# Oxidative Stress Biomarkers in Silicosis: A Systematic Review

**Authors:** Maria Carmina Pau, Elisabetta Zinellu, Barbara Piras, Alice Nardi, Maria Roberta Lacana, Chiara Scala, Angelo Zinellu, Arduino A. Mangoni, Ciriaco Carru, Alessandro G. Fois, Gaetano Caramori, Pietro Pirina

PMC · DOI: 10.3390/diseases14030098 · 2026-03-06

## 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.

## Key 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.

## Linked entities

- **Chemicals:** Malondialdehyde (PubChem CID 10964)
- **Diseases:** silicosis (MONDO:0005960)

## Full-text entities

- **Genes:** TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, NOS2 (nitric oxide synthase 2) [NCBI Gene 4843] {aka HEP-NOS, INOS, NOS, NOS2A}, CAT (catalase) [NCBI Gene 847], IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, GSR (glutathione-disulfide reductase) [NCBI Gene 2936] {aka CNSHA10, GR, GSRD, HEL-75, HEL-S-122m}, SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}
- **Diseases:** COPD (MESH:D029424), mitochondrial dysfunction (MESH:D028361), fibrotic lung disorders (MESH:D008171), lung injury (MESH:D055370), pneumoconiosis (MESH:D011009), asbestosis (MESH:D001195), injury to (MESH:D014947), IPF (MESH:D054990), inflammation (MESH:D007249), fibrotic remodeling (MESH:D020257), pulmonary fibrosis (MESH:D011658), Silicosis (MESH:D012829), tissue injury (MESH:D017695), fibrosis (MESH:D005355), epithelial injury (MESH:D009375)
- **Chemicals:** lipid (MESH:D008055), RNS (MESH:D011886), peroxides (MESH:D010545), 8-iso-prostaglandin F2alpha (MESH:C075750), superoxide (MESH:D013481), F2-isoprostane (MESH:D028441), MDA (MESH:D008315), TBARS (MESH:D017392), aldehydes (MESH:D000447), 8-iso-prostaglandin F2 (-), isoprostanes (MESH:D028421), NO (MESH:D009569), silica (MESH:D012822), ATP (MESH:D000255), 8-OH-dG (MESH:D000080242), Vitamin C (MESH:D001205), arachidonic acid (MESH:D016718), GSH (MESH:D005978), hydrogen peroxide (MESH:D006861), ROS (MESH:D017382), reactive nitrogen species (MESH:D026361), hydroxyl radical (MESH:D017665), creatinine (MESH:D003404), GSSG (MESH:D019803), lipid peroxides (MESH:D008054)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]
- **Cell lines:** BEAS-2B — Homo sapiens (Human), Transformed cell line (CVCL_0168)

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13025893/full.md

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Source: https://tomesphere.com/paper/PMC13025893