Hydrogen Sulphide and Vitamin B6

A number of gases are known to function as signal molecules in animals. The role for nitric oxide as a signal molecule in endothelial cell is well established, and in this role it is able to allow the relaxation of smooth muscle in response to increasing blood flow and pressure. For this reason nitric oxide is also known as endothelium derived relaxing factor. Another gas that functions as a signal molecule in animals is hydrogen sulphide, a product of the transsulfuration pathway that mediates cysteine production from homocysteine catabolism. Hydrogen sulfide is known to induce the relaxation of smooth muscles through the opening of potassium channels in the cell membranes. This pathway required activity from two enzymes, cystathionine β-synthase and cystathionine β-lyase, both of which require the presence of a vitamin B6 molecule, in the form of pyridoxal 5’-phosphate. Low availability of vitamin B6 may therefore impair the formation of hydrogen sulphide in cells and this may have health implications.

Research into the role of vitamin B6 in hydrogen sulphide production is still limited, but a number of well resigned studies have investigated the relationship between pyridoxal 5’-phosphate (the activated form of vitamin B6 present in tissues) and hydrogen sulphide production. For example, in one study1, researchers used cultured human hepatoma cells to evaluate the production of hydrogen sulphide under conditions of various cellular levels of pyridoxal. This was done by measurements of hydrogen sulphide biomarkers such as lanthionine and homolanthionine. Severe vitamin B6 deficiency (15 nmol/L pyridoxal) resulted in a 50 and 46 % lower production of lanthionine and homolanthionine, respectively, compared to adequate vitamin B6 concentrations (210 nmol/L). A dose response production of lanthionine and homolanthionine was evident with lower concentrations of vitamin B6 concentrations producing lower amounts of hydrogen sulphide and lower amounts of hydrogen sulphide metabolites.

Therefore the availability of vitamin B6 to cells may result in modification to the synthesis rates of hydrogen sulphide, and this may have implications for the relaxation of smooth muscle in animals. Low vitamin B6 intakes are associated with cardiovascular disease, because the vitamin B6 dependent enzyme cystathionine β-synthase is required for the metabolism of homocysteine. High homocysteine concentration, as can occur under conditions of low vitamin B6 intake, are a risk factor for cardiovascular disease, perhaps because homocysteine can initiate free radical generation in the endothelial lining of the arteries. The resulting oxidative stress then inhibits the synthesis of the signal molecule nitric oxide. Evidence from this study suggest that low vitamin B6 availability may also decrease production of hydrogen sulphide, another signal molecule with smooth muscle relaxing properties. The role of vitamin B6 in hydrogen sulphide production may therefore have implication for cardiovascular disease and other aspects of health.

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1DeRatt, B. N., Ralat, M. A., Kabil, O., Chi, Y., Banerjee, R. and Gregory, J. F. 2014. Vitamin B-6 restriction reduces the production of hydrogen sulphide and its biomarkers by the transsulfuration pathway in cultured human hepatocytes. Journal of Nutrition. 144(10): 1501-1508

About Robert Barrington

Robert Barrington is a writer, nutritionist, lecturer and philosopher.
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