Abstract
An increased concentration of homocysteine (Hcy) is considered an independent and graded cardiovascular risk factor. Hcy can be non-specifically activated by methionyl-tRNA synthetase to Homocysteine thiolactone (HTL). HTL is hydrolyzed to Hcy by the paraoxonase/Thiolactonase (PON1) enzyme. PON1 is a calcium-dependent esterase synthesized in the liver and contained in plasma High-Density Lipoproteins (HDLs). The PON1 gene is polymorphic. High thiolactonase activity was associated with L55 and R192 alleles, whereas low thiolactonase activity was associated with M55 and Q192 alleles. This study provides a brief overview of some of the mechanisms by which Hcy affects vascular function and the evidence that accounts for their relevance in hypertension. The hypothesis by which alleles encoding high thiolactonase forms of PON1 might confer vascular protection under certain environmental conditions is discussed. We also evaluated these alleles and conditions in patients and controls from our institutional records.
Keywords: Hypertension, homocysteine, thiolactone, lactonase, paraoxonase, oxidative stress
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