Malondialdehyde (MDA) is a compound that is derived from the peroxidation of polyunsaturated fatty acids. It has been used as a biomarker to measure oxidative stress in various biological samples in patients who are affected by a wide range of diseases. The aim of our work is to provide an updated overview of the role of MDA as a marker of oxidative stress in allergy-related diseases. We considered studies involving both paediatric and adult patients affected by rhinitis, asthma, urticaria and atopic dermatitis. The measurement of MDA was performed on different types of samples. The reported data highlight the role of serum MDA in inflammatory airway diseases. According to the literature review, the oxidative stress status in asthmatic patients, assessed via MDA determination, appears to worsen in the presence of other allergic airway diseases and in relation to the disease severity. This suggests that MDA can be a suitable marker for monitoring the disease status. However, there are several limitations in the considered studies due to the different samples used and the lack of phenotyping and description of the clinical period of patients examined. In cutaneous allergic diseases, the role of MDA is controversial because of the smallness of the studies and the heterogeneity of the samples and patients.

Regulation of leukocyte migration and activation by chemokines are recognized as potentially important functions in the induction of acute and chronic inflammatory reactions. Regulated upon activation normal T cell expressed and presumably secreted (RANTES), monocyte chemotactic protein-1 (MCP-1), and related molecules constitute the C-C class of the  chemokine supergene family with inflammatory properties. Here we report that in experimental studies RANTES and MCP-1 provoke mast cell activation and increase histidine decarboxylase mRNA expression in a dose-dependent manner. Moreover, injections of RANTES and MCP-1 in the rat skin cause mast cell, eosinophil, and macrophage recruitment, and prostaglandin E₂(PGE₂) generatioll. In a chronic inflammatory model MCP-1 was found to mediate the recruitment of mononuclear cells in calcified granulomas. In addition, MCP-1 mediated parasitic infections caused by Trichinella spiralis. In accordance with other studies, RANTES and MCP-1 were found to play an important role in the lung allergic inflammation, lung leukocyte infiltration, bronchial hyperresponsiveness, and the recruitment of eosinophils in the pathogenesis of asthma. Here for the first time we propose a new mechanism of pulmonary airway inflammation where RANTES and MCP-1 are deeply involved. We also studied the apparent role played by RANTES in the pathogenesis of relapsing-remitting multiple sclerosis enhancing the inflammatory response within the nervous system.

Owing to their radical scavenging and UV-filtering properties, ceria nanoparticles (CeO₂-NPs) are currently used for various applications, including as catalysts in diesel particulate filters. Because of their ability to filter UV light, CeO₂-NPs have garnered significant interest in the medical field and, consequently, are poised for use in various applications. The aim of this work was to investigate the effects of short-term (24 h) and long-term (10 days) CeO₂-NP exposure to A549, CaCo2 and HepG2 cell lines. Cytotoxicity assays tested CeO₂-NPs over a concentration range of 0.5 μg/mL to 5000 μg/mL, whereas genotoxicity assays tested CeO₂-NPs over a concentration range of 0.5 μg/mL to 5000 μg/mL. In vitro assays showed almost no short-term exposure toxicity on any of the tested cell lines. Conversely, long-term CeO₂-NP exposure proved toxic for all tested cell lines. NP genotoxicity was detectable even at 24-h exposure. HepG2 was the most sensitive cell line overall; however, the A549 line was most sensitive to the lowest concentration tested. Moreover, the results confirmed the ceria nanoparticles’ capacity to protect cells when they are exposed to well-known oxidants such as H₂O₂. A Comet assay was performed in the presence of both H₂O₂ and CeO₂-NPs. When hydrogen peroxide was maintained at 25 μM, NPs at 0.5 μg/mL, 50 μg/mL, and 500 μg/mL protected the cells from oxidative damage. Thus, the NPs prevented H₂O₂-induced genotoxic damage.