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Long-term exposure to benzo(a)pyrene (BaP) poses a serious genotoxic threat to human beings. This in vitro study investigated the potential of inactivated Bifidobacterium animalis subsp. lactis BI-04 in alleviating the damage caused by BaP in colon epithelial cells. A concentration of BaP higher than 50 μM strongly inhibited the growth of colon epithelial cells. The colon epithelial cells were treated with 50 μM BaP in the presence or absence of inactivated strain BI-04 (~5 × 108 CFU/mL). The BaP-induced apoptosis of the colon epithelial cells was retarded in the presence of B. lactis BI-04 through activation of the PI3K/ AKT signaling pathway, and p53 gene expression was decreased. The presence of the BI-04 strain reduced the intracellular oxidative stress and DNA damage incurred in the colon epithelial cells by BaP treatment due to the enhanced expression of antioxidant enzymes and metabolism-related enzymes (CYP1A1). The data from comet assay, qRT-PCR, and western blot analysis showed that the cytotoxic effects of BaP on colon epithelial cells were largely alleviated because the bifidobacterial strain could bind to this carcinogenic compound. The in vitro study highlights that the consumption of commercial probiotic strain BI-04 might be a promising strategy to mitigate BaP cytotoxicity.

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The purpose of this study was to explore the hydrolytic ability of Lactobacillus helveticus CICC 22171 with regard to protein and the expression of enzyme genes during protein utilization. The results revealed that the strain hydrolyzed casein from the C-terminal, reached the maximum level in 6 h, and the number of amino acids in the hydrolyzed peptide was 7–33. The molecular weight was 652.4–3432.74 kDa. Hydrophobic peptides produced by hydrolysis were the source of β-casein bitterness. Leucine and glutamine were the preferred cleavage points after 1 h; tyrosine and tryptophan subsequently increased. The first step of hydrolysis was controlled by PrtP and PrtM genes and coordinated with the action of PrtH1 and PrtH2. The transport system consisted of DtpT, OppB, OppD and OppF. The hydrolytic third step endopeptidase system consisted of the aminopeptidases (PepN, PepC, PepM and PepA), the endopeptidases (PepE, PepF and PepO); the dipeptidases (PepV and PepD), the tripeptidase PepT; the proline peptidases (PepX, PepP, PepQ, PepR and PepI). The expression of CEP genes was significantly different, and the expression level of genes related to the transport system significantly increased from 0 to 1 h. The specificity of the substrate and action site of endopeptidase was abundant.

This study's previous work showed that the carcinogen and mutagen benzo(a)pyrene (BaP) can be adsorbed by Lactobacillus cells in vitro. However, in vivo BaP detoxification by lactic acid bacteria has not yet been investigated. The present study evaluates the effects of orally administered Lactobacillus plantarum CICC 23121 in BaP‐treated mice. Oral administration of 50 mg kg−1 BaP perturbed the intestinal microflora, caused Proteobacteria to predominate, and severely damaged DNA. However, oral administration of 5 × 1010 CFU mL−1 CICC 23121 in BaP‐treated mice enhances fecal BaP excretion from 181.70 ± 1.04 µg/(g∙h) to 271.47 ± 11.71 µg/(g∙h) after 6 h. Fecal BaP excretion reaches up to 280.66 ± 22.97 µg/(g∙h) after the first 4 days of orally administered CICC 23121 and decreased to 94.31 ± 2.64 µg/(g∙h) by day 11. Intestinal microbiota are restored and Firmicutes predominates. CICC 23121 alleviates BaP‐induced DNA damage and reduces tail length from 56.37 ± 5.31  to 39.69 ± 4.27 µm. Therefore, oral CICC23121 consumption is a promising strategy for reducing BaP toxicity in mice. To the best of our knowledge, this report is the first report to demonstrate in vivo that Lactobacillus cells can detoxify BaP.