ABSTRACT
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.
Subject(s)
Oxyphil Cells/enzymology , Peroxiredoxins/analysis , Salivary Glands/enzymology , Adenocarcinoma/enzymology , Adenocarcinoma/pathology , Adenolymphoma/enzymology , Adenolymphoma/pathology , Adenoma, Oxyphilic/enzymology , Adenoma, Oxyphilic/pathology , Antioxidants/analysis , Biomarkers/analysis , Carcinoma, Mucoepidermoid/enzymology , Carcinoma, Mucoepidermoid/pathology , Free Radical Scavengers/analysis , Gene Expression Regulation, Enzymologic , Granular Cell Tumor/enzymology , Granular Cell Tumor/pathology , Humans , Hydrogen Peroxide/analysis , Hyperplasia , Lysosomes/pathology , Metaplasia , Mitochondria/pathology , Oxyphil Cells/pathology , Reactive Oxygen Species/analysis , Salivary Gland Neoplasms/enzymology , Salivary Gland Neoplasms/pathology , Salivary Glands/pathology , Thyroid Gland/pathologyABSTRACT
We recently established diagnostic criteria for granular cell changes in the distal female reproductive tract of rats. In a review of control animals from 9 carcinogenicity studies, we found that approximately 23% of animals had granular cell alterations. Because estrogen may play a role in the pathogenesis of granular cell alterations, we reviewed tissue sections from carcinogenicity studies with 2 aromatase inhibitors and found compound-related decreases in the incidence of granular cell changes. Since these aromatase inhibitors selectively prevent the conversion of androgenic steroids to the corresponding estrogens, these data further suggest that estrogen may play a role in the pathogenesis of granular cell tumors of the reproductive tract of rats.
