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The accumulation of ROS can initiate apoptosis through several key mechanisms: Firstly, ROS can damage the mitochondrial membrane, leading to a decrease in mitochondrial membrane potential, which in turn promotes the release of proteins like cytochrome C (Liu et al., 2024c)

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Conversely, if Drug A is an inhibitor of a CYP that also metabolizes Drug B, it will slow metabolism of Drug B, possibly raising its concentration to toxic levels

Elevated levels of ferritin and transferrin, markers of iron dysregulation, have been observed in clinical ARDS cases, linking iron metabolism to disease severity ( Mitochondrial dysfunction exacerbates iron-driven ferroptosis by impairing the organelles ability to sequester and regulate iron levels

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As mercury can readily cross the placenta (WHO, 2003), fetal exposure represents a concern in association with the inhalation of mercury by pregnant women (WHO, 1991