it is on peripheral blood mononuclear cells, so i dont know how much it applies to whole body biotin status.
Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. - PubMed - NCBI
A transporter present in intestinal cells and in choriocarcinoma cells has been shown to transport both pantothenic acid and biotin at similar transporter affinities. However, the concentration of pantothenic acid in most foods and biological fluids is approximately 200 times the concentration of biotin; theoretically, pantothenic acid might substantially reduce biotin transport via competition. In the present study, we sought to determine whether pantothenic acid reduces biotin transport by the biotin transporter in peripheral blood mononuclear cells (PBMC). PBMC were isolated from human blood by gradient centrifugation. Incubations with [(3)H]biotin and pantothenic acid were conducted at physiologic concentrations. Intracellular [(3)H]biotin was quantified after washing by liquid scintillation counting. Pantothenic acid at 10 to 1,000 nmol/L reduced biotin (475 pmol/L) uptake by less than 12% (P < 0.05). Based on Lineweaver-Burk plots, the competition was reversible. Several structural analogs of pantothenic acid at 1,000 nmol/L reduced biotin transport by only 7 to 15% (P = 0.13). No pattern of molecular structure required for recognition by the transporter was apparent. Extracellular pantothenic acid did not affect biotin efflux from [(3)H]biotin-loaded PBMC (P > 0.05), suggesting that countertransport of extracellular pantothenic acid and intracellular biotin does not increase biotin efflux from PBMC. We conclude that the physiologic effects of pantothenic acid on the transport of biotin in PBMC are likely to be quantitatively minor.
in the previous studies either biotin concentra-
tions, pantothenic acid concentrations, or both were mod-
erately to substantially greater than those normally encoun-
tered in human plasma and thus may have led to masking of
a transporter of low V
max
resembling the PBMC transporter.
For example, in our studies of biotin transport across the
blood-brain barrier and the published studies using the
functionally expressed vitamin transporter from rat pla-
centa, biotin concentrations were 3 nmol/L and 35 nmol/L,
respectively 4,5 ; the biotin concentration in normal human
plasma is approximately 0.5 nmol/L. 17 In the same transport
studies, pantothenic acid concentrations were 250 m mol/L
and 100 m mol/L, respectively 4,5 ; the pantothenic acid con-
centration in normal human plasma is 0.1 m mol/L. 6 In the
study that addressed the inhibition of pantothenic acid
transport in human placental choriocarcinoma cells by
biotin, biotin concentrations were approximately 2 3 10
5
times higher than the physiologic serum concentrations. 1
Human peripheral blood mononuclear cells: ; Inhibition of biotin transport by reversible competition with pantothenic acid is quantitatively minor. - PubMed - NCBI
A transporter present in intestinal cells and in choriocarcinoma cells has been shown to transport both pantothenic acid and biotin at similar transporter affinities. However, the concentration of pantothenic acid in most foods and biological fluids is approximately 200 times the concentration of biotin; theoretically, pantothenic acid might substantially reduce biotin transport via competition. In the present study, we sought to determine whether pantothenic acid reduces biotin transport by the biotin transporter in peripheral blood mononuclear cells (PBMC). PBMC were isolated from human blood by gradient centrifugation. Incubations with [(3)H]biotin and pantothenic acid were conducted at physiologic concentrations. Intracellular [(3)H]biotin was quantified after washing by liquid scintillation counting. Pantothenic acid at 10 to 1,000 nmol/L reduced biotin (475 pmol/L) uptake by less than 12% (P < 0.05). Based on Lineweaver-Burk plots, the competition was reversible. Several structural analogs of pantothenic acid at 1,000 nmol/L reduced biotin transport by only 7 to 15% (P = 0.13). No pattern of molecular structure required for recognition by the transporter was apparent. Extracellular pantothenic acid did not affect biotin efflux from [(3)H]biotin-loaded PBMC (P > 0.05), suggesting that countertransport of extracellular pantothenic acid and intracellular biotin does not increase biotin efflux from PBMC. We conclude that the physiologic effects of pantothenic acid on the transport of biotin in PBMC are likely to be quantitatively minor.
We speculate that pantothenic acid
is unlikely to confound studies of biotin nutritional status
using biotin concentrations or carboxylase activities in
PBMC as indices. In addition, pantothenic acid in incuba-
tion medium is unlikely to confound transport studies of
biotin in PBMC.