Chromium (Cr) is the seventh most abundant chemical element in the Earth’s crust, and Cr(III) and Cr(VI) are common stable valence states of Cr. Several Cr-containing substances, such as FeOCr2O3 and stainless-steel products, exist in nature and in life. However, Cr(VI) is toxic to soil, microorganisms, and plants and poses a serious threat to human health through direct and indirect exposure. By collecting published journal literature, we found that Cr(VI) can cause acute and chronic toxicity in organisms and has carcinogenic effects, and the mechanisms causing these toxicity include endoplasmic reticulum stress, autophagy and apoptosis. However, the relationship between these mechanisms remains unclear. Many methods have been researched to purify chromium, but each of these methods has its own advantages and disadvantages. Therefore, this review summarizes the hazards of chromium and the mechanisms of chromium toxicity after entering cells and provides a number of methods for chromium contamination management, providing a direction for the next step in chromium toxicology and contamination decontamination research.

Hexavalent chromium (Cr(VI)) is a widespread heavy metal that has been identified as a human carcinogen, and acute or chronic exposure to Cr(VI) can cause organ damage. Platycodon grandiflorus polysaccharide (PGPS) is a constituent extracted from the Chinese herb Platycodon grandiflorus, which has various pharmacological effects. Therefore, the author investigated the role of PGPSt in Cr(VI)-induced apoptosis in chicken embryo fibroblast cell lines (DF-1 cells). Firstly, this study infected DF-1 cells using Cr(VI) to set up a model for cytotoxicity and then added PGPSt. Then, the intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and apoptosis rate were evaluated. The results showed that PGPSt could inhibit Cr(VI)-induced mitochondrial damage and increase the apoptosis rate. For further exploration of the mechanism of regulation of PGPSt, the ROS-Drp1 pathway was investigated. The antioxidant N-acetyl-L-cysteine (NAC) and mitochondrial division inhibitor 1(Mdivi-1) were added, respectively. The results showed that the NAC and Mdivi-1 restored abnormal mitochondrial fission and cell apoptosis. Thus, PGPSt can alleviate Cr(VI)-induced apoptosis of DF-1 cells through the ROS-Drp1 signaling pathway, which may suggest new research ideas for developing new drugs to alleviate Cr(VI) toxicity.