Rabbit Anti-Homocysteine Polyclonal Antibody

Homocysteine (HCY) is a sulfur-containing amino acid formed after the demethylation of methionine and is an intermediate product of the methionine cycle. Homocysteine cannot be synthesized in the body and can only be converted from methionine. Methionine cannot be synthesized in the human body and must be supplied by food. In normal plasma, 80% of homocysteine is bound to proteins through disulfide bonds. Most of the unconjugated homocysteine exists as cystine or cysteine-homocysteine, with only a small portion free. Homocysteine, whether in bound or free form, is collectively referred to as total homocysteine. The main factors that affect homocysteine levels are genetics and dietary deficiencies. Homocysteine metabolism requires vitamin B6, vitamin B12, and folic acid. If the concentration of vitamin B12, vitamin B6, and folic acid in the blood is too low, the concentration of homocysteine in the blood will increase. The first reports of homocysteine metabolism disorders came from the observation of homocystinuria in patients with congenital cystathionine synthase deficiency. Since then, several other metabolic disorders caused by changes in enzymes or coenzymes involved in HCY metabolism have been discovered. In recent years, with the improvement of measurement technology and methods, it has been possible to measure HCY existing in various forms in normal human plasma. Studies have found that HCY metabolic disorders exist in patients with heart, brain and peripheral vascular diseases, chronic renal insufficiency, dermatophytes, vitamin By2 deficiency and other diseases.

Figure 1. Homocysteine (Hcy) metabolic pathway.(Source: Alexey Chubarov. 2021)

HCY comes from methionine in the daily diet. It is the product of the hydrolysis reaction of S-adenosine HCY in the methionine cycle. At the same time, it is the substrate for the synthesis of cystathionine by cystathionine beta synthase. The total HCY in the blood includes three forms: HCY, HCY disulfide and cystine-HCY. Most of them exist in protein-bound form, and a small part is in a free state. There are three metabolic pathways for HCY. 1. HCY is remethylated into methionine, also known as the remethylation pathway. The remethylation reaction requires the participation of methionine synthase and vitamin B12 as a coenzyme. Under these conditions, HCY synthesizes methionine and tetrahydrofolate with 5'-methyltetrahydrofolate. There is another remethylation pathway in the liver, which uses betaine as a methyl donor and synthesizes methionine and dimethylglycine under the catalysis of betaine HCY methyltransferase. 2. The reaction of condensation of HCY and serine into cystathionine, also known as the transsulfurization pathway. The reaction is catalyzed by cystathionine synthase, with vitamin Br as a coenzyme, and is condensed into cystathionine and water. This reaction is irreversible under physiological conditions and is beneficial to the transport of HCY. The generated cystathionine is cleaved into cysteine and α-ketobutyric acid by γ-cystathionase. 3. Directly released into the extracellular fluid. This part is closely related to plasma concentration. Increased release of HCY outside cells reflects disturbances in its production and metabolism. Studies have shown that the concentration of methionine can affect the release of HCY from cells. At low concentrations, cellular release is affected by methionine synthase; while at high concentrations, cellular release is affected by cystathionine synthase.

Elevated homocysteine levels are found in atherosclerotic vascular disease, stroke, rheumatoid arthritis, various cancers, etc. Elevated levels of homocysteine produce superoxide and peroxide, which can cause damage to vascular endothelial cells and oxidation of low-density lipoprotein, leading to sustained contraction of vascular smooth muscle and hypoxia, accelerating the process of atherosclerosis. It can also disrupt normal clotting mechanisms and increase the risk of thrombosis. If homocysteine levels are elevated due to inadequate intake of vitamin B6, vitamin B12 and folic acid, you can reduce plasma homocysteine levels through diet or increase intake of B vitamins and folic acid, thereby reducing the risk of cardiovascular and cerebrovascular disease.

L-Homocysteine
Thiohomocysteine
Hcy