Mitochondrial depolarization and repolarization in the early stages of acetaminophen hepatotoxicity in mice.

ABSTRACT: Mitochondrial injury and depolarization are primary events in acetaminophen hepatotoxicity. Previous studies have shown that restoration of mitochondrial function in surviving hepatocytes, which is critical to recovery, is at least partially accomplished via biogenesis of new mitochondria. However, other studies indicate that mitochondria also have the potential to spontaneously repolarize. Although repolarization was previously observed only at a sub-hepatotoxic dose of acetaminophen, we postulated that mitochondrial repolarization in hepatocytes outside the centrilobular regions of necrosis might contribute to recovery of mitochondrial function following acetaminophen-induced injury. Our studies utilized longitudinal intravital microscopy of millimeter-scale regions of the mouse liver to

SUBMITTER: Dunn KW 

PROVIDER: S-EPMC7270714 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature