Abstract
It is well known that neuronal damage following a stroke has been attributed to the over stimulation of excitatory amino acids such as glutamate and aspartate through activation of NMDA receptors. The brain is exposed to most of the constituents of plasma including homocysteine as a result of the disruption of the blood–brain barrier after stroke, head trauma and stress. The question, therefore, arises as to whether or not homocysteine is able to selectively stimulate the release of excitatory amino acids in stroke. This review article will address the importance of homocysteine in nervous system specifically how these amino acids may trigger the release of catecholamines. Our data will thus strengthen the view that a mechanism for the association of hyperhomocysteinemia with increased brain lesion in stroke. As hypothalamus also controls the cardiac function via sympathetic system, the contractility of heart will be compromised. Homocysteine is also known to mediate cardiovascular problems by its adverse effects on cardiovascular endothelium and smooth muscle cells with resultant alterations in subclinical arterial structure and function. The present review will thus summarize both central and peripheral effects of homocysteine and will highlight some of the controversies associated with hyperhomocysteinemia-induced cardiovascular problems.
Highlights
Homocysteine has been under a lot of speculation since its discovery in 1932
There are two types of hyperhomocysteinemia: (1) the rare but severe forms are due to major genetic mutations of the enzymes implicated in homocysteine metabolism; (2) the more common forms cause moderately elevated homocysteine levels related to a pathogenesis such as genetic and environmental factors [2]
The published literature indicates that homocysteine is an independent cardiovascular disease risk factor modifiable by nutrition and exercise
Summary
Homocysteine has been under a lot of speculation since its discovery in 1932. Its chemical properties showed a similarity to cysteine, the name homocysteine. There are two types of hyperhomocysteinemia: (1) the rare but severe forms are due to major genetic mutations of the enzymes implicated in homocysteine metabolism; (2) the more common forms cause moderately elevated homocysteine levels related to a pathogenesis such as genetic and environmental factors [2]. Vitamin B12 and to a lesser extent, vitamin B6 are related inversely to total homocysteine; a person with a nutritional deficiency that leads to low blood concentrations of the aforementioned is at increased risk of hyperhomocysteinemia [4,9].
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