to disruption of the antioxidant system. These findings suggest that TCEP may exert hepatotoxic effects on zebrafish by disrupting the HPT and gut− liver axes and thereafter inducing hepatic inflammation and oxidative stress.

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