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Vitamin B6 Pyridoxal 5 Phosphate

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Vitamin B6

In addition, PLP works as antioxidant molecule by quenching oxygen reactive species (ROS) (Ehrenshaft et al., 1999) and counteracting the formation of Advanced Glycation End products (AGEs), genotoxic compounds associated with senescence and diabetes (Booth et al., 1997). Deficiency of vitamin B6 has been implicated in several clinically relevant diseases including autism, schizophrenia, Alzheimer, Parkinson, epilepsy, Down’s syndrome, diabetes, and cancer.

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The expression of Bax and caspase-8 was tested after the 24h exposure.
Pyridoxine induced cell death in a concentration-dependent way in SHSY5Y cells. Moreover, both pyridoxal-5-phosphate dependent enzymes were inhibited by pyridoxine. In conclusion, the present study indicates that the neuropathy observed after taking a relatively high dose of vitamin B6 supplements is due to pyridoxine.
The inactive form pyridoxine competitively inhibits the active pyridoxal-5′-phosphate. Consequently, symptoms of vitamin B6 supplementation are similar to those of vitamin B6 deficienc.

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Test Catalog

Vitamin B6 status, including in persons who present with progressive nerve compression disorders, such as carpal tunnel and tarsal tunnel syndromes

Markedly elevated PLP in conjunction with low levels of pyridoxic acid are observed in cases of hypophosphatasia, a disorder characterized by low levels of alkaline phosphatase and a range of skeletal abnormalities.
Persons who present chronic, progressive nerve compression disorders may be deficient in vitamin B6 and should be evaluated. Vitamin B6 deficiency is associated with symptoms of scaling of the skin, severe gingivitis, irritability, weakness, depression, dizziness, peripheral neuropathy, and seizures. Describes reference intervals and additional information for interpretation of test results.
May include intervals based on age and sex when appropriate. If an interpretive report is provided, the reference value field will state this. The following are interpretative guidelines based upon PLP and PA results:

-If PLP is greater than 100 mcg/L; or -If PLP is greater than 100 mcg/L and PA is less than or equal to 30, the increased pyridoxal 5-phosphate is suggestive of hypophosphatasia.
Consider analysis of serum alkaline phosphatase isoenzymes (ALKI / Alkaline Phosphatase, Total and Isoenzymes, Serum) and urinary phosphoethanolamine (AAPD / Amino Acids, Quantitative, Random, Urine). -If PLP is greater than 100 mcg/L and PA is 31 to 100 mcg/L; or PLP is 81 to 100 mcg/L and PA is less than or equal to 30 mcg/L, the increased pyridoxal 5-phosphate is likely related to dietary supplementation; however a mild expression of hypophosphatasia cannot be excluded. Consider analysis of serum alkaline phosphatase isoenzymes (ALKI / Alkaline Phosphatase, Total and Isoenzymes, Serum) and urinary phosphoethanolamine (AAPD / Amino Acids, Quantitative, Random, Urine).
-If PLP is 51 to 80 mcg/L or PLP is 81 to 100 mcg/L and PA is greater than 30; or PLP is greater than 100 mcg/L and PA is greater than 100 mcg/L, the elevated pyridoxal 5-phosphate is likely due to dietary supplementatio.

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Abstract

Low vitamin B-6 status, based on plasma concentrations of pyridoxal-5-phosphate (PLP), has been identified in inflammatory diseases, including cardiovascular disease, rheumatoid arthritis, inflammatory bowel disease, and diabetes. Our objective was to examine the association between plasma PLP and multiple markers of inflammation in a community-based cohort [n = 2229 participants (55% women, mean age 61 ± 9 y)].
Multivariable-adjusted regression analysis was used to assess the associations between the IS and plasma PLP. Geometric mean plasma PLP concentrations were lower in the highest tertile category of IS relative to the lowest (61 vs. 80 nmol/L; P-trend < 0.0001). These relationships persisted after accounting for vitamin B-6 intake.

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