Low Dose Acetaminophen Induces Reversible Mitochondrial Dysfunction Associated with Transient c-Jun N-Terminal Kinase Activation in Mouse Liver

In conclusion, low dose APAP produces reversible MPT-dependent mitochondrial dysfunction and steatosis in hepatocytes without causing ALT release or necrosis, whereas high dose leads to irreversible mitochondrial dysfunction and cell death associated with sustained JNK activation. Thus, nontoxic APAP has the potential to cause transient mitochondrial dysfunction that may synergize with other stresses to promote liver damage and steatosis.

Source: Toxicological Sciences - February 25, 2016 Category: Toxicology Authors: Hu, J., Ramshesh, V. K., McGill, M. R., Jaeschke, H., Lemasters, J. J. Tags: Mitochondrial Effects of Low Dose Acetominophen Source Type: research