Activated carbon attenuates nicotine and Candida albicans-induced oral leukoplakia via modulation of IL-17R signaling and oxidative stress: an in vivo study

OBJECTIVES: This study evaluated the therapeutic potential of coconut-shell-derived activated carbon (AC) in attenuating oral leukoplakia induced by cigarette smoke condensate (CSC) nicotine and Candida albicans, focusing on nicotine burden, fungal growth, interleukin-17 receptor (IL-17R) expression, oxidative stress (malondialdehyde, MDA), and mucosal cytotoxicity. MATERIALS AND METHODS: An in vivo experimental study was conducted using Rattus norvegicus (n = 25), divided into five groups: negative control (CSC-nicotine + C. albicans), positive control (triamcinolone acetonide 1%), and AC-treated groups (1:10, 1:20, 1:30). Oral mucosal changes were assessed macroscopically and histologically. Free nicotine was measured by FTIR, IL-17R, and MDA by ELISA, and cell viability by MTT assay. Statistical analyses included ANOVA, the Kruskal–Wallis test, and correlation tests (p < 0.05). RESULTS: CSC-nicotine and C. albicans induced progressive leukoplakia-like lesions with high dysplasia scores, elevated IL-17R (182.4 ± 11.2 pg/mL), MDA (3.1 ± 0.2 nmol/mg), and low cell viability (46.2 ± 4.8%). AC at 1:10 significantly reduced fungal growth (− 53.3%), free nicotine (39 ± 7 µg/mL), IL-17R (101.5 ± 7.9 pg/mL), and MDA (1.7 ± 0.3 nmol/mg), while restoring cell viability (94.6 ± 6.1%), comparable to the positive control. Strong correlations were observed between nicotine, IL-17R, and MDA (r > 0.97). CONCLUSIONS: Activated carbon at 1:10 effectively reduces nicotine burden, inflammation, oxidative stress, and mucosal cytotoxicity, limiting oral leukoplakia progression in vivo.