eNOS and XRCC4 VNTR variants contribute to formation of nicotine dependence and/or schizophrenia
Göster/ Aç
Erişim
info:eu-repo/semantics/openAccessTarih
2017Yazar
Pehlivan, SacideUysal, Mehmet Ali
Aydın, Pelin C.
Pehlivan, Mustafa
Nursal, Ayşe Feyda
Yavuzlar, Hazal
Kurnaz, Serdar
Sever, Ülgen
Yavuz, Ferhat K.
Uysal, Sezer
Aydın, Nazan
Üst veri
Tüm öğe kaydını gösterKünye
Pehlivan, S., Uysal, M.A., Aydin, P., Pehlivan, M., Nursal, A.F., Yavuzlar, H., Kurnaz, S., Sever, U., Yavuz, F., Uysal, S., & Aydin, N. (2017). eNOS and XRCC4 VNTR variants contribute to formation of nicotine dependence and/or schizophrenia. Bratislavske lekarske listy, 118 (8), 467-471 .Özet
BACKGROUND: This study aimed to evaluate whether VNTR variants in the Endothelial Nitric Oxide Synthase (eNOS) and the XRCC4 gene play any role in nicotine dependence (ND) and/or Schizophrenia+ND (Sch+ND) ethiopathogenesis. METHODS: Present study included 100 individuals with ND, 60 patients with Sch+ND, and 70 healthy controls. These variants were analyzed using PCR. RESULTS: The cases with ND had higher eNOS VNTR-BB genotype than the healthy control subjects (p = 0.001). eNOS-AA genotype was lower in cases with Sch+ND and ND groups compared to the controls (p = 0.001, p = 0.001, respectively). eNOS-B allele was found significantly more frequently in Sch+ND group compared to the controls (p = 0.001). eNOS-A allele was significantly lower in ND group than the controls (p = 0.001). XRCC4-ID genotype was more common in the ND group than the control group (p = 0.001) as heterozygosity disadvantage. XRCC4-DD genotype was more common in the Sch+ND group compared to the controls (p = 0.035). The frequency of XRCC4-I allele was lower in the Sch+ND group compared to the controls (p = 0.012). CONCLUSIONS: Our results showed that eNOS and XRCC4 VNTR variants might play a potential role in Sch+ND and/or ND pathophysiology.
Kaynak
Bratislava Medical JournalCilt
118Sayı
8Koleksiyonlar
- Makale Koleksiyonu [517]
- Scopus İndeksli Yayınlar Koleksiyonu [2695]
- WoS İndeksli Yayınlar Koleksiyonu [2986]