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dc.contributorDepartment of Applied Biology and Chemical Technologyen_US
dc.contributor.advisorKwok, Wing-hin Kevin (FSN)en_US
dc.creatorWu, Manhui-
dc.identifier.urihttps://theses.lib.polyu.edu.hk/handle/200/14162-
dc.languageEnglishen_US
dc.publisherHong Kong Polytechnic Universityen_US
dc.rightsAll rights reserveden_US
dc.titleFood emulsifiers increase toxicity of food contaminantsen_US
dcterms.abstractEmulsifiers are used extensively in processed food to enhance product stability while emulsifiers mostly have low toxicity, recent studies have found that they could lead to alteration of gut microbiota community and subsequently gut inflammation. Such effects opened up further questions as to whether emulsifiers could lead to higher sensitivity of the individual due to higher chemical uptake and/or increased toxicity as a result of impaired gut lining integrity. Importantly, food emulsifiers are typically used in food products containing other food additives and contaminants. For example, food emulsifiers are used in baked products which also contain process contaminant acrylamide. We performed a local survey of over 100 baked products (e.g. bread, cookies, etc.) and all contains at least one food emulsifier. Therefore in this study we hypothesized that toxicity of two food contaminants of opposite spectrum of water solubility, namely acrylamide (AA) and benzo[a]pyrene (BAP), will be increased in the presence of two food emulsifiers of opposite spectrum of hydrophilic–lipophilic balance (HLB) values, namely polyoxyethylene sorbitan monooleate (Tween80; TW) and glycerol monostearate (G).en_US
dcterms.abstractThe hypothesis was first tested using three human cell lines (liver carcinoma cell line HepG2, small intestine epithelial cell HIEC-6, colorectal adenocarcinoma cell Caco-2), representing three organs of the GI tract. When AA or BAP was combined with low concentration of TW, toxicity significantly increased and decrease in cell viability compared to treatments without TW. When Tween80 was added, IC50 value of AA decreased by 56.1% in HepG2, 20.4% in HIEC-6 and 50% in Caco-2 at 72h. Co-exposure of TW led to significant different expression of inflammation and redox related genes compared with AA or BAP alone. Investigating with Caco-2 cells, uptake of contaminants and cell membrane permeability were enhanced by TW. Tight junction proteins expressions of Caco-2 monolayer also be influenced by TW. There was no significant effect caused by the addition of G. Our results suggested that TW have the ability to increase uptake and aggravate the inflammatory, oxidate stress and toxicity of AA and BAP.en_US
dcterms.abstractMixtures of emulsifiers (TW and G) and food contaminants (AA and BAP) were also tested using zebrafish via dietary exposure. In this whole animal model, both food emulsifiers increased the toxic effect of both food contaminants and significantly increased biomarkers expression related oxidative stress, inflammation, and cell death. Ingestion of AA and BAP contaminated diets with emulsifiers induced more severe damages to the liver and gut than the AA and BAP treatments alone, including fusion of villi, change in cell populations, inflammation and infiltration of immune cells, and foci of necrosis. Acute uptake of AA and BAP in liver and gut were also increased after emulsifiers addition.en_US
dcterms.abstractTo better understand the interaction of the mixtures to human, C57BL/6J mice were given AA and emulsifiers by oral gavage for 2 weeks. BAP was not carried out in this study due to the weaker effect of BAP. Similar to earlier chapters, AA combined with either emulsifier was found to have significantly higher expression pro-inflammatory cytokines and obesity biomarker of ileum than AA alone treatment. Moreover, the intestine barriers were more attenuated by AA in the presences of emulsifiers. Interestingly, AA and emulsifier mixture led to significant increase in mice weight but AA or either emulsifier alone had no significant effect on weight. Acute uptake experiment in SD rats showed that when co-exposed with TW or G, glycidamide, the primary metabolite of acrylamide, was significantly higher in the liver and gut. Transcriptome analysis of mice ileum carried out by RNAseq confirmed our findings by indicating lipid metabolic pathways, nervous system and immune pathways were more disrupted after addition of emulsifiers. The behavior test confirmed the higher neurotoxicity. Microbiota community analyzed through 16s sequencing of mice fecal pellets also showed addition of emulsifiers aggravated microbiota dysbiosis by increasing abundance of harmful bacteria that are associated with inflammation and obesity and decreased in bacteria that are associated with weight-loss.en_US
dcterms.abstractEffects of this mixture on human microbiota were investigated using in vitro fermentation and an ex vivo gastro-intestinal simulator SHIME for 1 day and 21 days respectively. 16S sequencing of microbial community data showed that emulsifiers aggravate effect of AA-induced gut dysbiosis which are associated with increased permeability, Crohn's disease, metabolic disorders and obesity. Results supported that effects observed in previous chapters have high potential to occur in humans.en_US
dcterms.abstractLastly, study was concluded by giving a general discussion of all results and their implications on human health. Limitations of this study and potential further research were also discussed.en_US
dcterms.abstractIn conclusion, exposure of emulsifiers and food contaminants caused leaky gut by disrupt gut barriers to increase absorption of food contaminants, followed by over-absorption of contaminants and their mixtures, contributing to activate inflammation, weigh gain and microbiota dysbiosis. The propose of subject is to draw the attention of risk assessors to make an adequate evaluation of emulsifiers and improve the toxicity assessment of mixtures of food contaminants and emulsifiers.en_US
dcterms.extentxix, 177 pages : color illustrationsen_US
dcterms.isPartOfPolyU Electronic Thesesen_US
dcterms.issued2023en_US
dcterms.educationalLevelPh.D.en_US
dcterms.educationalLevelAll Doctorateen_US
dcterms.accessRightsopen accessen_US

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