Homocysteine Detection Service

Homocysteine is a substrate in the biosynthesis process of methionine, its abnormal level in the blood may be result from the deficiency of vitamin B₁₂, vitamin B₆ or folate, and on the other hand, it perhaps also due to genetic mutations in some related enzymes. Homocysteine abnormalities are associated with a variety of diseases, including cardiovascular disease, Alzheimer's disease, and atherosclerosis. Creative BioMart Biomarker offers high quality detection service for homocysteine, ensuring high detection accuracy, sensitivity and efficiency for each sample.

Introduction

Homocysteine, which is a compound present in the blood, is a homologue of cysteine. The methionine in the body is generally derived from proteins in the body and food. Homocysteine is formed in the metabolic pathway of methionine, and it can be recycled to build other proteins. Homocysteine is a key substrate in methylation, remethylation, and transsulfuration pathways. The homeostasis of homocysteine is maintained by its formation and consumption in the folate cycle, the methionine cycle, and the transsulfuration pathway. In the methionine pathway, homocysteine reacts with N⁵-methyltetrahydrofolate to form methionine with the participation of methionine synthase (MS) and vitamin B₁₂. Among them, vitamin B₁₂ is used as a cofactor and N⁵-methyltetrahydrofolate is used as a methyl donor. N⁵-methyltetrahydrofolate is formed by N^{5, 10}-methylenetetrahydrofolate in the folate cycle under the catalysis of the enzyme methylenetetrahydrofolate reductase (MTHFR). Meanwhile, S-adenosylhomocysteine (SAH) undergoes a reversible reaction to form homocysteine by the hydrolysis of S-adenosylhomocysteine hydrolase (SAHH). In the transsulfuration pathway, homocysteine, as the first substrate in this reaction, forms cystathionine under the catalysis of cystathionine β-synthase (CBS), and then a further reaction is proceeded under the action of cystathionase γ-lyase (CSE) to form cysteine. Thus, vitamin B₁₂ and folate are required in the metabolic pathway of homocysteine. If a person lacks vitamin B₁₂ or folate, homocysteine is not efficiently recycled and therefore accumulates in the blood, resulting in an increase level of intracellular homocysteine. Abnormal elevation of homocysteine in plasma often results in hyperhomocysteinemia and homocystinuria. In addition to vitamin B₁₂ and folate deficiency, mutations in MTHFR, MS, and CBS can also cause severe hyperhomocysteinemia and homocystinuria. Moreover, abnormal levels of homocysteine are also associated with cardiovascular disease, venous thrombosis, cognitive decline and pregnancy complications.

Figure 1. Homocysteine pathway: breakdown and recycling. (Moll, et al. 2015)

Application of Homocysteine Detection

• Serum and plasma homocysteine levels as biomarkers to predict bone diseases, such as atherosclerosis, cognitive decline, cardiovascular disease

Our Advantages

• Guarantee high accuracy and sensitivity for homocysteine detection
• Ensure high repeatability of homocysteine detection
• Short turn-around time of detection service
• Competitive price in the market of detection services
• Provide multiple homocysteine detection methods, including ELISA and fluorescent
• Accept a wide range of sample types (serum, plasma, etc.)

Workflow of Homocysteine Detection at Creative BioMart Biomarker

Creative BioMart Biomarker strictly controls each specific experimental step in the homocysteine detection procedure to ensure accurately quantify the level of homocysteine in each sample.

At Creative BioMart Biomarker, we offer homocysteine detection service which includes several technical methods, you can communicate with our experts according to your research needs, and we will determine the final detection technological scheme based on the communication results. Please feel free to contact us, Creative BioMart Biomarker is here to offer you professional and thoughtful service.

References:

1. Hannibal, L.; Blom, H.J. Homocysteine and disease: causal associations or epiphenomenons? Molecular Aspects of Medicine. 2016, 53: 36-42.
2. Moll, S.; Varga, E.A. Homocysteine and MTHFR mutations. Circulation. 2015, 132(1): e6-9.