Abstract
The present preliminary case-control study was undertaken to detect the potential association of six single nucleotide polymorphisms (SNPs) in oxidative stress-related genes: SOD2 (c.47T > C; rs4880), CAT (c.-89A > T; rs7943316), GPX4 (c.660T > A; rs713041), NOS1 (g.117803515C > T; rs1879417) and NOS2 (c.1823C > T; rs2297518 and c.-227G > C; rs10459953) and the occurrence of a stroke. The SNPs were determined using the TaqMan® Allelic Discrimination Assay in 107 patients with strokes and 107 age- and sex-matched individuals who had not experienced cerebrovascular accidents. The T alleles of the rs4880 were positively correlated with a stroke (bootstrap OR 1.31; 1.07–1.59 95% CI). In the case of the rs713041, an association with the T allele was found (bootstrap OR 1.36; 1.12–1.67). In addition, the occurrence of a stroke was associated with the presence of the C allele of the rs1879417 (bootstrap OR 1.32; 1.09–1.61). We also found that the C/C genotype and C allele of the rs2297518 increased the risk of a stroke (bootstrap ORs 7.00; 4.34–11.29 and 4.96; 3.88–6.34, respectively). Moreover, the C allele of the rs10459953 was associated with an increased occurrence of this disease (bootstrap OR 1.31; 1.08–1.60). These results indicated that genetics variants in the SOD2, GPX4, NOS1 and NOS2 might be associated with susceptibility to strokes in the Polish population.
Highlights
IntroductionStroke leads to energy deficits of nerve tissue, which are clinically manifested focal or global neurological deficits, including: paresis, disorders of the cerebellar, body axis control and extrapyramidal, as well as cognition impairment and depressive syndromes [2]
The odds ratios (ORs) values and the corresponding p-values for the genotypes/alleles increasing the risk of stroke are shown in red, and in blue are the genotypes/alleles with a protective effect
Numerous studies have shown that excessive oxidative stress, which is caused by genetic predisposition/susceptibility and environmental stress, results in the excessive production of reactive oxygen species, inflammation in the arterial atheromatous plaque, unstable atherosclerotic plaque formation, and eventually an ischemic stroke onset [29,32,33]
Summary
Stroke leads to energy deficits of nerve tissue, which are clinically manifested focal or global neurological deficits, including: paresis, disorders of the cerebellar, body axis control and extrapyramidal, as well as cognition impairment and depressive syndromes [2]. Important social consequences caused by cerebrovascular disease cause the implementation of general strategies to reduce the risk of a stroke. To this end, modifiable risk factors of a stroke should be eliminated, and associated diseases properly treated, including smoking, high blood pressure, diabetes, physical inactivity and obesity, atrial fibrillation (AFib) or other heart disease, carotid or other artery disease, certain blood disorders, and excessive alcohol intake [3]. Risk of subsequent stroke should be reduced by using effective secondary prevention methods [4]
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