Oxidative Stress Biomarkers in Silicosis: A Systematic Review

TL;DR

This review examines how oxidative stress contributes to silicosis, a lung disease caused by silica exposure, by analyzing biomarkers in patients compared to healthy individuals.

Contribution

The study systematically reviews oxidative stress biomarkers in silicosis, revealing consistent patterns of oxidative imbalance.

Findings

Malondialdehyde (MDA) levels were significantly higher in silicosis patients, indicating increased lipid peroxidation.

Superoxide Dismutase (SOD) levels were lower, showing impaired antioxidant defense in affected individuals.

Elevated oxidant molecules confirmed oxidative, nitrosative, and DNA damage in silicosis patients.

Abstract

Background: Silicosis is a progressive fibrotic lung disease caused by chronic inhalation of crystalline silica. Increasing evidence indicates that oxidative stress plays a central role in linking silica exposure to inflammation, tissue injury, and fibrosis. We conducted a systematic review to critically appraise the current evidence on the imbalance between oxidant and antioxidant markers in patients with silicosis compared with unexposed healthy controls. Methods: A systematic literature search was conducted in PubMed, Scopus, and Google Scholar from their inception to 30 November 2025. Eligible studies assessed oxidative stress biomarkers in biological samples from patients with silicosis and non-exposed controls. Results: Malondialdehyde (MDA) and Superoxide Dismutase (SOD) were the most frequently assessed oxidative and antioxidant markers, respectively, with MDA significantly increased and SOD decreased in patients with silicosis, highlighting amplified lipid peroxidation and impaired antioxidant defense. In addition, elevated levels of other oxidant molecules confirmed the presence of lipid, nitrosative, and DNA oxidative damage. Overall, antioxidant defenses were compromised, although some markers appeared to vary with disease stage. Conclusions: This review highlights the central role of oxidative stress in the pathogenesis and progression of silicosis. Future studies with larger cohorts and a broader range of biomarkers are needed to better understand oxidative imbalance and its potential utility for monitoring disease progression and assessing severity in this population.

Figures