Open AccessNitrative and oxidative DNA damage in oral lichen planus in relation to human oral carcinogenesis
Author(s) -
Chaiyarit Ponlatham,
Ma Ning,
Hiraku Yusuke,
Pinlaor Somchai,
Yongvanit Puangrat,
Jintaka Darunee,
Murata Mariko,
Oikawa Shinji,
Kawanishi Shosuke
Publication year - 2005
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2005.00096.x
Subject(s) - oral lichen planus , pathology , cancer , epithelium , nitrotyrosine , oral mucosa , dna damage , carcinogenesis , biopsy , cancer research , biology , medicine , nitric oxide , nitric oxide synthase , dna , biochemistry
Oral lichen planus (OLP) is a chronic inflammatory disease, which has been clinically associated with development to oral cancer. A double immunofluorescence labeling study found that 8‐nitroguanine and 8‐oxo‐7,8‐dihydro‐2′‐deoxyguanosine (8‐oxodG) accumulated in oral epithelium in OLP and oral squamous cell carcinoma (OSCC) biopsy specimens, whereas little or no immunoreactivity was observed in normal oral mucosa. Colocalization of 8‐nitroguanine and inducible nitric oxide synthase (iNOS) was found in oral epithelium of OLP and OSCC. Immunoreactivity of 3‐nitrotyrosine, which is formed by protein tyrosine nitration and is considered to be a biochemical marker for inflammation, was also observed in oral epithelial cells and colocalized with 8‐nitroguanine. Accumulation of p53 was more strongly observed in oral epithelium in OSCC than OLP, whereas there was no p53 accumulation in normal oral mucosa. Our findings demonstrate that iNOS‐dependent DNA damage in OLP may lead to p53 accumulation in not only OLP but also OSCC. We conclude that the formation of potentially mutagenic DNA lesions including 8‐nitroguanine and 8‐oxodG may contribute to the development of oral cancer from OLP. ( Cancer Sci 2005; 96: 553 –559)