SRP researchers collaborate with the National Toxicology Program to study biomarkers, mechanism of PCB toxicity

James Swenberg, PhD, DVM

Dr. Swenberg’s research team has been at the forefront of developing and validating a comprehensive set of biomarkers that can be used to identify oxidative DNA damage, which is well-known to play a role in carcinogenicity. In an effort to illuminate the mechanism of PCB toxicity and carcinogenesis in rodents, researchers at NTP exposed rats to multiple concentrations of either PCB 126, 153 or a mixture of the two at 14, 31 and 53 weeks of age. PCB 126 is dioxin-like and is the most potent PCB in the environment while PCB 153 is a non-dioxin-like PCB that has been found in high concentrations in human tissue. The UNC research team analyzed tissue samples from the rats provided by NTP, measuring eight DNA adducts arising from oxidative stress and implicated in cancer studies.  Results revealed an increase of oxidative DNA adducts associated with the liver in response to PCB 126, 153 or the binary mixture.  The binary mixture generally induced more adducts than either single PCB congener alone.

“This research suggests that an increase in oxidative DNA damage in rats may be a contributing factor in liver disease and carcinogenesis,” Swenberg explains, noting that there is still much to be learned about the mechanism of PCB-induced oxidative stress in order to improve the risk assessment process.

Results were published online July 20, 2016 and can be found in the August 15, 2016 print issue of Chemical Research in Toxicology (Volume 29, Issue 8).