Total 25-OH Vitamin D ELISA Kit (DEIA4458)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
Serum, plasma
Species Reactivity
Human
Intended Use
The Total 25-OH Vitamin D ELISA kit is for the quantitative determination of 25-hydroxyvitamin D (D2 and D3) in human serum and plasma. Please read the complete kit insert before performing this assay. The kit is for RESEARCH USE ONLY. It is not intended for use in diagnostic procedures.
Storage
1. Upon receipt of the Total 25-OH Vitamin D ELISA kit, store it at 2-8°C and avoid light exposure (do not freeze the kit or hold it at temperatures above 25°C).
2. The kit should not be used after the expiration date.
Precision
The assay has a within-run and total precision of CV ≤ 10%.
Detection Range
The Total 25-OH Vitamin D ELISA Kit has an assay range from 10-160 ng/mL.
Detection Limit
The limit of detection of the assay is 5.5 ng/mL.
General Description
Vitamin D is a group of secosteroids of which vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol) are the most important to humans. In animals, vitamin D3 is generated in the skin by the reaction of sunlight with a precursor molecule. In plants, vitamin D2 is formed via a related photochemical process from ergosterol. In either case, vitamin D3 and D2 are biologically inactive and metabolized into 25-hydroxyvitamin D3 (25-OH vitamin D3) and 25-hydroxyvitamin D2 (25-OH vitamin D2), the main forms of vitamin D in the body. Due to its abundance and long circulating half-life, 25-OH vitamin D levels are the best indicator of vitamin D status. 25-OH vitamin D can also be converted to 1,25-(OH)2 vitamin D, but it has a short half-life in the body and does not typically correlate as directly to vitamin D levels. Vitamin D deficiency is an important risk factor for bone health (rickets, osteomalacia and senile osteoporosis), cancer, and pregnancy outcomes. Vitamin D toxicity can cause general symptoms such as weight loss, heart arrhythmias, and anorexia as well as more severe complications including kidney, heart, and blood vessel damage.

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References


Make hey while sun shines! Hormone 25 OH D (vitamin D3) in follicular fluid: a determinant factor for top grade blastocyst formation?

HUMAN REPRODUCTION

Authors: Chimote, N. M.; Chimote, B.

Vitamin D regulation of HAS2, hyaluronan synthesis and metabolism in triple negative breast cancer cells

JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY

Authors: Narvaez, C. J.; Grebenc, D.; Balinth, S.; Welsh, J. E.

The vitamin D receptor (VDR) and its ligand 1,25(OH)(2)D-3 (1,25D) exert anti-tumor effects, but considerable heterogeneity has been reported in different model systems. In general, cell lines derived from aggressive tumor subtypes such as Triple Negative Breast Cancer (TNBC) express low levels of VDR and are less sensitive to 1,25D than those derived from more differentiated tumor types. We have previously reported that 1,25D inhibits hyaluronic acid synthase 2 (HAS2) expression and hyaluronic acid (HA) synthesis in murine TNBC cells. Here we confirmed the inhibitory effect of 1,25D on HA synthesis in human Hs578T cells representative of the mesenchymal/stem-like (MSL) subtype of TNBC. Because HA synthesis requires the production of hexoses for incorporation into HA, we predicted that the high HA production characteristic of Hs578T cells would require sustained metabolic changes through the hexosamine biosynthetic pathway (HBP). We thus examined metabolic gene expression in Hs578T cell variants sorted for High (HA(High)) and Low (HA(Low)) HA production, and the ability of 1,25D to reverse these adaptive changes. HA(High) populations exhibited elevated HA production, smaller size, increased proliferation and higher motility than HA(Low) populations. Despite their more aggressive phenotype, HA(High) populations retained expression of VDR protein at levels comparable to that of parental Hs578T cells and HA(Low) subclones. Treatment with 1,25D decreased production of HA in both HA(High) and HA(Low) populations. We also found that multiple metabolic enzymes were aberrantly expressed in HA(High) cells, especially those involved in glutamine and glucose metabolism. Notably, Glutaminase (GLS), a known oncogene for breast cancer, was strongly upregulated in HA(High) vs. HA(Low) cells and its expression was significantly reduced by 1,25D (100 nM, 24 h). Consistent with this finding, Seahorse extracellular flux analysis indicated that respiration in HA(High) cells was significantly more dependent on exogenous glutamine than HA(Low) cells, however, acute 1,25D exposure did not alter metabolic flux. In contrast to GLS, the glutamate transporter SLC1A7 was significantly reduced in HA(High) cells compared to HA(Low) cells and its expression was enhanced by 1,25D. These findings support the concept that 1,25D can reverse the metabolic gene expression changes associated with HA production in cancer cells with aggressive phenotypes.

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