Anka Tıp Dergisi

Yazarlar: Ahmet ÖZAYDIN, Ayla KERİMOVA, İlhan ONARAN

Konular:Tıbbi Araştırmalar Deneysel

DOI:10.38175/phnx.869878

Anahtar Kelimeler:MtDNA4977 deletion,Ischemic heart disease,Platelet,ATP

Özet: Objective: It is known that point mutations, duplications and deletions occur in mitochondrial DNAs (mtDNA) of different tissues of individuals. Among the deletions observed, mt4977 mutation, which is located at nucleotide positions 8470-8482 and 13447-13459 and causes the loss of 4977 base pairs, is the most common. mtDNA 4977 deletion leads to the loss of 8 genes encoding subunits of respiratory chain complexes. Consequently, the deletion could be expected to inhibit the oxidative function and reduce ATP production level. It is known that mitochondrial ATP production has an important role on platelet functions. However, there is no information about this in the literature. Since platelet activation in ischemic heart disease (IHD) has been shown to play an important role in the pathophysiology of the disease, we wanted to examine the relationship between platelet function and mtDNA 4977 deletion in ischemic heart disease. Material and Method: Platelet functions were studied by giving ADP stimulus with the help of lumiaggregometer device to evaluate in terms of secretion and aggregation. ATP measurement was performed with the bioluminescence assay kit. mtDNA 4977 deletion was determined by the modified simultaneous quantitative polymerase chain reaction method. Results: The frequency of mtDNA 4977 deletion and mtDNA copy number were higher in platelets of the patients compared with the healthy control group (p<0.05). However, no significant differences in platelet ATP content, and in their slope (Ω) and % amplitude values were observed between both groups (p>0.05). Conclusion: It was observed that increased deletion in patients with IHD did not have a significant effect on platelet dysfunction compared with healthy control subjects.

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