Abstract: To investigate the regulatory effect of lactic acid bacteria on the toxicity by perfluorooctane sulfonate (PFOS) in mice and its possible mechanism, 36 male C57BL/6J mice were randomized into six groups. The control group and the PFOS model group were treated with 30 g/L (sucrose) solution, while the four strain intervention groups (Lactobacillus bulgaricus D2A49, Lactobacillus bulgaricus DQHXNS3L9, Pediococcus pentosaceus FFSCDJY63L2 and Pediococcus pentosaceus JSNJPK1-1) were treated with lactic acid bacteria resuspended in 30 g/L(sucrose) solution for 30 days (109 CFU/mL). From day 16 to 30, the PFOS model group and the strain intervention groups were exposed with 3 μg/(g BW·d) PFOS. Liver parameters such as liver index, IL-1β, TNF-α and serum liver enzymes levels were determined; histopathological analysis was performed for liver and colon; the levels of IL-10, TNF-α and the tight junction protein in colon and short-chain fatty acids in faces were also examined. The results indicated that PFOS exposed mice developed hallmark features of liver and intestinal damage, and lactic acid bacteria attenuated the development of the damage. Further analysis demonstrated that supplementation with L. bulgricus DQHXNS3L9 and L. bulgricus D2A49 significantly decreased the liver index, serum liver enzyme content and intestine inflammation, attenuated the pathological changes in liver and colon tissues, and elevated the level of the tight junction protein in colon and short-chain fatty acids in stool. Therefore, lactic acid bacteria showed the capabilities in preventing and alleviating liver and intestinal damage caused by PFOS exposure through short-chain fatty acids regulation with individual differences.
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