MnSOD Polymorphism May Modify the Association between Exposure to Dioxin and Diabetes

摘要

Background/Aim: Manganese superoxide dismutase (MnSOD) is an antioxidant, and might play an important role to diabetes (DM) pathogenesis. Dioxin may also cause effects with aryl hydrocarbon receptor (AhR) and induce DM. The interaction between exposure to dioxin and MnSOD gene polymorphism has not been investigated yet. Our study was to assess the joint effects of MnSOD polymorphism and exposure to dioxin on the risk of DM. Methods: A total of 282 individuals were selected from Central Taiwan to conduct a cross-sectional study. We used real-time polymerase chain reaction (RT-PCR) to analyze the four single-nucleotide polymorphisms (SNPs) of MnSOD (rs5746136, rs2855116, rs4880, rs2758346) and performed Haploview v4.1 software to test the MnSOD gene for Hardy-Weinberg equilibrium. The dioxin data were measured by chromatography/mass spectrometry (HRGC/HRMS) and divided dioxins levels into four groups: reference group (<25th), low exposure group (25th to <50th), middle exposure group (50th to <75th) and high exposure group (>75th). We performed logistic regression models to assess the risk for diabetes and applied Rothman index (s) to estimate interaction in additive scale. Result: After adjusting for confounding, we found that the risk of DM was associated with the low and middle combined exposure group of OCDF(aOR=3.25; 95% Cl=1.07-9.81), PCDDs(aOR=5.12; 95% CI=1.46-18.62), 1,2,3,7,8-PeCDD(aOR=4.03; 95% CI=1.18-13.78), 1,2,3,4,7,8-HxCDD(aOR=3.79; 95% CI=3.79-13.37) and OCDD(aOR=4.00; 95% CI=1.42-11.26) as compared with reference group. Additive interactions between SNP (rs2758346) and the specific dioxin (PCDDs: S=1.592; 1,2,3,7,8-PeCDD: S=2.138; 1,2,3,6,7,8-HxCDD: S=1.642) on the risk of diabetes was found. Conclusions: Our study suggests that MnSOD (rs2758346) may modify the association between exposure to specific dioxin (PCDDs, 1,2,3,7,8-PeCDD and 1,2,3,6,7,8-HxCDD) and DM.