Molecular mechanisms of nickel carcinogenesis.
Humans are exposed to carcinogenic nickel (Ni) compounds both occupationally and environmentally. In this paper, molecular mechanisms of nickel carcinogenesis are considered from the point-of-view of the uptake of nickel sulfide particles in cells, their dissolution and their effects on heterochromatin. Molecular mechanisms by which nickel induces gene silencing, DNA hypermethylation and inhibition of histone acetylation, will be discussed.
Cangul
H
H
Department of Environmental Medicine, New York University School of Medicine, 550 First Avenue, New York, USA.
Broday
L
L
Salnikow
K
K
Sutherland
J
J
Peng
W
W
Zhang
Q
Q
Poltaratsky
V
V
Yee
H
H
Zoroddu
M A
MA
Costa
M
M
D000107:Acetylation / Q000187:drug effects; D000818:Animals; D002273:Carcinogens / Q000009:adverse effects* / Q000493:pharmacokinetics / Q000633:toxicity; D002470:Cell Survival / Q000187:drug effects; D004249:DNA Damage; D053938:DNA Fragmentation / Q000187:drug effects; D019175:DNA Methylation / Q000187:drug effects; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism; D020868:Gene Silencing / Q000187:drug effects; D006657:Histones / Q000378:metabolism; D006801:Humans; D009369:Neoplasms / Q000139:chemically induced* / Q000235:genetics / Q000378:metabolism; D009532:Nickel / Q000009:adverse effects* / Q000493:pharmacokinetics / Q000633:toxicity
D002273:Carcinogens; D006657:Histones; D009532:Nickel