Archives of Clinical Toxicology

Non-alcoholic fatty liver disease (NAFLD) is an increasing health problem when left untreated. NAFLD is defined as accumulation of fat in 5% of the hepatocytes. NAFLD can convert into non-alcoholic steatohepatitis (NASH) which is defined as inflammatory NAFLD. Both NAFLD and NASH are observed in individuals suffering from metabolic syndrome and type 2 diabetes (T2D).

In normal cells, homologous recombination (HR) is strictly regulated and precise and plays an important role in preserving genomic integrity by accurately repairing DNA damage. RAD51 is the recombinase which mediates homologous base pairing and strand exchange during DNA repair by HR. We have previously reported that HR is spontaneously elevated (or dysregulated) in esophageal adenocarcinoma (EAC) and contributes to ongoing genomic changes and instability. The purpose of this study was to evaluate the impact of RAD51 inhibitor on genomic toxicity caused by etoposide, a chemotherapeutic agent.

Non-alcoholic fatty liver disease (NAFLD) is an increasing health problem when left untreated. NAFLD is defined as accumulation of fat in 5% of the hepatocytes. NAFLD can convert into non-alcoholic steatohepatitis (NASH) which is defined as inflammatory NAFLD. Both NAFLD and NASH are observed in individuals suffering from metabolic syndrome and type 2 diabetes (T2D).

Non-alcoholic fatty liver disease (NAFLD) is an increasing health problem when left untreated. NAFLD is defined as accumulation of fat in 5% of the hepatocytes. NAFLD can convert into non-alcoholic steatohepatitis (NASH) which is defined as inflammatory NAFLD. Both NAFLD and NASH are observed in individuals suffering from metabolic syndrome and type 2 diabetes (T2D).

In normal cells, homologous recombination (HR) is strictly regulated and precise and plays an important role in preserving genomic integrity by accurately repairing DNA damage. RAD51 is the recombinase which mediates homologous base pairing and strand exchange during DNA repair by HR. We have previously reported that HR is spontaneously elevated (or dysregulated) in esophageal adenocarcinoma (EAC) and contributes to ongoing genomic changes and instability. The purpose of this study was to evaluate the impact of RAD51 inhibitor on genomic toxicity caused by etoposide, a chemotherapeutic agent.