Serum CA19-9 and CEA levels, serum CAT, GSH, oxidised glutathione levels, 8-dihidro-2'-deoksiguanosina and F2-isoprostanes levels in colorectal cancer patients and Lactobacillus: A randomised double-blind controlled trial.

BACKGROUND: Oxidative stress (OS) plays a crucial role in colorectal cancer (CRC) progression. Lactobacillus has been proposed as a potential modulator of OS. This randomised controlled trial aimed to evaluate the effects of Lactobacillus supplementation on OS markers and its related signalling pathways in CRC patients after surgery. METHODS: A total of 76 CRC patients were enrolled and randomised into two groups: the study group (n=39) received Lactobacillus supplementation, while the control group (n=37) received a placebo. The intervention lasted for six months following surgery. Serum levels of catalase (CAT), glutathione (GSH), oxidised glutathione (GSSG), 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), and F2-isoprostanes (F2-IsoPs) were measured. In addition, the nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1 (NRF2/KEAP1), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK) signalling pathways were assessed via western blot analysis. RESULTS: Following Lactobacillus supplementation, serum carcinoembryonic antigen (CEA) levels significantly decreased, whereas carbohydrate antigen 19-9 (CA19-9) levels remained unchanged. OS marker analysis demonstrated increased CAT, GSH, and F2-IsoPs levels and decreased GSSG and 8-oxodG levels in the study group compared to the control group. Western blot results revealed that NRF2, ASK1, MKK3, p-p38, and MKK4 protein levels were significantly reduced after Lactobacillus intervention, while KEAP1 and p-JNK remained unchanged. CONCLUSIONS: Oral administration of Lactobacillus for six months reduced OS marker levels and inhibited NRF2/KEAP1, p38 MAPK, and JNK signalling pathways in CRC patients after surgery. These findings suggest that Lactobacillus may contribute to CRC management by modulating oxidative stress.