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| Gene | Clinical relevance | References |
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| Glutathione S-transferases M1 (GSTM1) and P1 (GSTP1) | GSTs conjugate endogenous byproducts of OS with glutathione, enabling rapid elimination and thus defending tissues against oxidant damage; common polymorphisms exist in genes coding for various GSTs including glutathione S-transferases M1 (GSTM1) and P1 (GSTP1) | [19] |
|
Antioxidant defence enzymes (ADE)
Glutamate cysteine ligase (GCLM)
Glutathione peroxidase (GPX1)
Myeloperoxidase (MPO)
NADPH oxidase (CYBA, p22phox subunit)
NAD(P)H: quinone oxidoreductase type 1 (NQO1)
Microsomal epoxide hydrolase (EPHX1)
Glutamate cysteine ligase (GCLM) | They are associated with allergic and nonallergic asthma, inducing increased oxidative stress status | [11, 20, 21] |
|
| Tumor necrosis factor G-308A | It may have a protective role in asthma pathogenesis, depending on airway oxidative stress levels | [22] |
|
Methylenetetrahydrofolate reductase (MTHFR)
ORM1-like 3 (ORMDL3)
Gasdermin A and B (GSDM) | In addition to foetal smoke exposure, it seems to be associated with lower airway responsiveness, lung function, and increased risk of transient wheezing, a phenotype of childhood asthma | [23]
[24]
[25] |
|
| Antioxidant enzyme paraoxonase (PON1) | It is inversely correlated to plasma total oxidant status and to severity of asthma | [26] |
|
| Nuclear factor (NF), erythroid-derived 2-related factor 2 (NRF2) | It has been found to be a critical regulator in protecting cells and tissues under highly oxidative microenvironments, including airways that interface with the external environment and are exposed to pollutants and other oxidant stressors | [27] |
|
| Toll-like receptor 4 (Tlr4) | It is associated with O3-induced lung inflammation and increased airway hyperpermeability | [28] |
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| Heme oxygenase-1 (HMOX-1) | In addition to ozone exposure, it is responsible for the onset of allergic asthma | [29] |
|
| Transforming growth factor- (TGF-) beta1 C-509T polymorphism | This genotype is associated with an increased risk of asthma in addition to maternal smoking exposure in the uterus or to traffic-related emissions | [30] |
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| Arginases (ARG1 and ARG2) | It may play an important role in asthma pathogenesis through effects on nitrosative stress | [31] |
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