Abstract
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.
Highlights
Malignant ascites, a condition in which fluid containing cancer cells accumulates in the abdomen, is frequently observed in patients with progressive carcinomas such as ovarian (37%), pancreatobiliary (21%), gastric (18%), esophageal (4%), colorectal (4%), and breast (3%) cancers 1
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 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
Summary
Malignant ascites (ma), a condition in which fluid containing cancer cells accumulates in the abdomen, is frequently observed in patients with progressive carcinomas such as ovarian (37%), pancreatobiliary (21%), gastric (18%), esophageal (4%), colorectal (4%), and breast (3%) cancers 1. Oxidative stress, defined as loss of the balance between production of reactive oxygen species (ros) and antioxidant defenses, is considered to cause oxidative damage to lipids, proteins, and dna. In the absence of an adequate antioxidant system, the accumulated dna damage may result in dna mutation. Mutations in dna and decreased efficacy of dna repair cause further dysfunction and apoptosis in many kinds of cells, including lymphocytes, possibly playing a pivotal role in cell carcinogenesis and dissemination of cancer cells 3. 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; the relationship between oxidative stress and dna damage to tumour-associated lymphocytes (tals) in ma is unclear
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
