serum, plasma, tissue homogenates, other biological fluids
Species Reactivity
Human
Detection Method
cELISA
Intended Use
HCY ELISA Kit allows for the in vitro quantitative determination of HCY concentrations in serum, plasma, tissue homogenates and other biological fluids.
Contents of Kit
Storage
2-8°C for 6 months.
Precision
Intra-Assay: CV<8% Inter-Assay: CV<10%
Detection Range
7.813-500pmol/ml
Sensitivity
< 4.688pmol/ml
Standard Curve
Citations
Publication ()
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Background
Homocysteine is a naturally occurring sulfur-containing amino acid that is an intermediate product in the metabolism of the essential amino acid methionine. It plays a crucial role in several important biological pathways within the human body. Homocysteine undergoes a series of enzymatic reactions to convert into methionine. Methionine synthase (MS), with the help of vitamin B12, transfers a methyl group from 5-methyltetrahydrofolate (5-methyl-THF) to homocysteine. This process results in the production of methionine. Methionine is then converted into S-adenosylmethionine (SAM) by methionine adenosyl transferase (MAT). SAM acts as a methyl donor for various cellular processes. It is eventually converted to S-adenosylhomocysteine (SAH), which can be reversed back to homocysteine through a hydrolase-catalyzed reaction. Homocysteine can be either remethylated back to methionine or undergo trans-sulfuration to form cystathionine with the help of cystathionine β-synthase (CBS), which requires vitamin B6. Methylene tetrahydrofolate reductase (MTHFR) is involved in the remethylation pathway, facilitating the conversion of homocysteine back to methionine.
Figure 1. 2 Simplified schematic diagram of homocysteine metabolic pathways. (Source: Bhatt, N. et al., 2021)
When the level of homocysteine in the blood is high (hyperhomocysteinemia), it increases the risk of endothelial cell injury, leading to inflammation in the blood vessels. This inflammation can contribute to the development of atherosclerosis, a condition where plaque builds up in the arteries, potentially causing restricted blood flow and ischemic injury. Hyperhomocysteinemia is therefore considered a potential risk factor for coronary artery disease, which occurs when atherosclerotic plaque blocks blood flow to the heart's oxygenated blood supply.
Moreover, extensive research has explored the potential mechanisms by which elevated homocysteine may contribute to the development and progression of diseases such as stroke, dementia, Alzheimer's disease, osteoporosis, and pregnancy complications. Homocysteine appears to exert its deleterious effects through pathways involving endothelial dysfunction, oxidative stress, inflammation, and other cellular processes. Understanding the metabolism and clinical implications of homocysteine is crucial for disease prevention, diagnosis, and potential therapeutic targeting.
Alternative Names
Human HCY ELISA Human Homocysteine ELISA Human HCY ELISA Kit Human Homocysteine ELISA Kit
References
1. Bhatt N, et al. Anti-inflammatory role of anthocyanins in the prevention of hyperhomocysteinemia-mediated cardiometabolic diseases. Nutritional Management and Metabolic Aspects of Hyperhomocysteinemia. 2021: 33-49.
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References
Hyperhomocysteinemia Concurrent with Metabolic Syndrome Is Independently Associated with Chronic Kidney Disease among Community-Dwelling Adults in an Urban Korean Population
INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
Elevated homocysteine (Hcy) levels and metabolic syndrome (MetS) are associated with chronic kidney disease (CKD). We investigated the combined effects of hyperhomocysteinemia (HHcy) and MetS on CKD among community-dwelling adults in an urban area of South Korea. We also identified the combination of HHcy and individual MetS components associated with the maximal risk of CKD. A retrospective cross-sectional study involving 19,311 health examinees between 2 January 2011 and 31 December 2015 was conducted. The participants were divided into four groups-namely, the HHcy-/MetS-, HHcy-/MetS+, HHcy+/MetS-, and HHcy+/MetS+ groups. CKD was defined as a low eGFR <60 mL/min/1.73 m(2) or albuminuria. The HHcy+/MetS+ group had a higher risk of CKD than the HHcy-/MetS+ group (odds ratio (OR): 1.750, p = 0.002 for males; OR: 3.224, p < 0.001 for females). The HHcy+/MetS+ group had a higher CKD risk than the HHcy+/MetS- group; however, the difference was not statistically significant (OR: 1.070, p = 0.712 for males; OR: 1.847, and p < 0.074 for females). HHcy concurrent with MetS increased the CKD risk. Among the combinations of HHcy and MetS components, the coexistence of HHcy and central obesity had the greatest effect on CKD. Therefore, the timely detection and treatment of HHcy and MetS are important for preventing CKD.
Role of homocysteine in the development of cardiovascular disease
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.
COA
Publication 
Figure 1. 2 Simplified schematic diagram of homocysteine metabolic pathways.
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