Homocysteine, Vitamins B6 and Folic Acid in Experimental Models of Myocardial Infarction and Heart Failure—How Strong Is That Link?

Abstract

Cardiovascular diseases are the leading cause of death and the main cause of disability. In the last decade, homocysteine has been found to be a risk factor or a marker for cardiovascular diseases, including myocardial infarction (MI) and heart failure (HF). There are indications that vitamin B6 plays a significant role in the process of transsulfuration in homocysteine metabolism, specifically, in a part of the reaction in which homocysteine transfers a sulfhydryl group to serine to form α-ketobutyrate and cysteine. Therefore, an elevated homocysteine concentration (hyperhomocysteinemia) could be a consequence of vitamin B6 and/or folate deficiency. Hyperhomocysteinemia in turn could damage the endothelium and the blood vessel wall and induce worsening of atherosclerotic process, having a negative impact on the mechanisms underlying MI and HF, such as oxidative stress, inflammation, and altered function of gasotransmitters. Given the importance of the vitamin B6 in homocysteine metabolism, in this paper, we review its role in reducing oxidative stress and inflammation, influencing the functions of gasotransmitters, and improving vasodilatation and coronary flow in animal models of MI and HF.

Men with oligozoospermia had lower level of seminal plasma pyridoxine compared to normozoospermic men

“…Further, pyridoxal 5′-phosphate, an active form of pyridoxine, is considered as key coenzyme for cystathionine-β-synthase, which is a multidomain enzyme catalyzes the conversion of homocysteine into cystathionine and cysteine [ 53 , 54 ]. Decreased levels of pyridoxine may lead to accumulation of homocysteine and hyperhomocysteinemia (increased level of homocysteine in the blood) [ 55 , 56 ]. It has been shown that deficiencies in B vitamins, including pyridoxine, is associated with hyperhomocysteinemia and altered sperm differentiation and maturation [ 16 , 54 , 57 ].…”

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“…This leads to a reduction in cellular DNA synthesis and impaired tissue repair [ 81 ]. Hcy also has a negative effect on myocytes and myocardial contractility [ 85 ].…”

“…Stimulation of the synthesis of reactive oxygen species is one of the most important links between Hcy, particularly its oxidized sulfhydryl groups, and the development of atherosclerosis [ 138 ]. Atherosclerosis is also favoured by Hcy-induced hyperuricemia, which further promotes the formation of reactive oxygen species and subsequent vascular endothelium dysfunction [ 85 ].…”

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