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Your Environment. Your Health.

Progress Reports: University of California-Davis: Critical Role of Mitochondrial Oxidative Stress (MOS) in Chemical Induced Cardiac Toxicity

Superfund Research Program

Critical Role of Mitochondrial Oxidative Stress (MOS) in Chemical Induced Cardiac Toxicity

Project Leader: Nipavan Chiamvimonvat
Grant Number: P42ES004699
Funding Period: 2017-2022
View this project in the NIH Research Portfolio Online Reporting Tools (RePORT)

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Progress Reports

Year:   2019  2018  2017 

Current hazardous waste and chemical pollution, together with new forms of chemicals and hazardous waste being generated each year, pose major threats to the environment in the U.S. and the world. As such, people are frequently exposed to xenobiotic and environmental toxins. The acute short-term effects of many of these hazardous man-made chemicals have been well studied with the support of the Superfund Research Program (SRP). The most studied aspect of environmental toxins has been its role in cancer. While relatively few studies investigating chronic exposure to environmental toxins has focused on the heart, some SRP chemicals have been shown to be toxic to cardiac cells. This is important because cardiovascular disease (CVD) continues to be the leading cause of mortality in the U.S., affecting one out of every three individuals. The mechanism(s) by which xenobiotics contribute to CVD is not well understood. Project data obtained to date demonstrate that mitochondrial dysfunction and mitochondrial oxidative stress (MOS) represent one main contributor to cell death in the heart. The researchers are currently carrying out experiments to understand the roles of MOS as a critical mechanism by which chronic exposure to xenobiotics leads to proteasome dysfunction, apoptosis, cardiac fibrosis, and cell death.

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