Product Usage:To qualitatively detect MTHFR 677C>T and 1298A>C in EDTA anticoagulated venous whole blood samples, MTRR gene 66A>C gene polymorphism, tailored folic acid quantity supplementation and supplementation cycles.
Features and Advantages:1. High Specificity: The use of Taqman-MGB probe method, effectively enhance the genotyping specificity
2. High Accuracy: Paraffin sealed sample, the whole process is carried out in a closed tube with beta-actin internal control system that effectively prevents product contamination and false negatives
3. High Sensitivity: accurate genotyping of CYP2C19 down to 1ng/μl in DNA samples
4. Simplicity and Fastness: the kit is simple and easy to operate, the detection cycle is short (1.5 hours), and the result is reliable.
Applicable Instrument Model: - AB 7500 and AB 7900 fluorescent quantitative PCR instrument. - SLAN-48P and SLAN-96P fluorescence quantitative PCR instrument.
Folic Acid Supplementation Dosage Guidance:Folic acid belonging to the B vitamins, cannot be synthesized by the human body itself, and can only be supplemented in vitro. In the body folic acid effect through folic acid reductase, reduces the physiological activity of tetrahydrofolate. It is an important factor in the body’s different biochemical reactions, involved in the nucleic acids, proteins and phospholipids metabolism for the DNA and RNA synthesis, cell proliferation and tissues growth. Folic acid deficiency or excess supplementation can cause physical impact on the foetus and couples preparing for pregnancy.
Folic acid Excess effect:Increase colorectal adenocarcinoma and breast cancer risk, concealment of vitamin B12 deficiency, resulting in the pregnant woman's body asthenia, neurasthenia, nausea and anemia, which affect zinc absorption and cause health impairment, leading to folic acid hypersensitivity.
Population, Man:Folic acid Deficiency effect:Sperm low density and decreased activity, abnormal chromosome count.
Background:Abnormalities in enzyme activity resulting from mutations in the human MTHFR and MTRR genes are the major causes of folic acid metabolism disorders. MTHFR is a key enzyme in folic acid metabolism, with many loci variations. The most studied loci are 677C>T and 1298A>C. MTHFR 677 locus is located on exon 4 and its mutation causes Cytosine (C) to be replaced by Thymine (T), causing Alanine to become Valine. The 1298 locus is located in exon 7, and its mutation causes Adenine (A) to be replaced by cytosine (C), and the corresponding glutamic acid is replaced by alanine. These loci’s mutation lead to decreased enzyme activity and thermal stability, hinder the conversion of 5-10MTHF to 5MTHF, homocysteine accumulation in the body, hyperhomocysteinemia, hyperhomocysteineuria, and low blood-Met disorders. Homocysteine is converted into Met, reducing the production of S-adenosyl methionine (SAM), a direct donor of methyl, and affects the body's metabolism due to insufficient DNA, protein and lipid methylation in vivo and causes chromosomal instability. MTRR and vitamin B12 synergism maintain the MTR reductive activity and participate in the homocysteine -Met cycle in the body. The second exon on the 66 locus A is replaced by G, and the corresponding isoleucine is converted into Met. MTRR 66A > G mutation cannot maintain MTR activity, and can inhibit the transformation of homocysteine into Met in coordination with MTR 2756A >G, resulting in homocysteine increase.
Storage and Stability:Store powder at 4°C liquid at -20°C. Store other components at 4°C. Stable for 6 months For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.
