Exposing to cadmium stress cause profound toxic effect on microbiota of the mice intestinal tract.
Cadmium (Cd), one of the heavy metals, is an important environmental pollutant and a potent toxicant to organism. It poses a severe threat to the growth of the organism, and also has been recognized as a human carcinogen. However, the toxicity of cadmium and its influences on microbiota in mammal's intestine are still unclear. In our experiment, the changes of intestinal microbiota in two groups of mice were investigated, which were supplied with 20 and 100 mg kg(-1) cadmium chloride respectively for 3 weeks. The control group was treated with water free from cadmium chloride only. This study demonstrated that Cd accumulated in some tissues of mice after Cd administration and the gut barrier was impaired. Cd exposure also significantly elevated the colonic level of TNF-α. On the other hand, Cd-treatment could slow down the growth of gut microbiota and reduced the abundance of total intestinal bacteria of the mice. Among them, the growth of Bacteroidetes was significantly suppressed while Firmicutes growth was not. The probiotics including Lactobacillus and Bifidobacterium were notably inhibited. We also observed that the copies of key genes involved in the metabolism of carbohydrates to short-chain fatty acids (SCFAs) were lower in Cd-treated groups than control. As a result, the levels of short-chain fatty acids in colonic decreased significantly. In summary, this study provides valuable insight into the effects of Cd intake on mice gut microbiota.
School of Public Health, Anhui Medical University, Hefei, Anhui Province, People's Republic of China.
Yehao
Y
Liu
Department of Biological and Environmental Engineering, Hefei Univeristy, Hefei, Anhui Province, People's Republic of China.
Yuhui
Y
Li
School of Public Health, Anhui Medical University, Hefei, Anhui Province, People's Republic of China.
Kaiyong
K
Liu
School of Public Health, Anhui Medical University, Hefei, Anhui Province, People's Republic of China.
Jie
J
Shen
D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics; D041963:Bacteroidetes / Q000187:drug effects / Q000235:genetics / Q000254:growth & development; D001644:Bifidobacterium / Q000187:drug effects / Q000235:genetics / Q000254:growth & development; D002104:Cadmium / Q000097:blood / Q000378:metabolism / Q000633:toxicity*; D015256:Coenzyme A-Transferases / Q000235:genetics; D003106:Colon / Q000187:drug effects / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005232:Fatty Acids, Volatile / Q000378:metabolism; D005243:Feces / Q000382:microbiology*; D005260:Female; D005574:Formate-Tetrahydrofolate Ligase / Q000235:genetics; D015964:Gene Expression Regulation, Bacterial / Q000187:drug effects; D007422:Intestines / Q000382:microbiology*; D007778:Lactobacillus / Q000187:drug effects / Q000235:genetics / Q000254:growth & development; D051379:Mice; D008807:Mice, Inbred BALB C; D064307:Microbiota / Q000187:drug effects*; D009093:Mucus / Q000187:drug effects / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D001426:Bacterial Proteins; D005232:Fatty Acids, Volatile; D014409:Tumor Necrosis Factor-alpha; D002104:Cadmium; D015256:Coenzyme A-Transferases; D005574:Formate-Tetrahydrofolate Ligase