Exploring Oxidative Stress Markers Catalase and Malondialdehyde in Chemotherapy-Induced Neuropathy in Head and Neck Cancer Patients: A Prospective Study

Abstract

Background: Chemotherapy-induced neuropathy (CIPN) is a common and debilitating side effect of cancer treatment, significantly impacting patients' quality of life. Oxidative stress has been implicated in the pathogenesis of CIPN, with markers such as catalase and malondialdehyde (MDA) serving as indicators of oxidative damage and antioxidant defense. This study aims to explore the roles of catalase and MDA as oxidative stress markers in CIPN.

Methods: A prospective cohort study was conducted with 42 patients undergoing chemotherapy for Head and neck solid tumors. Blood samples were collected to measure serum levels of catalase and MDA. Neuropathy severity was assessed using the National Cancer Institute’s Common Terminology Criteria for Adverse Events (CTCAE). Statistical analyses, including Pearson correlation and multiple regression, were performed to evaluate the relationships between catalase, MDA levels, and neuropathy severity.

Results: Patients with severe neuropathy exhibited significantly higher levels of MDA (mean: 7.8 ± 1.5 µmol/L) compared to those with mild or no neuropathy (mean: 4.2 ± 1.1 µmol/L, p<0.001). Conversely, catalase activity was significantly lower in patients with severe neuropathy (mean: 45.3 ± 10.2 U/mg protein) than in those with mild or no neuropathy (mean: 68.7 ± 12.5 U/mg protein, p<0.001). A significant positive correlation was found between MDA levels and neuropathy severity (r=0.52, p<0.001), while catalase activity showed a significant negative correlation with neuropathy severity (r=-0.46, p<0.001). Multiple regression analysis identified MDA levels (β=0.38, p<0.001) and catalase activity (β=-0.32, p<0.001) as independent predictors of neuropathy severity.

Conclusion: Elevated MDA levels and reduced catalase activity are significantly associated with increased severity of chemotherapy-induced neuropathy, highlighting the role of oxidative stress in CIPN pathogenesis. These findings suggest that oxidative stress markers such as MDA and catalase could serve as potential biomarkers for CIPN risk and severity. Further research is warranted to explore antioxidant-based interventions as potential therapeutic strategies for mitigating CIPN.