Publications by authors named "A A Tinkov"

Manganese (Mn) is an essential trace element crucial for various physiological processes, but excessive exposure can lead to significant health concerns, particularly neurotoxicity. This review synthesizes current knowledge on Mn-induced oxidative stress and its role in cellular dysfunction and disease. We discuss how Mn promotes toxicity through multiple mechanisms, primarily through reactive oxygen species (ROS) generation, which leads to oxidative stress and disruption of cellular processes.

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Exposure to metal nanoparticles (NPs) is known to induce inflammatory responses in various tissues, thus limiting their therapeutic potential. NOD-like receptor protein 3 (NLRP3) inflammasome activation is an essential component of innate immunity playing a significant role in inflammation and development of inflammatory diseases. Therefore, the objective of the present review was to summarize data on the role of NLRP3 inflammasome in proinflammatory effects induced by metal NPs, and to discuss the underlying molecular mechanisms, including its dependence on the physical and chemical properties of metal NPs.

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Integration of various types of omics data is an important trend in contemporary molecular oncology. In this regard, high-throughput analysis of trace and essential elements in cancer biosamples is an emerging field that has not yet been sufficiently addressed. For the first time, we simultaneously obtained gene expression profiles (RNA sequencing) and essential and trace element profiles (inductively coupled plasma mass spectrometry) for a set of human cancer samples.

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The objective of the present study was to assess serum and cancerous tissue biometal levels in colorectal cancer (CRC) patients, and its relation to disease severity. A total of 90 CRC patients and 97 controls were involved in the present study. The level of biometals in blood serum and colon tissues (only in CRC cases) was evaluated by inductively-coupled plasma mass-spectrometry.

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Copper (Cu) is essential for brain development and function, yet its overload induces neuronal damage and contributes to neurodegeneration and other neurological disorders. Multiple studies demonstrated that Cu neurotoxicity is associated with mitochondrial dysfunction, routinely assessed by reduction of mitochondrial membrane potential. Nonetheless, the role of alterations of mitochondrial dynamics in brain mitochondrial dysfunction induced by Cu exposure is still debatable.

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