👤 Andrey Y. Abramov

While various metal complexes demonstrate immunogenic cell death (ICD)-inducing properties, there is a lack of studies comparing ICD properties in structurally similar complexes with different metal centers. In this study, we synthesized four structurally similar Rh(I) and Ir(I) complexes with redox-active 1,2-bis(arylimino)acenaphthene (Ar-bian) ligands and assessed their anticancer and ICD-inducing properties. Analysis of damage-associated molecular patterns (DAMPs), ROS localization and dying cell populations highlighted the distinct roles of the metal center and the ligands. Specifically, only Rh(I) complexes induced the release of the three essential DAMPs and high levels of late apoptotic cells, while the Ir(I) complexes failed to trigger crucial “eat-me” signals. This work offers valuable insights into structure–activity relationships in metal complexes in the context of ICD. Show less

AbstractThe world's population aging progression renders age‐related neurodegenerative diseases to be one of the biggest unsolved problems of modern society. Despite the progress in studying the development of pathology, finding ways for modifying neurodegenerative disorders remains a high priority. One common feature of neurodegenerative diseases is mitochondrial dysfunction and overproduction of reactive oxygen species, resulting in oxidative stress. Although lipid peroxidation is one of the markers for oxidative stress, it also plays an important role in cell physiology, including activation of phospholipases and stimulation of signaling cascades. Excessive lipid peroxidation is a hallmark for most neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and many other neurological conditions. The products of lipid peroxidation have been shown to be the trigger for necrotic, apoptotic, and more specifically for oxidative stress‐related, that is, ferroptosis and neuronal cell death. Here we discuss the involvement of lipid peroxidation in the mechanism of neuronal loss and some novel therapeutic directions to oppose it. Show less