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In the body, homocysteine can be recycled into methionine or converted into cysteine with the aid of vitamin B 6, B 9, and B 12. [3] High levels of homocysteine in the blood (hyperhomocysteinemia) is regarded as a marker of cardiovascular disease, likely working through atherogenesis, which can result in ischemic injury.
A blood test can be performed to quantify total homocysteine concentration in the plasma, of which approximately 80% is generally protein-bound. Classification of hyperhomocysteinemia is defined with respect to serum concentration as follows: [citation needed] Moderate: 15–30 nmol/mL (or μmol/L) Intermediate: 30–100 nmol/mL; Severe: > 100 ...
Methylenetetrahydrofolate reductase deficiency is the most common genetic cause of elevated serum levels of homocysteine (hyperhomocysteinemia). It is caused by genetic defects in MTHFR, which is an important enzyme in the methyl cycle. [1] Common variants of MTHFR deficiency are asymptomatic and have only minor effects on disease risk. [2]
Blood tests: A blood test can measure vitamin B12 levels, along with other markers such as homocysteine and methylmalonic acid, which may also indicate a deficiency. Imaging studies: If gastrointestinal cancer is suspected, imaging techniques like CT scans, MRIs, or endoscopy are used to identify tumors or other abnormalities in the digestive ...
Homocystinuria (HCU) [2] is an inherited disorder of the metabolism of the amino acid methionine due to a deficiency of cystathionine beta synthase or methionine synthase. [3] It is an inherited autosomal recessive trait, which means a child needs to inherit a copy of the defective gene from both parents to be affected.
In contrast, the steady-state enzyme kinetics of rat CBS yields intersecting lines, indicating that the β-substituent of serine is not released from the enzyme prior to binding of homocysteine. [9] One of the alternate reactions involving CBS is the condensation of cysteine with homocysteine to form cystathionine and hydrogen sulfide (H 2 S). [13]
Elevated homocysteine is an independent risk factor for cardiovascular disease and inversely correlated to consumed vitamin B12/B6 and folate levels. [37] Homocysteine methylation to methionine is catalyzed by MTR, resulting in appropriate intracellular levels of methionine and tetrahydrofolate, alongside non-toxic homocysteine levels.
S-Adenosyl-L-homocysteine (SAH) is the biosynthetic precursor to homocysteine. [1] SAH is formed by the demethylation of S -adenosyl- L -methionine . [ 2 ] [ 3 ] Adenosylhomocysteinase converts SAH into homocysteine and adenosine .