TCDD inhibits the proliferation of C17.2 cells through the activation of the c-Cbl/β-catenin signaling pathway.

2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD) belongs to the category of persistent environmental pollutants, and gestational exposure to TCDD can lead to cognitive, memory, and motor deficits, as well as altered neuron development in rodents. However, the molecular mechanisms underlying TCDD's neurotoxicity remine unclear. Neural stem cells (NSCs) possess the capacity for self-renewal and can generate various cell types within the brain, playing fundamental roles in brain development and regeneration.

2,3,7,8-Tetrachlorodibenzo-p-dioxin induces liver lipid metabolism disorder via the ROS/AMPK/CD36 signaling pathway.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is widely considered as the most toxic and common carcinogen in the world. Exposure to TCDD causes liver lipid metabolism disorder and steatosis. However, the molecular mechanism of TCDD-induced liver lipid accumulation is not completely clear.

Antimony trichloride induces a loss of cell viability via reactive oxygen species-dependent autophagy in A549 cells.

Antimony (Sb) is one of the most prevalent heavy metals and frequently leads to biological toxicity. Although autophagy is believed to be involved in metal-associated cytotoxicity, there is no evidence of its involvement following exposure. Moreover, the underlying mechanism of autophagy remains unclear.