Moreover, Cd is also associated with airway inflammation, cardiovascular diseases, diabetes, neurological diseases and several cancers. The gastrointestinal tract acts as the first organ susceptible to the xenobiotics. The Senegenin normal microflora comprises diverse populations of bacteria and has mutual relationship with intestinal epithelial cells. They are known to live and in symbiosis and play an essential role in the development and health of the host by improving the intestinal tract microbial balance as well as detoxification and elimination of poisonous compounds from the body by removing metals through precipitation and other ways. The indigenous GI tract microflora has profound effects on the physiological and immunological development of the host. The intestinal microflora of mammals is involved in host nutrition. The presence of commensal bacteria in the intestinal tract also provides the first barrier of defense against pathogenic bacteria. The indigenous microflora stimulates the host immune system to respond more quickly to outer challenges. It is well known that the imbalance in the relationship between intestinal epithelial cells and bacteria results in GI disorders. However, early studies of the effects of xenobiotics on gut microbiota were limited by the use of culture-based technologies that identified,5% of the extant GI tract microbes. Culture-independent investigation of ribosomal RNA sequences allows the microbial population and structure of the gut microbiota to be profiles with greater Ganoderic-acid-F resolution. Toxicants, including heavy metals and pathogens reach intestine following ingestion of contaminated food and water, and interact with an ecosystem of eukaryotic and prokaryotic cells. Since microorganisms play a major role in the host homeostasis, the effect of heavy metal toxicity on gut microflora has received attentions in recent years. However, the toxicological effect of heavy metals, especially Cd on GI microflora, is still remains unclear. The present study explores the toxic effects of Cd on the changes of intestinal bacteria quantity and SCFAs metabolism. Here, we used a murine model to gain insight into the toxicity of Cd to intestinal microbiota. In this study, we focused on the microbiota and its response to host consumption of water containing Cd. We found that the growth rate of intestinal microbiota was inhibited significantly in vitro under Cd stress. Gut barrier was impaired as a result of Cd accumulation in intestine. Probiotic Bifidobacteria and Lactobacilli received more stress from Cd than other components of gut bacteria. Cd intake resulted in a decrease of butyrate-producing bacteria, which leads to the increase in cecal pH, and decrease in fecal SCFAs. This study provides a gut microbe-based framework for evaluating responses to Cd intake. The existence of heavy metals in living organisms can generate different degrees of adverse effects on liver, brain, intestinal systems and et.al.. For example, previous data suggest that heavy metals contribute to gut barrier alterations because intestine is the main absorbing section. However, the different mechanisms of the interaction between heavy metals and the host that affect gut barrier function have not been fully elucidated. We determined Cd levels for different duration of exposure. As shown in this study, administration of CdCl2 resulted in clearly elevated Cd level in some tissue samples. Since the accumulation of Cd, the histological structure and function of intestine could be harmed, definitely including the intestinal microbiota. However, different effects of Cd toxicity would be exhibited according to the exposure duration and dosage to Cd.