Exposure to Toxic Heavy Metals Can Influence Homocysteine Metabolism?
Caterina Ledda,
Emanuele Cannizzaro,
Piero Lovreglio,
Ermanno Vitale,
Angela Stufano,
Angelo Montana,
Giovanni Li Volti,
Venerando Rapisarda
Affiliations
Caterina Ledda
Department of Clinical and Experimental Medicine, University of Catania, 95123 Catania, Italy
Emanuele Cannizzaro
Department of Health Promotion Sciences Maternal and Infantile Care, Internal Medicine and Medical Specialities “Giuseppe D’Alessandro”, University of Palermo, 90127 Palermo, Italy
Piero Lovreglio
Interdisciplinary Department of Medicine, University of Bari “Aldo Moro”, 70124 Bari, Italy
Ermanno Vitale
Department of Clinical and Experimental Medicine, University of Catania, 95123 Catania, Italy
Angela Stufano
Interdisciplinary Department of Medicine, University of Bari “Aldo Moro”, 70124 Bari, Italy
Angelo Montana
Department of Medical Science, Surgical Science and advanced Technologies “G.F, Ingrassia”, University of Catania, 95123 Catania, Italy
Giovanni Li Volti
Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy
Venerando Rapisarda
Department of Clinical and Experimental Medicine, University of Catania, 95123 Catania, Italy
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’-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.
