Honors Theses and Capstones

Date of Award

Spring 2014

Project Type

Senior Honors Thesis

College or School



Biological Sciences; Molecular, Cellular and Biomedical Sciences

Program or Major

Biomedical Science

Degree Name

Bachelor of Science

First Advisor

Gale Carey


Vitamin D deficiency in the Unites States has become more prevalent in recent years. Research has shown that environmental chemicals such as flame-retardants induce hepatic enzymes in the cytochrome P450 family such as CYP24 and CYP3A that are important in vitamin D metabolism. To determine if exposure to one class of flame-retardants known as polybrominated diethyl ethers (PBDEs) promotes vitamin D deficiency, 15 rats consumed a diet marginally deficient in Vitamin D - 85 IU Vitamin D/kg diet - for 56 days. On day 28 of the experiment, 7 rats were gavaged daily with 7 mg/kg BW PBDEs and 8 rats were gavaged daily with corn oil, for 28 days. Body weight and food intake were measured three times a week, vitamin D status markers in the urine were measured at weeks 4 and 8 and blood Vitamin D metabolites along with liver weight were measured at euthanization. Liver microsomal vitamin D metabolism, composition and CYP3A enzyme activity were also measured. The final body weight tended to be lower in the treatment animals than in the control but was not significantly different (370.29±40.12 vs. 400.63±31.99, respectively, p = 0.0636). Liver from PBDE-treated rats was significantly heavier than liver from control rats (15.67±1.99 vs. 12.71±0.98, respectively) p < 0.05. Liver as a percent of body weight was also significantly greater in treatment (4.24±0.2) compared to control (3.18±0.13). There was no significant difference in the lipid composition of the liver or urine metabolites between PBDE-treated and control rats. The inactive metabolites 24, 25-dihydroxy vitamin D3 and 4β, 25-dihydroxy vitamin D3 did not show significant difference between control and treatment groups. The active form of 1, 25-vitamin D3 tended to be lower in the PBDE-treated rats than in the control (0.071±0.027 vs. 0.082±0.018, respectively, p = 0.187). When expressed as a ratio to 25(OH)D3, 4β, 25-dihydroxyD3 was significantly lower in treatment rats compared to control (0.96±0.18 vs. 1.28±0.38, respectively) and 1, 25-dihydroxyD3 tended to be lower in treatment compared to control (3.62±0.96 vs. 4.44±0.97, p = 0.068). Enzymatic CYP3A levels were significantly higher in PDBE-treated rats than in control (6.047±1.53 vs. 0.103±0.032 nmol/min/mg protein, respectively). The hypothesis that the induction of CYP3A by PBDEs may accelerate vitamin D inactivation, leading to vitamin D deficiency was not supported by the findings, as there was no significant change in serum vitamin D levels in the PBDE-treated rats.