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Protein Carbonylation as the Pathogenesis of Oral Hyperkeratosis: A Pilot Study

Akiko Kumagai and Koichi Tsunoda

Objective: We examined the etiology of hyperkeratosis of the oral mucosa, focusing on antioxidant actions and oxidative stress related to the accumulation of oxidized and damaged molecules.

Materials and Methods: The subjects were non-smoking females with squamous cell hyperplasia, oral lichen planus, epithelial dysplasia, or squamous cell carcinoma. Proteins were extracted from hyperkeratosis tissue specimens. Carbonylated proteins, serving as oxidative stress markers, were detected by western blotting and identified by nano-liquid chromatography-tandem mass spectrometry. In addition, we performed immunohistochemical staining of oral mucosa tissue sections using an anti-hexanoyl-lysine (HEL) antibody.

Results: Several carbonylated proteins from hyperkeratosis tissue of the oral mucosa were detected by western blot and identified asalpha-actinin-1 isoform a, tumor rejection antigen (gp96) 1, alpha-actinin 4, and neutral alphaglucosidase AB isoform 3 precursors. On immunohistochemical staining with the anti-HEL antibody, the prickle to basal cell layers in cornified lesions were positive. These results indicate the presence of local oxidative stressinduced changes in hyperkeratosis tissues and suggest a new approach for treating oral mucosal keratotic lesions.