Numerous studies have confirmed that the apoptosis induced by the methacrylate resin monomers triethyleneglycol-dimethacrylate (TEGDMA), 2-hydroxy ethyl methacrylate (HEMA), etc., in pulp cells and odontoblast-like cells is caused mainly by oxidative stress (OS). Reactive oxygen species (ROS), recognized as the most important risk factor for apoptosis in cells of the pulp–dentin complex, are produced mainly via the mitochondrial respiratory chain. When the free resin monomers in the oral cavity and pulp reach a toxic level, the monomers induce oxidative DNA damage, activate ATM-p53 in the nucleus, and mediate the intrinsic apoptotic pathway in the presence of Bcl-2 family proteins. A vicious cycle is established between OS cellular responses and abnormalities in mitochondrial dynamics that accelerate apoptosis. Despite numerous products generated via iteration, complete polymerization of resin monomers is not currently possible. The cytotoxicity of free monomers may lead to adverse reactions, such as pulp sensitivity. This review is based on the most important papers describing the roles of resin monomers in mediating apoptosis in the pulp–dentin complex and provides an overview of the precise mechanisms related to mitochondrion-mediated cytotoxicity, suggesting ways to reduce or eliminate their cytotoxicity in the future through advancements in material technology.

A simple monitoring method has been proposed by measuring uranium (U) concentration and its chemical form in serum. The droplet of the 1 µL rat serum specimen was then examined by subjecting it to high energy synchrotron radiation X-ray fluorescence spectroscopy (SR-XRF) and X-ray absorption fine structure (XAFS) to determine the concentration and chemical form of U. The detection limit of U in 1 µL droplet was calculated to be 0.071 µg/g. The U concentration in the specimen obtained from the rat exposed to U was consistent with that determined by inductively coupled plasma mass spectrometry. Uranium in the rat serum was estimated to be hexavalent U based on the standard specimens of tetravalent and hexavanet U. This method developed might be used for monitoring and decorporation of patients at nuclear disasters and environmental pollution.

Chlorfenapyr is a novel pyrrole compound with the chemical formula C15H11BrClF3N2O, exhibiting potent insecticidal and acaricidal effects. It primarily acts on the multi-functional oxidases in the mitochondria of insects, inhibiting the conversion of adenosine diphosphate to adenosine triphosphate, leading to cellular dysfunction due to energy depletion. With increased production and market availability, the population’s exposure to chlorfenapyr has risen, resulting in a growing number of fatal poisoning incidents. This report describes the clinical presentation, disease progression, and treatment outcomes of a 2-year and 11-month-old toddler poisoned with chlorfenapyr. The child exhibited symptoms of nausea and vomiting two hours post-poisoning, received gastric lavage and fluid replacement at the local hospital, and was subsequently transferred to our facility. On admission, the child's vital signs were stable for the first two days, with normal laboratory findings. On the third day, the child showed signs of fatigue and diaphoresis, followed by high fever, profuse sweating, altered consciousness, and muscle tremors on the fourth day. By the fifth day, the child displayed rigid muscles in the limbs and trunk, respiratory and circulatory failure, despite rescue efforts proving futile, leading to eventual demise.

Ferroptosis, a mode of cell death involving iron-dependent lipid peroxidation, has attracted widespread attention in the development of anticancer drugs and toxicological studies as a potential mechanism of chemical-induced cytotoxicity. This process is regulated by several antioxidant enzymes, of which the selenium-containing glutathione peroxidase 4 (GPx4) is the prime regulator. However, accurately and reproducibly evaluating ferroptosis in cultured cells is challenging since numerous experimental factors in in vitro setting can influence the results. In the present study, we found that the expression levels of selenoproteins, such as GPx4 and GPx1, fluctuate across several cell lines depending on the selenium content of different origin of fetal bovine serum (FBS). Cells cultured in FBS containing higher selenium concentrations exhibited elevated GPx4 expression, and were resistant to ferroptosis induced by erastin and RSL3. These findings suggest that the variability of selenium content in different FBS batches can significantly influence the susceptibility of cells to ferroptosis, highlighting the importance of standardizing these factors to enhance the reproducibility of ferroptosis-related experiments.