Insights into the mechanism of transcription factors in Pb2+-induced apoptosis.

The health risks associated with exposure to heavy metals, such as Pb2+, are increasingly concerning the public. Pb2+ can cause significant harm to the human body through oxidative stress, autophagy, inflammation, and DNA damage, disrupting cellular homeostasis and ultimately leading to cell death. Among these mechanisms, apoptosis is considered crucial. It has been confirmed that transcription factors play a central role as mediators during the apoptosis process. Interestingly, these transcription factors have different effects on apoptosis depending on the concentration and duration of Pb2+ exposure. In this article, we systematically summarize the significant roles of several transcription factors in Pb2+-induced apoptosis. This information provides insights into therapeutic strategies and prognostic biomarkers for diseases related to Pb2+ exposure.

Mitochondrion: a sensitive target for Pb exposure.

Pb exposure is a worldwide environmental contamination issue which has been of concern to more and more people. Exposure to environmental Pb and its compounds through food and respiratory routes causes toxic damage to the digestive, respiratory, cardiovascular and nervous systems, etc. Children and pregnant women are particularly vulnerable to Pb. Pb exposure significantly destroys children's learning ability, intelligence and perception ability. Mitochondria are involved in various life processes of eukaryotes and are one of the most sensitive organelles to various injuries. There is no doubt that Pb-induced mitochondrial damage can widely affect various physiological processes and cause great harm. In this review, we summarized the toxic effects of Pb on mitochondria which led to various pathological processes. Pb induces mitochondrial dysfunction leading to the increased level of oxidative stress. In addition, Pb leads to cell apoptosis via mitochondrial permeability transition pore (MPTP) opening. Also, Pb can stimulate the development of mitochondria-mediated inflammatory responses. Furthermore, Pb triggers the germination of autophagy via the mitochondrial pathway and induces mitochondrial dysfunction, disturbing intracellular calcium homeostasis. In a word, we discussed the effects of Pb exposure on mitochondria, hoping to provide some references for further research and better therapeutic options for Pb exposure.