Adsorption Characterization of Lactobacillus sp. for Di-(2-ethylhexyl) phthalate.

Di-(2-ethylhexyl) phthalate (DEHP) is the widely detected plasticizer in foods whose exposure is associated with a myriad of human disorders. The present study focused on identifying Lactobacillus strains with high adsorption potential towards DEHP and further elucidating the mechanism of binding using HPLC, FTIR and SEM. Two strains, Lactobacillus rhamnosus GG and Lactobacillus plantarum MTCC 25,433, were found to rapidly adsorb more than 85% of DEHP in 2 h. Binding potential remained unaffected by heat treatment. Moreover, acid pre-treatment enhanced the DEHP adsorption. Chemical pre-treatments, such as NaIO4, pronase E or lipase, caused reduction in DEHP adsorption to 46% (LGG), 49% (MTCC 25,433) and 62% (MTCC 25,433), respectively, attributing it to cell wall polysaccharides, proteins and lipids. This was also corroborated by stretching vibrations of C = O, N-H, C-N and C-O functional groups. Furthermore, SDS and urea pre-treatment, demonstrated the crucial role of hydrophobic interactions in DEHP adsorption. The extracted peptidoglycan from LGG and MTCC 25,433 adsorbed 45% and 68% of DEHP, respectively, revealing the imperative role of peptidoglycan and its integrity in DEHP adsorption. These findings indicated that DEHP removal was based on physico-chemical adsorption and cell wall proteins, polysaccharides or peptidoglycan played a primary role in its adsorption. Owing to the high binding efficiency, L. rhamnosus GG and L. plantarum MTCC 25,433 were considered to be a potential detoxification strategy to mitigate the risk associated with the consumption of DEHP-contaminated foods.

Ameliorative potential of synbiotic combination of Lactobacillus sp. and polyphenols against Benzo[a]pyrene-induced toxicity in Caco-2 cell line.

Exposure to benzo[a]pyrene (B[a]P), a major global food safety concern, is often associated with increasing incidence of colorectal cancers. This in-vitro study was focused on the identification of potential B[a]P-adsorbing Lactobacillus strains and evaluation of the ameliorative effect of synbiotic combination of selected Lactobacillus sp. and polyphenols (quercetin or resveratrol) against B[a]P-induced intestinal toxicity in Caco-2 cells. Preliminary studies lead to the selection of Lactiplantibacillus plantarum MTCC 25433 strain that showed 86% of B[a]P adsorption in 2 h as compared to L. rhamnosus GG that showed 74% of B[a]P adsorption. B[a]P adsorption by MTCC 25433 was reduced to 9%, 16% and 20% upon pre-treatment with SDS, NaIO4 and mutanolysin, attributing the involvement of cell wall proteins and polysaccharides in the adsorption. Additionally, peptidoglycan of both strains adsorbed >50% of B[a]P. In-vitro assays revealed that the selected LAB mitigated the B[a]P-induced epithelial cell damage. Among the polyphenols, quercetin, resveratrol and curcumin, varied in their potency to mitigate B[a]P-induced oxidative stress, with curcumin being least effective. Combinations of selected Lactobacillus sp. and polyphenols were more potent in averting B[a]P-induced toxicity via increase in GSH (17-30 %), SOD (50-88 %), catalase (19-45 %), and reduction in IL-8 secretion (14-28 %) and barrier dysfunction. Principal component analysis affirmed the superior potency of combination of L. plantarum MTCC 25433 and quercetin in averting B[a]P-induced toxicity. Overall, this study highlighted a novel promising strategy of synbiotic combination of Lactobacillus sp. and polyphenols (quercetin or resveratrol) in alleviating the B[a]P-induced toxicity in intestinal epithelial cells.

An insight into the critical role of gut microbiota in triggering the phthalate-induced toxicity and its mitigation using probiotics.

Exposure to phthalates, a major food safety concern, has been implicated in various chronic human disorders. As dietary exposure serves as a primary exposure route for phthalate exposure, understanding the detrimental impact on the gastrointestinal tract and resident gut microbiota is indispensable for better managing public health risks. Various reports have explored the intricate interplay between phthalate exposure, gut microbiota dysbiosis and host pathophysiology. For instance, oral exposure of dibutyl phthalate (DBP) or di-(2-ethylhexyl) phthalate (DEHP) affected the Firmicutes/Bacteroidetes ratio and abundance of Akkermansia and Prevotella, ensuing impaired lipid metabolism and reproductive toxicity. In some cases, DEHP exposure altered the levels of gut microbial metabolites, namely short-chain fatty acids, branched-chain amino acids or p-cresol, resulting in cholesterol imbalance or neurodevelopmental disorders. Conversely, supplementation of gut-modulating probiotics like Lactococcus or Lactobacillus sp. averted the phthalate-induced hepatic or testicular toxicity through host gene regulation, gut microbial modulation or elimination of DEHP or DBP in faeces. Overall, the current review revealed the critical role of the gut microbiota in initiating or exacerbating phthalate-induced toxicity, which could be averted or mitigated by probiotics supplementation. Future studies should focus on identifying high-efficiency probiotic strains that could help reduce the exposure of phthalates in animals and humans.