6533b7d3fe1ef96bd1260b90

RESEARCH PRODUCT

Exposure to Toxic Heavy Metals Can Influence Homocysteine Metabolism?

Caterina LeddaAngelo MontanaErmanno VitalePiero LovreglioGiovanni Li VoltiAngela StufanoVenerando RapisardaEmanuele Cannizzaro

subject

0301 basic medicinemedicine.medical_specialtyHyperhomocysteinemiamercury6HomocysteinePhysiologycadmiumvitamin b<sub>6</sub>Clinical BiochemistryCadmium; Chromium; Folate; Lead; Mercury; Methionine; MTHFR; Vitamin B; 12; Vitamin B; 6TranssulfurationReview010501 environmental sciencesfolate01 natural sciencesBiochemistryvitamin B603 medical and health scienceschemistry.chemical_compoundInternal medicinemedicineVitamin B12Vitamin BMolecular Biology0105 earth and related environmental sciencesmethionineleadMethioninebiologybusiness.industrylcsh:RM1-950Cell BiologyMetabolismvitamin B12medicine.diseaseCystathionine beta synthase12lcsh:Therapeutics. Pharmacology030104 developmental biologyEndocrinologychemistryMethylenetetrahydrofolate reductaseMTHFRbiology.proteinchromiumbusinessvitamin b<sub>12</sub>

description

Background: Homocysteine is a sulfur amino acid whose metabolism is activated in two pathways: remethylation to methionine, which requires folate and vitamin B12, and transsulfuration to cystathionine, which needs pyridoxal-5&#8217;-phosphate. High homocysteine level increases the risk of developing heart disease, stroke, peripheral vascular diseases, and cognitive impairment. Some evidence showed that exposure to these metals increased plasma homocysteine levels. Methods: A systematic review was carried out to clarify the relationship between homocysteine blood levels and exposure to toxic heavy metals (Lead, Cadmium, Mercury, and Chromium). Results: The results of this systematic review indicate that exposure to Pb, Cr, Cd, and Hg is connected with nonphysiological homocysteine levels or vitamin B12 and folate serum concentrations. Conclusions: These findings reinforce the importance of involvement in exposure to heavy metals in homocysteine metabolism. This supports the role of blood metals as potential upstream modifiable risk factors to prevent the development of other established risk factors as hyperhomocysteinemia.

10.3390/antiox9010030http://europepmc.org/articles/PMC7022705