Abstract
The antioxidant paraoxonase-1 (PON1) may be involved in the response to radiation-induced oxidative stress and possibly prevent cell apoptosis. The correlation of PON1 with the risk of cancer recurrence after radiotherapy (RT) is not yet explored. We investigated changes in the activity of PON1 in patients with prostate cancer (PCa) undergoing RT, and the relation of PON1 activity to the risk of recurrence after RT. We included 56 men with PCa. Blood samples were obtained before irradiation and after the completion of RT. Patients were followed for an average of 51.2 months. Each case of biochemical recurrence was confirmed with biopsy. The control group was composed of 60 healthy men. There was no significant difference in PON1 activity between the control group and patients pre-radiotherapy. Irradiation was associated with a significant decrease in PON1 activity. Patients with PCa recurrence had significantly higher serum PON1 activity than those recurrence-free, both before and after RT. PON1 activity was a predictor of PCa recurrence, with sensitivity over 80% and specificity over 64%. Our results suggest that PON1 activity may be a predictor of PCa recurrence risk after RT. Studies with a larger number of patients and longer follow-up are needed to confirm this hypothesis.
Highlights
Prostate cancer (PCa) is one of the most common forms of cancer in men worldwide, with radiotherapy (RT) being one of the main modalities used to treat it at the present time [1]
PON1 activity was a predictor of PCa recurrence, with sensitivity over 80%
PCa cells have a higher level of reactive oxygen species (ROS) compared with normal prostate cells and maintaining a balance of ROS levels in cancer is an important mechanism of radioresistance; RT induces antioxidant defense systems, which may lead to radioresistance [6,7,8,9]
Summary
Prostate cancer (PCa) is one of the most common forms of cancer in men worldwide, with radiotherapy (RT) being one of the main modalities used to treat it at the present time [1]. PCa cells have a higher level of ROS compared with normal prostate cells and maintaining a balance of ROS levels in cancer is an important mechanism of radioresistance; RT induces antioxidant defense systems, which may lead to radioresistance [6,7,8,9]. All these reasons justify the interest in the antioxidative mechanisms in the response of cancer cells to radiation-induced damage
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