Abstract
Cadmium (Cd) is a toxic metal inducing a range of adverse effects on organs including liver and kidneys. However, the underlying molecular mechanisms of Cd-induced intestinal toxicity through dietary intake is poorly studied. This study evaluated the toxic effects of Cd on intestinal physiology and confirmed the effectiveness of the protective mechanism of the probiotic Lactobacillus plantarum CCFM8610 against chronic Cd toxicity. After treatment with Cd, the HT-29 cell line was subjected to iTRAQ analysis, which revealed that changes in the proteomic profiles after Cd exposure were related to pathways involved in the stress response and carbohydrate metabolism. The results of an animal trial also indicated that 10 weeks of Cd exposure decreased the fecal water content and contractile response of colonic muscle strips in mice, and delayed the excretion time of the first black feces. L. plantarum CCFM8610 treatment provided protective effects against these Cd-induced intestinal motility dysfunctions by recovering the levels of neurotransmitters, including substance P, acetyl cholinesterase, vasoactive intestinal peptide, 5-hydroxytryptamine, calcitonin gene-related peptide, and nitric oxide, and suppressing the cellular stress response in mice (e.g., the inhibition of mitogen-activated protein kinase pathways). The administration of this probiotic was also observed to reduce Cd levels in the tissues and blood of the mice. Our results suggest a newly identified protective mechanism of probiotics against Cd toxicity that involves the recovery of intestinal motility and increase in fecal cadmium excretion.
Highlights
Cadmium (Cd) is a heavy metal widely distributed in the environment
Gene ontology (GO) analysis (Figure 2) indicated that the differentially expressed proteins after Cd exposure had a wide range of functions that could be categorized as biological processes, cellular components, and molecular functions
Of the proteins altered in the global stress response (Supplemental Table 2), eight heat-shock proteins were upregulated by a factor of 2–3 after Cd exposure
Summary
Cadmium (Cd) is a heavy metal widely distributed in the environment. Once Cd has accumulated in the host, it can induce a range of adverse effects on the liver, kidney, brain, bone, and reproductive systems [1,2,3,4]. The mechanisms of Cd toxicity have been well studied, including its competitive interference with the metabolism of essential divalent metals such as zinc and manganese, Lactobacilli Against Cadmium Toxicity cytotoxicity induced by the abnormal production of reactive oxide species, and disruption of protein structures by the binding of Cd to sulfhydryl groups [5,6,7]. A number of studies have demonstrated that the liver, kidneys, and lungs are the main targets of long-term Cd exposure [10], reports on the toxic effects of this heavy metal on the gut are relatively limited. Animal studies have shown that the oral administration of Cd induce pathological changes in gastric mucosa and intestinal villi [11]. The underlying molecular mechanisms of Cdinduced intestinal toxicity are not thoroughly understood
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