Groundbreaking Technology Measures Drug-induced Mitochondria Toxicity

The liver plays a central role in metabolizing synthetic chemicals and is therefore the most common target for drug-induced toxicity. Drug toxicity is often due to an accumulation of damage to the cell’s mitochondria. Current methods to evaluate mitochondrial function rely on indirect tests, which provide limited prognostic information. Now researchers from the Hebrew University of Jerusalem have found a way to directly measure mitochondrial damage caused by drug toxicity.

Liver-on-Chip devices measure tiny changes in cellular metabolism in real time (seconds to minutes). This test relies on a computer-controlled switchboard that reports cellular changes when exposed to new drugs, permitting detection of chemical toxicity before any effects on cell or tissue viability can be observed.

Past research using this liver-on-chip technology allowed the Hebrew University team to identify a new cause of acetaminophen (Tylenol®) toxicity, suggesting the drug could directly block respiration in the kidneys and skin.

In a recently reported study, the team tested the new technology on troglitazone (Rezulin®), an antidiabetic and anti-inflammatory drug that has been removed from the U.S. market in 2000 due to severe drug-induced liver injury, costing Pfizer Inc. over $750 million in lawsuits. The researchers found that even at low concentrations previously regarded as safe, in which traditional tests do not reveal any damage to the cells, the new liver-on-chip technology was able to detect mitochondrial stress that forced the liver to increase its reliance on glucose metabolism.

This cutting edge technology may now allow laboratory researchers to pinpoint mitochondrial damage caused by pharmaceuticals and also has the potential to redefine the study of neurodegenerative diseases (Alzheimer’s, Parkinson’s), metabolic diseases (diabetes, obesity) virology and cancer, in addition to drug discovery.

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