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Role of SOD2 Ala16Val polymorphism in primary brain tumors.

ABSTRACT: The present study aimed to investigate the possible association between the genetic polymorphism of the enzyme superoxide dismutase 2 (SOD2, also known as manganese-dependent SOD), Ala16Val (rs4880), and primary brain tumor risk in the Turkish population. Frequency of the SOD2 gene rs4880 polymorphism was identified in 225 Turkish individuals (120 controls and 105 patients with primary brain tumor) by polymerase chain reaction-restriction fragment length polymorphism. Subject demographics and clinical characteristics were also recorded. The findings were evaluated using logistic regression and ?2 tests. Logistic regression analysis indicated that smoking did not increase the risk for primary brain tumor [odds ratio (OR)=0.77, 95% confidence interval (CI)= 0.44-1.33, ?2=0.352, P=0.860]. Similarly, there was no statistically significant difference in the family history of cancer incidence between the control subjects and the primary brain tumor patients (OR=0.81, 95% CI=0.39-1.71, ?2=0.340, P=0.560). There was no significant association of the histopathological type, genotype/allele frequencies and inheritance models of tumor with the gene variants among the patients with primary brain tumor. In summary, the results of the present study indicated that the Ala16Val polymorphism of the SOD2 gene was not associated with primary brain tumor risk in the Turkish population studied.

SUBMITTER: Tas A

PROVIDER: S-EPMC6403480 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature

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Project description:Methotrexate (MTX) is a folic acid antagonist used in high doses as an anti-cancer treatment and in low doses for the treatment of some autoimmune diseases. MTX use has been linked to oxidative imbalance, which may cause multi-organ toxicities that can be attenuated by antioxidant supplementation. Despite the oxidative effect of MTX, the influence of antioxidant gene polymorphisms on MTX toxicity is not well studied. Therefore, we analyzed here whether a genetic imbalance of the manganese-dependent superoxide dismutase (SOD2) gene could have some impact on the MTX cytotoxic response. An in vitro study using human peripheral blood mononuclear cells (PBMCs) obtained from carriers with different Ala16Val-SOD2 genotypes (AA, VV and AV) was carried out, and the effect on cell viability and proliferation was analyzed, as well as the effect on oxidative, inflammatory and apoptotic markers. AA-PBMCs that present higher SOD2 efficiencies were more resistance to high MTX doses (10 and 100 µM) than were the VV and AV genotypes. Both lipoperoxidation and ROS levels increased significantly in PBMCs exposed to MTX independent of Ala16Val-SOD2 genotypes, whereas increased protein carbonylation was observed only in PBMCs from V allele carriers. The AA-PBMCs exposed to MTX showed decreasing SOD2 activity, but a concomitant up regulation of the SOD2 gene was observed. A significant increase in glutathione peroxidase (GPX) levels was observed in all PBMCs exposed to MTX. However, this effect was more intense in AA-PBMCs. Caspase-8 and -3 levels were increased in cells exposed to MTX, but the modulation of these genes, as well as that of the Bax and Bcl-2 genes involved in the apoptosis pathway, presented a modulation that was dependent on the SOD2 genotype. MTX at a concentration of 10 µM also increased inflammatory cytokines (IL-1β, IL-6, TNFα and Igγ) and decreased the level of IL-10 anti-inflammatory cytokine, independent of SOD2 genetic background. The results suggest that potential pharmacogenetic effect on the cytotoxic response to MTX due differential redox status of cells carriers different SOD2 genotypes.

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Role of SOD2 Ala16Val polymorphism in primary brain tumors.

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