Abstract
We investigated whether the C1245G polymorphism of human 8-oxoguanine glycosylase 1 (hOGG1) gene confers the susceptibility to systemic lupus erythematosus (SLE) occurrence of lupus nephritis and affects the plasma level of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in patients with SLE. A total of 45 healthy controls and 85 SLE patients were recruited. The C1245G polymorphism of the hOGG1 gene was determined by direct sequencing. The frequency of occurrence of the hOGG1 1245 GG genotype in SLE patients was 31.8% (27/85), which is lower than that of healthy controls of 53.3% (24/45). Thirty-three (33/85, 38.8%) SLE patients developed lupus nephritis. Significantly, SLE patients harboring the hOGG1 1245 GG genotype had a higher incidence to develop lupus nephritis than did those harboring the hOGG1 1245 CC or CG genotype (15/27, 55.6% vs.18/58, 31.0%, p = 0.031). Divided into subgroups, SLE patients harboring the hOGG1 1245 GG genotype had the highest plasma levels of 8-OHdG among patients with all genotypes, with regard to the coexistence of lupus nephritis (p = 0.020, ANOVA), including those with nephritis harboring the hOGG1 1245 CC or CG genotypes (p = 0.037), those without nephritis harboring the hOGG1 1245 GG genotype (p = 0.050), and those without nephritis harboring the hOGG1 1245 CC or CG genotype (p = 0.054). We conclude that the C1245G polymorphism of hOGG1 may be one of the factors that confer the susceptibility to lupus nephritis and modulate the plasma level of 8-OHdG in patients with SLE.
Highlights
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the generation of arrays of pathogenic auto-antibodies that cause cascades of organ damages [1]
Similar to several human degenerative diseases, elevated reactive oxygen species (ROS) and ROS-triggered oxidative damages have been demonstrated to be involved in the pathogenesis of systemic lupus erythematosus (SLE) [2,3,4,5]
For the subsequent comparative analysis, CC genotype plus CG genotype were gathered as one group in this study (Table 1)
Summary
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the generation of arrays of pathogenic auto-antibodies that cause cascades of organ damages [1]. ROS can attack the intracellular molecules randomly, e.g., protein, lipid, RNA and DNA, and thereby cause cellular dysfunction Among these oxidative DNA damages, the formation of. There have been three hOGG1 genotypes identified because of a C to G shifting at base-pair (bp) 1245 (C1245G) in exon 7 of the hOGG1 gene Such a shifting causes a serine (Ser) to cysteine (Cys) substitution at codon 326 during translation. Studies revealed that excessive ROS production and oxidative stress may exacerbate inflammation, dampen antioxidant capacity and lead to tissue damage and the formation of lupus nephritis in SLE patients [3,17]. In one of our previous studies, we demonstrated that SLE patients had higher plasma levels of 8-OHdG than did healthy controls [20]. GG genotype modulates the plasma level of 8-OHdG in SLE patients with or without nephritis
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