In solid cancer surgery, oxidative stress (OS) is of particular interest because both the malignancy itself and the surgical intervention are major contributors to the modulation of OS levels. This study aimed to investigate the effects of solid cancer surgery on OS levels. Because solid cancer is often accompanied by intense cell death, the study specifically focused on the pathway leading to uric acid formation, (i.e. adenosine deaminase (ADA) and xanthine oxidase (XO). Ische-mia-modified albumin (IMA), a recognized marker of oxidative stress, and plasma redox poten-tial (RP) were also measured. Thirty-six patients undergoing major solid cancer surgery (median age 68 years (58-76), 23 men and 13 women) and thirty controls (62 years (51-80)) were included.
During the surgical procedure, serum ADA levels did not change significantly (10.4 International Units (IU) (6.9 – 13.7) vs. 8 IU (6 – 12); p = 0.47). In contrast, XO (IU), IMA (Arbitrary Units(AU)) and redox potential (mV) decreased significantly (22.5 IU (11 – 63) vs. 8.4 IU (5 – 27); p = 0.0041, 89 AU (69 – 105) vs. 74 AU (66 – 80); p = 0.01 and 98 mV (78 – 118) vs. 79 mV (65 – 101); p = 0.033). The correlation between XO and IMA or redox potential was positive (Spearman’s r = 0.32 ; p = 0.007, and r = 0.58; p < 0.001, respectively). XO was negatively correlated with ADA (r = -0.26; p = 0.03). Redox potential was positively correlated with IMA (r = 0.26; p = 0.04) and nega-tively correlated with ADA (r = -0.25 ;p = 0.04).
We found that a major source of OS in solid cancer could be the result of an increase in xanthine oxidase activity and that the global effect of solid cancer surgery is a significant decrease in OS levels. We also found that ADA and XO were inversely correlate, suggesting the existence of a negative retrocontrol between the production of free radicals and the production of their sub-strate. Finally, our study highlights the potential value of XO inhibitors as adjuvant therapy in solid tumor surgery.