Vitamin B6 deficiency is associated with cardiovascular disease. In some studies this has been shown to be related to the role of vitamin B6 in the metabolism of homocysteine. In short, vitamin B6 is required for the metabolism of homocysteine to cysteine, and a deficiency increases the concentration of homocysteine in tissues, leading to tissue damage through the generation of free radicals. However, vitamin B6 also plays another important role in metabolic regulation that may relate to cardiovascular effects. Hydrogen sulphide is produced in cells by a transsulfuration reaction involving cystathionine β-synthase and cystathionine γ-lyase that require vitamin B6 in its coenzyme form, pyridoxal 5’-phosphate. Hydrogen sulphide promotes vasodilation through the opening of potassium channels and thus aids in correct cardiovascular function. Measurements of hydrogen sulphide under various vitamin B6 intakes is therefore of interest, but hydrogen sulphide is not easy to measure because it is volatile.
Lanthionine and homolanthionine are formed concurrently with hydrogen sulphide and may be useful markers for its production. Researchers have measured the levels of lanthionine and homolanthionine in healthy adults before and after a 28 day period of vitamin B6 restriction, but neither lanthionine nor homolanthionine were affected by vitamin B6 restriction. However, there was a large variation in the individual response of both lanthionine and homolanthionine to the restriction. Interestingly following restriction, those with the highest concentration of homolanthionine had the greatest severity of vitamin B6 deficiency symptoms, which is the opposite of what the researcher hypothesised. The measurement of the metabolism of hydrogen sulphide is therefore not straightforward to undertake, and use of lanthionine and homolanthionine may be problematic. However, this does not mean that hydrogen sulphide levels are not affected by vitamin B6 restriction, just that it is not easy to measure the changes.
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