Abstract

Cadmium (Cd), widely present in food and drinking water at low doses, can cause health risks. However, the mechanistic effects of long-term Cd exposure at low dose through dietary intake is poorly studied. The aim of this study is to elucidate whether the dysbiosis of gut microbiota caused by Cd at an environmental low dose can aggravate the injury of mice liver, and the possible mechanism is investigated. In order to explore the potential underlying mechanism, the analyses of the variation of gut microbiota composition, intestinal permeability, and hepatic transcriptome were conducted. Our results showed that gut microbiota was disturbed. The rise of intestinal permeability induced by the dysbiosis of gut microbiota resulted in more Cd ions accumulating in mice liver, but it could be restored partly through depleting gut microbiota by antibiotics cocktail. Transcriptomic analyses indicated that 162 genes were significantly differentially expressed including 59 up-regulated and 103 down-regulated in Cd treatment. These genes were involved in several important pathways. Our findings provide a better understanding about the health risks of cadmium in the environment.

Highlights

  • Cd, a non-essential toxic metal, is widely distributed in soils, air dust and water

  • Since Cd usually enter the host by food or drinking water, the composition of gut microbiota might be altered after contact with Cd in the digestive tract

  • These results suggested that even low-level Cd treatment can induce the alteration of gut microbiota

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Summary

Introduction

A non-essential toxic metal, is widely distributed in soils, air dust and water. It can produce multiple health risks even at environmental low dose [1,2]. Apart from that, several studies based on transcriptional analyses discovered that the expression of some hepatic genes is altered under Cd toxicity in animals [9,10,11]. These genes are involved in transcriptional regulation, cell proliferation, stress response, apoptosis, nutrition metabolism. The health risk at low-level exposure and its underlying mechanism need further study

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