Exposure to Toxic Heavy Metals Can Influence Homocysteine Metabolism?

Antioxidants

Giovanni Li Volti¹  Ermanno Vitale²  Caterina Ledda²  Venerando Rapisarda²  Emanuele Cannizzaro³  Angelo Montana⁴  Piero Lovreglio⁵  Angela Stufano⁵ 

[1] Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy;Department of Clinical and Experimental Medicine, University of Catania, 95123 Catania, Italy;Department of Health Promotion Sciences Maternal and Infantile Care, Internal Medicine and Medical Specialities “Giuseppe D’Alessandro”, University of Palermo, 90127 Palermo, Italy;Department of Medical Science, Surgical Science and advanced Technologies “G.F, Ingrassia”, University of Catania, 95123 Catania, Italy;Interdisciplinary Department of Medicine, University of Bari “Aldo Moro”, 70124 Bari, Italy;

关键词: methionine;    mthfr;    vitamin b₆;    vitamin b₁₂;    folate;    lead;    chromium;    cadmium;    mercury;   

DOI  :  10.3390/antiox9010030

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown