Reactive metabolites of AP bind to hepatic and renal DNA and hepatotoxic doses initiate oligonucleosomal fragmentation of nuclear DNA. Despite generation of the reactive metabolites of AP primarily in the endoplasmic reticulum, alterations of mitochondrial proteins by reactive metabolites of AP also have been observed; however, the effects of AP metabolites on mitochondrial DNA have not been investigated. Fasted male ICR mice were given 400 mg/kg of AP or equal volumes of saline, killed at 2 h, mitochondria isolated, and DNA extracted. The mitochondrial DNA was amplified by polymerase chain reaction, using sets of primers that collectively span the entire mitochondrial genome and which were selected to amplify the common deletions that have been identified in studies of aging and degenerative diseases as critical targets for damage to mitochondrial DNA. Our studies to date do not indicate that significant increases in common deletions of mitochondrial DNA are associated with acutely hepatotoxic doses of AP, although results indicative of altered PCR amplification of the mitochondrial DNA in the AP-treated mice suggest other forms of damage to the DNA, such as alkylation. The correlation between cumulative ingestion of AP and incidence of end stage renal disease in humans [NEJM 1675, 1994] suggests a chronic injury, which may include DNA damage and mitochondrial dysfunction. Therefore, the investigations of alterations of mitochondrial DNA in relevant models of chronic exposure to AP are needed. Supported by GM44263 and a summer research fellowship (to SAM) from the Society for Pediatric Research.