Geology ReportsSearch

Geology topics

Catherine M. Maddox

Publications and source records attributed to Catherine M. Maddox.

3 recordsLinked to original sources

Sex- and developmental stage-related differences in the hepatic transcriptome of Japanese quail (Coturnix japonica) exposed to 17β-Trenbolone

Endocrine-disrupting chemicals can cause transcriptomic changes that may disrupt biological processes associated with reproductive function including metabolism, transport, and cell growth. We investigated effects from in ovo and dietary exposure to 17β-trenbolone (at 0, 1, and 10 ppm) on the Japanese quail ( Coturnix japonica ) hepatic transcriptome. Our objectives were to identify differentially expressed hepatic genes, assess perturbations of biological pathways, and examine sex- and developmental stage–related differences. The number of significantly differentially expressed genes was higher in embryos than in adults. Male embryos exhibited greater differential gene expression than female embryos, whereas in adults, males and females exhibited similar numbers of differentially expressed genes (>2-fold). Vitellogenin and apovitellenin-1 were up-regulated in male adults exposed to 10 ppm 17β-trenbolone, and these birds also exhibited indications of immunomodulation. Functional grouping of differentially expressed genes identified processes including metabolism and transport of biomolecules, enzyme activity, and extracellular matrix interactions. Pathway enrichment analyses identified as perturbed peroxisome proliferator–activated receptor pathway, cardiac muscle contraction, gluconeogenesis, growth factor signaling, focal adhesion, and bile acid biosynthesis. One of the primary uses of 17β-trenbolone is that of a growth promoter, and these results identify effects on mechanistic pathways related to steroidogenesis, cell proliferation, differentiation, growth, and metabolism of lipids and proteins.

Environmental Toxicology and Chemistry

Thyroid disruption and oxidative stress in American kestrels following embryonic exposure to the alternative flame retardants, EHTBB and TBPH

Brominated flame retardant chemicals, such as 2-ethylhexyl-2,3,4,5-tetrabromobenzoate (EHTBB) (CAS #: 183658–27-7) and bis(2-ethylhexyl)-2,3,4,5-tetrabromophthalate (TBPH) (CAS #: 26040–51-7), have been detected in avian tissues and eggs from remote regions. Exposure to EHTBB and TBPH has been shown to cause oxidative stress and altered thyroid function in rodents and fish, yet no controlled studies have examined potential adverse effects of exposure in birds. Because flame retardants have been detected in wild raptors, we used American kestrels ( Falco sparverius ) as a model raptor to determine whether in ovo exposure to EHTBB or TBPH affected growth, hatching success, oxidative stress, or thyroid function. We exposed kestrel embryos to nominal concentrations (10, 50, or 100 ng g −1 egg weight) of EHTBB and TBPH via egg-injection on embryonic day 5. Embryonic exposure (~23 d) to EHTBB increased thyroid gland mass, reduced glandular colloid and total thyroxine (T4) in hatchling males and females, whereas deiodinase enzyme activity increased in males but decreased in females. Hatchlings exposed to TBPH in ovo exhibited reduced colloid and increased oxidative stress. Although exposure to EHTBB and TBPH caused several physiological effects (e.g., heart and brain mass), only exposure to 50 ng g −1 EHTBB appeared to reduce hatching success. Our results suggest these flame retardants may be hazardous for predatory birds. Future research should evaluate long-term survival and fitness consequences in birds exposed to these chemicals.

Environment International

Effects on circulating steroid hormones and gene expression along the hypothalamus–pituitary–gonadal axis in adult Japanese quail exposed to 17β-trenbolone across multiple generations

We investigated the effects of the androgenic growth promoter 17β-trenbolone (17βTB) on adult Japanese quail ( Coturnix japonica ) exposed across three generations. The F0 generation was exposed after sexual maturity to 0, 1, 5, 10, 20, and 40 ppm through feed. The F1 generation was exposed in ovo by maternal transfer and through feed at the same doses as their parents. The F2 generation was exposed in ovo only. Levels of plasma sex steroids, gonadal Cytochrome P450 aromatase (CYP19A1) mRNA and select brain neuroendocrine peptide mRNAs were measured. In males, testosterone levels did not differ in any generation from those in controls. Estradiol was significantly elevated in 17βTB treated F0 and F1 males. In F0 and F1 females, testosterone was suppressed by 17βTB, whereas estradiol was significantly higher at 40 ppm in F0 and at 10 ppm in F1 females. CYP19A1 expression in F1 males and females increased suggesting a compensatory response to the androgenic effects of 17βTB. Few significant effects were observed in the F2 birds indicating that in ovo exposure had limited effects on the monitored endpoints. Overall, our results confirmed endocrine disrupting effects of dietary 17βTB in Japanese quail but the response was dependent on sex, developmental stage at initiation of exposure, and dose.

Toxicological Sciences