OBJECTIVE: To assess long-term variations in arsenic methylation and oxidative DNA lesions of chronic high arsenic-exposed populations. METHODS: A follow-up study was conducted in 64 chronic high arsenic-exposed subjects from 2004 to 2006. Urinary arsenic species and 8-hydroxydeoxyguanine were measured. RESULTS: Percentages of urinary inorganic arsenic, monomethylarsonate and urinary 8-hydroxydeoxyguanine (8-OHdG) level were significantly higher, but the percentage of dimethylarsinate, the primary methylation index (PMI) and secondary methylation index (SMI) was lower in the ninth year of arsenic exposure compared with the seventh year. Substantial differences in relative arsenic methylation capacity were observed between the seventh and ninth year. Percentages of arsenic species, PMI and SMI were significantly correlated between siblings, and between parents and children. CONCLUSIONS: Arsenic methylation may decrease, but oxidative DNA lesions may increase with the increase of cumulative arsenic exposure level. Both genetic and environmental factors may contribute to variability in arsenic methylation.
OBJECTIVE: To assess long-term variations in arsenic methylation and oxidative DNA lesions of chronic high arsenic-exposed populations. METHODS: A follow-up study was conducted in 64 chronic high arsenic-exposed subjects from 2004 to 2006. Urinary arsenic species and 8-hydroxydeoxyguanine were measured. RESULTS: Percentages of urinary inorganic arsenic, monomethylarsonate and urinary 8-hydroxydeoxyguanine (8-OHdG) level were significantly higher, but the percentage of dimethylarsinate, the primary methylation index (PMI) and secondary methylation index (SMI) was lower in the ninth year of arsenic exposure compared with the seventh year. Substantial differences in relative arsenic methylation capacity were observed between the seventh and ninth year. Percentages of arsenic species, PMI and SMI were significantly correlated between siblings, and between parents and children. CONCLUSIONS:Arsenic methylation may decrease, but oxidative DNA lesions may increase with the increase of cumulative arsenic exposure level. Both genetic and environmental factors may contribute to variability in arsenic methylation.
Authors: Andrew D Kligerman; Carolyn L Doerr; Alan H Tennant; Karen Harrington-Brock; James W Allen; Ernest Winkfield; Patricia Poorman-Allen; Bijit Kundu; Kunihiro Funasaka; Barbara C Roop; Marc J Mass; David M DeMarini Journal: Environ Mol Mutagen Date: 2003 Impact factor: 3.216
Authors: Julia E Heck; Mary V Gamble; Yu Chen; Joseph H Graziano; Vesna Slavkovich; Faruque Parvez; John A Baron; Geoffrey R Howe; Habibul Ahsan Journal: Am J Clin Nutr Date: 2007-05 Impact factor: 7.045
Authors: Christopher A Loffredo; H Vasken Aposhian; Mariano E Cebrian; Hiroshi Yamauchi; Ellen K Silbergeld Journal: Environ Res Date: 2003-06 Impact factor: 6.498
Authors: Karin Schläwicke Engström; Karin Broberg; Gabriela Concha; Barbro Nermell; Margareta Warholm; Marie Vahter Journal: Environ Health Perspect Date: 2007-01-08 Impact factor: 9.031
Authors: Xi Shuhua; Sun Qingshan; Wang Fei; Liu Shengnan; Yan Ling; Zhang Lin; Song Yingli; Yan Nan; Sun Guifan Journal: J Expo Sci Environ Epidemiol Date: 2013-12-27 Impact factor: 5.563