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Peroxiredoxin I is overexpressed in oncocytic lesions of salivary glands
Author(s) -
Demasi Ana P. D.,
Furuse Cristiane,
Altemani Albina,
Junqueira José L. C.,
Oliveira Paulo R. G.,
Araújo Vera C.
Publication year - 2009
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.2009.00753.x
Subject(s) - peroxiredoxin , salivary gland , mitochondrion , reactive oxygen species , biology , oxidative stress , organelle , lesion , immunohistochemistry , cytoplasm , pathology , mitochondrial dna , microbiology and biotechnology , endocrinology , gene , immunology , medicine , biochemistry , enzyme , peroxidase
Background: Oncocytic lesions, particularly frequent in the salivary glands, are characterized by cells with an atypical accumulation of mitochondria. This accumulation has been recognized as a compensatory mechanism to intrinsic functional defects of these organelles, resulting in energy production impairment and increased generation of reactive oxygen species (ROS), including hydrogen peroxide (H 2 O 2 ). Peroxiredoxin I (Prx I) is a H 2 O 2 scavenging protein and the expression of its yeast homolog was reported to be influenced by mitochondrial function. Methods: In this study, we evaluated Prx I expression in oncocytic lesions of salivary glands by immunohistochemistry. Results: Our results showed that Prx I is overexpressed in oncocytes regardless of the salivary gland lesion where they appear. Conclusions: These results suggest that Prx I expression in oncocytes is related to its ability to decompose mitochondrial‐derived H 2 O 2 and that it could provide to the cells a protective role in an environment that, by continuously producing potential DNA‐damaging ROS, predisposes to genome instability and cellular transformation.