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.