Abstract
The single-nucleotide polymorphisms (SNPs) of apurinic/apyrimidinicendonuclease 1 (APE1), which has been implicated in cancers and the DNA base excision repair (BER) process, have not been thoroughly investigated in association with the risks of oxidative stress-related vitiligo. The aim of this study is to investigate associations between APE1 single-nucleotide polymorphisms 141T >G and 1349T >G and risk and prognosis of vitiligo. From June 2013 to June 2015, a total of 460 vitiligo patients were randomly recruited as a case group; 200 of these patients received narrow bound ultraviolet B (NB-UVB) treatment. Meanwhile, 460 healthy controls were included as a control group. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed to explore the distribution frequencies of genotypes. Significant differences were detected between the case group and the control group in the frequencies of the 141T >G and 1349T >G genotypes. At 141T >G, compared with patients carrying the TG + GG genotype, male patients carrying the TT genotype aged more than 20 years with active non-segmental vitiligo, without a family history of vitiligo or other autoimmune diseases, exhibited an increased risk of vitiligo. Binary logistic regression analysis demonstrated that the TT genotype at 141T >G and the non-TT genotype at 1349T >G were independent risk factors for vitiligo development. At 1349T >G, compared with patients carrying the TT genotype, male patients carrying the TG + GG genotype aged more than 20 years with active non-segmental vitiligo, without a family history of vitiligo or other autoimmune diseases, exhibited an increased risk of vitiligo. Moreover, patients carrying 141TG + GG or 1349 TT genotypes had better photochromic effects, lower cumulative radiation doses, shorter treatment times, and earlier first photochromic times.
Highlights
The single-nucleotide polymorphisms (SNPs) of apurinic/apyrimidinicendonuclease 1 (APE1), which has been implicated in cancers and the DNA base excision repair (BER) process, have not been thoroughly investigated in association with the risks of oxidative stress-related vitiligo
The results showed that a mutation of the SNPs at141T >G was associated with a decreased risk of vitiligo, while a mutation of 1349T >G confers a highly increased risk of vitiligo
It has been suggested that the loss of melanocytes from lesional skin may be a cause of the white spots, and research has shown an increase in DNA damage in the leucocytes of patients with vitiligo compared with healthy controls.[22]
Summary
The single-nucleotide polymorphisms (SNPs) of apurinic/apyrimidinicendonuclease 1 (APE1), which has been implicated in cancers and the DNA base excision repair (BER) process, have not been thoroughly investigated in association with the risks of oxidative stress-related vitiligo. DNA base excision repair (BER) is a process repairing base damage, including single-strand breaks, non-bulky adducts, oxidative DNA damage, alkylation adducts, and damage induced by ionizing radiation.[13] Evidence has shown that the induction of oxidative damage and expression of several BER genes are significantly increased in melanocytes.[14] The apurinic/apyrimidinic endonuclease (APE1) gene is the most important gene reported in close association with oxidative-stress-related disorders.[15,16] In addition, APE1 is known as redox effector factor 1 (Ref-1), and participates in the regulation of reoxidation and transcription.[17] Taking all this into account, the authors propose the hypothesis that APE1 may be involved in the development of vitiligo
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