Oxidative dna damage of lymphocytes in peripheral blood and ascites in cancer patients

Patients with malignant ascites (ma) usually experience poor quality of life, and treatment of this symptom remains a challenge. Oxidative stress, which can cause oxidative damage to dna, plays a pivotal role in carcinogenesis; however, the relationship between oxidative stress and dna damage to tumour-associated lymphocytes (tals) in ma is unclear.

We measured the total antioxidant capacity (tac) of plasma and ma supernatant in 31 cancer patients with ma, and we used a comet assay to assess dna damage to both peripheral blood mononuclear cells (pbmcs) and tals. Measurements in age- and sex-matched healthy volunteers were used as controls.

The tac of plasma was remarkably lower in cancer patients (9.73 ± 1.96 U/mL) than in healthy control subjects (11.31 ± 1.50 U/mL, p < 0.001). The tac of ma supernatant (6.34 ± 1.57 U/mL) was significantly lower than that of plasma in cancer patients (7.42 ± 1.36 U/mL, p < 0.001). The comet percentage of pbmcs was higher in cancer patients (17.26% ± 6.04%) than in healthy control subjects (9.44% ± 4.47%, p < 0.01). In cancer patients, the comet percentage of tals (36.14% ± 17.85%) was significantly higher than that of pbmcs (17.26% ± 6.04%, p < 0.001). In cancer patients with ma, negative correlations were observed between plasma tac and dna damage to pbmcs (r = -0.505, p = 0.004) and between the tac of ma supernatant and the comet percentage of tals (r = -0.588, p = 0.001).

Results indicate the presence of significant oxidative damage to the dna of lymphocytes in peripheral blood and ascites from patients with ma, being especially higher in the cells from ascites. The lower tac of ma supernatant may be related to a higher degree of dna damage to tals. The present study suggests that an oxidant-antioxidant imbalance may be one of the mechanisms leading to the dna damage detected in peripheral blood and local tals in patients with ma, which may provide a novel approach to the treatment of ma.