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Flame Retardants might also be active vitamin D retardants – Jan 2015

Do Flame Retardants Promote Vitamin D Deficiency?

Honor Thesis Audrey Petteruti University of New Hampshire -arc63 at wildcats.unh.edu

VitaminDWiki Summary

Rat Experiment
Added PBDE flame retardant to diet
Livers got somewhat larger
It appears that active vitamin D levels dropped somewhat
Did not notice if the flame retardant added to rat diet has any relationship to the amount
  from cloth, polyurethane foam, etc.
Note: PDBE is an organohalogen
 Download the PDF from VitaminDWiki.

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With only 7 rats the 20% decline was not statistically significant

ABSTRACT
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 4p, 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, 4p, 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.


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Attached files

ID Name Comment Uploaded Size Downloads
4920 Flame retard CYP3A.jpg admin 18 Jan, 2015 14:11 25.13 Kb 507
4919 Flame Retard.jpg admin 18 Jan, 2015 14:11 38.72 Kb 558
4918 Do Flame Retardants Promote Vitamin D Deficiency-.pdf PDF 2015 admin 18 Jan, 2015 14:10 1,019.16 Kb 503
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