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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. 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 0.97). Activated carbon at 1:10 effectively reduces nicotine burden, inflammation, oxidative stress, and mucosal cytotoxicity, limiting oral leukoplakia progression in vivo.
Arma et al. (Thu,) studied this question.