Sakshi Arora, Jaya Joshi, Rutuja Patil, Arushi Chaure, Astha Pusame, Nimisha Subhash
The findings showed higher expression of XRCC1 and HIF-1α in gutkha chewers without lesions, indicating that early stress-induced DNA damage and hypoxia may activate cellular DNA repair machinery and the release of protective transcription factors as an adaptive response. However, the finding of down-regulation in OSMF suggests depletion of repair proteins and cellular tolerance to the damage that occurs with persistent stress exposure.
OBJECTIVE: This study aimed to investigate the levels of deoxyribonucleic acid (DNA) repair under the hypoxic conditions of oral submucous fibrosis (OSMF) using X-ray repair cross-complementing protein 1 (XRCC1) and hypoxia-inducible factor 1-alpha (HIF-1α) in saliva samples.
MATERIALS AND METHODS: A cross-sectional study was conducted at Department of Oral and Maxillofacial Pathology and Oral Microbiology, Government College of Dentistry, Indore, India. A total of 45 participants were divided into three groups that is, controls without any history of gutkha use, gutka chewers without oral lesions, and gutka chewers with OSMF. Enzyme-linked immunosorbent assay (ELISA) test was performed to measure the expression of XRCC1 and HIF-1α in saliva samples.
RESULTS: Salivary XRCC1 levels were significantly higher in gutkha chewers without oral lesions compared to controls and OSMF patients (P = .023). Similarly, salivary HIF-1α levels were also significantly elevated in gutkha chewers without oral lesions compared to both controls and OSMF patients (P = .028). In addition, post hoc analysis confirmed that gutkha chewers without oral lesions and the two other participant groups differed significantly for both biomarkers. However, a statistically nonsignificant correlation was found between XRCC1 and HIF-1α.
CONCLUSION: The findings showed higher expression of XRCC1 and HIF-1α in gutkha chewers without lesions, indicating that early stress-induced DNA damage and hypoxia may activate cellular DNA repair machinery and the release of protective transcription factors as an adaptive response. However, the finding of down-regulation in OSMF suggests depletion of repair proteins and cellular tolerance to the damage that occurs with persistent stress exposure.