Mitochondrial DNA Damage and Histological Features in Liver Tissue of Azoxymethane-Treated <i>Apex1</i> Haploinsufficient Mice.

ABSTRACT: Mitochondrial dysfunction and loss of mitochondrial DNA (mtDNA) integrity are increasingly recognized as key contributors to liver diseases such as cirrhosis and hepatocellular carcinoma. However, the role of mtDNA repair in maintaining mitochondrial homeostasis during liver injury remains poorly understood. Apurinic/apyrimidinic endonuclease 1 (APE1), encoded by the Apex1 gene, is the primary endonuclease mediating base excision repair of mtDNA. We hypothesize that APE1 is required to preserve mtDNA integrity in response to genotoxic stress in the liver. To test this, wild-type (WT) and Apex1 haploinsufficient mice (Apex1^+/-) were treated with the alkylating agent azoxymethane (AOM), a carcinogen bioactivated in the liver, and tissues were collected 20 week

SUBMITTER: Perez-Perez CM 

PROVIDER: S-EPMC12731096 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature