Lydia M. Bilinsky
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
Researcher
Also affiliated: United States Food and Drug Administration (2018–2024); Duke University (2015); University of Michigan (2022); Arizona State University (2009–2017)
Unknown Researcher
Research Areas
Biomedical Subjects
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Biography and Research Information
OverviewAI-generated summary
Lydia M. Bilinsky's research focuses on the development and application of computational models to understand biological processes, particularly those related to cellular metabolism and stress responses. Her work has investigated the metabolism of endogenous hydrogen peroxide in hepatocytes, highlighting the role of glutathione (GSH) in its removal. Bilinsky has also developed computational models to predict intracellular hydrogen peroxide concentration and cell death during oxidative stress, with applications in pharmacokinetic/pharmacodynamic (PBPK/PD) modeling, such as for the trivalent arsenical DMA<sup>III</sup>.
Her research explores the regulatory mechanisms of mitochondrial energy metabolism and reactive oxygen species (ROS) production. By studying these processes, her work aims to provide insights into cell death pathways, the critical role of GSH depletion, and the tight regulation of intracellular hydrogen peroxide. Bilinsky's publications include work on theoretical models of biological systems and their application to toxicological studies.
Metrics
- h-index: 4
- Publications: 8
- Citations: 70
Selected Publications
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A computational model of endogenous hydrogen peroxide metabolism in hepatocytes, featuring a critical role for GSH (2024)
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A Computational Model of Hydrogen Peroxide Production in Liver and its Removal by Catalase and GSH-reliant Enzymes that Can Predict Intracellular H <sub>2</sub> O <sub>2</sub> Concentration and Cell Death During Incidents of Extreme Oxidative Stress: (1) Applications to PBPK/PD Modeling of the Trivalent Arsenical DMA <i> <sup>III</sup> </i> , (2) Insights Obtained into (a) the Role of Critical GSH Depletion in Apoptosis and (b) How Intracellular H <sub>2</sub> O <sub>2</sub> Concentration is So Tightly Regulated (2023)
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Using mathematical modeling to infer the valence state of arsenicals in tissues: A PBPK model for dimethylarsinic acid (DMAV) and dimethylarsinous acid (DMAIII) in mice (2018)
Collaboration Network
Top Collaborators
- Kinetic and thermodynamic regulation of mitochondrial energy metabolism and ROS production
- Kinetic and thermodynamic regulation of mitochondrial energy metabolism and ROS production
- Kinetic and thermodynamic regulation of mitochondrial energy metabolism and ROS production
- Kinetic and thermodynamic regulation of mitochondrial energy metabolism and ROS production
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