Abstract
The aim of the present study is to determine if Ahr ligands as PCB-126, a dioxin-like, might contribute to inhibition of the tumour suppressor p53 by promoting its degradation through proteasome-ubiquitin system (UPS). The findings show, in the presence of PCB-126, a significant increase in p53 immunoreactivity in fish compared to the control. Subsequently, there is a decrease in p53 immunoreactivity at 24 h which is maintained even at 72 h. There is also a slight decrease in ubiquitin immunoreactivity to 12 h compared to the control and a marked decrease to 24 and 72 h. It's very important to underline as in this study we demonstrate a marked decrease in ubiquitin and p53 immunoreactivity at 24 and 72 h. Our result emphasise the need to deeply the role of this receptor in UPS regulation as potential therapeutic target for cancer treatment.