Xylitol

Xylitol can be classified as a polyol and sugar alcohol, exhibiting inhibitory activity on cancer cell proliferation. It induces autophagy (Autophagy) and cell death in A549 cells by activating the autophagy signaling pathway, as evidenced by the increased expression of LC3-II and Atg5-Atg12 upon Xylitol treatment. Additionally, Xylitol inhibits acetaldehyde production by Candida species, thereby reducing their carcinogenic potential. In vivo, Xylitol induces alterations in the gut microbiota of mice, which may enhance cholesterol accumulation and upregulate hepatic ChREBP, while also slowing tumor growth in the B16F10 melanoma C57BL/6 mouse model^[1][2][3][4]. In Vitro:Xylitol (0.125% - 32%, 72 h) inhibits proliferation of A549, Caki, NCI-H23, HCT-15, HL-60, K562, and SK MEL-2 cells, with IC₅₀ ranging from 3.9% to 8.2%, and K562 being the most sensitive. Normal cells exhibited higher tolerance to Xylitol^[3].
Xylitol (6%, 24 h) induces cell death and autophagy in A549 cells^[3]. In Vivo:Xylitol (20%, i.t. (75%) + s.c. (25%), once daily for 2 weeks) transiently inhibits tumor growth in the B16F10 melanoma C57BL/6 mouse model, but fails to sustain inhibition, likely due to solution leakage^[1].
Xylitol (40 mg/kg and 194 mg/kg, drinking water intake, once daily for 16-18 weeks) modifies gut microbiota composition in HFD-fed C57Bl/6J mice but does not ameliorate HFD-induced dyslipidemia^[2].