Evaluation of the FAS and FASL Gene changes in women with premature ovarian failure: A case-control study

Abstract Background: Premature ovarian failure (POF), is menopause occurring before the age of 40, affecting 1-3% of women worldwide. The risk of POF increases with altered immunological parameters such as FAS and FASL genes, which play a fundamental role in embryogenesis and cellular homeostasis. O...

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Main Authors: Zhima Akhavansales (Author), Alimohammad Mosadeghmehrjardi (Author), Hamid Reza Ashrafzadeh (Author), Shadnaz Fakhteh Yavari (Author), Mohammad Taher Tahoori (Author), Morteza Bitaraf Sani (Author), Mahnaz Mohammadi (Author), Fateme Montazeri (Author), Nasrin Ghasemi (Author)
Format: Book
Published: Shahid Sadoughi University of Medical Sciences, 2022-12-01T00:00:00Z.
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Summary:Abstract Background: Premature ovarian failure (POF), is menopause occurring before the age of 40, affecting 1-3% of women worldwide. The risk of POF increases with altered immunological parameters such as FAS and FASL genes, which play a fundamental role in embryogenesis and cellular homeostasis. Objective: The study aimed to investigate the potential role of FAS and FASL genes in POF pathogenesis. Materials and Methods: In this case-control study, the polymorphisms of FAS-670A/G and FASLIVS2nt_124A/G apoptotic genes were analyzed in 51 Iranian women suffering from POF, and 61 healthy controls. Isolation of DNA was done using the salting-out method, and genotypic analysis was performed for all the subjects using the polymerase chain reaction-restriction fragment length polymorphism method. Results: Our results revealed that homozygous FAS-670A/A and G/G, and heterozygous FAS-670A/G are not significantly different between cases and controls (p = 0.99). Also, in different genotyping models of FASIVS2nt_124, polymorphisms were not related to POF risk (p = 0.23). Conclusion: There is no statistical association between these polymorphisms and POF risk in women referred to genetic counseling clinics.
Item Description:2476-4108
2476-3772
10.18502/ijrm.v20i12.12561