Dimetilarjinin dimetilaminohidrolaz (DDAH) enzim aktivitesi ölçüm yöntemi ve klinik uygulamaları
Method of DDAH(dimethylarginine dimethylaminohydrolase) enzyme activity measurement and clinical applications
- Tez No: 224391
- Danışmanlar: PROF.DR. M. KEMAL ERBİL
- Tez Türü: Tıpta Uzmanlık
- Konular: Biyokimya, Kardiyoloji, Biochemistry, Cardiology
- Anahtar Kelimeler: Epilepsy, Nitric Oxide, ADMA, Homocysteine pathway, Antiepileptic Drug, Erythrocyte DDAH enzyme activity, ADMA
- Yıl: 2007
- Dil: Türkçe
- Üniversite: Gata
- Enstitü: Tıp Fakültesi
- Ana Bilim Dalı: Biyokimya ve Klinik Biyokimya Ana Bilim Dalı
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: Belirtilmemiş.
Özet
Experimental data indicate that nitric oxide (NO) may play a role in the pathophysiology of epilepsy. It is also possible that NO-mediated events are involved in the expression of the anticonvulsant action of some antiepileptics. ADMA is an endogenous NO synthase inhibitor. Homocysteine is an established atherosclerotic risk factor. Vitamin B-12 and folate play important roles in homocysteine metabolism.The aims of this study are defined as, to manifest the functional interaction between epilepsy and NO by comparing serum ADMA, homocysteine, folate and vitamin B-12 levels before and after carbamazepine and valproic acid treatment; to investigate the role of NO in the action of mechanism of AEDs and to evaluate the atherosclerotic risk and metabolic changes in patients who are on long term AED therapy. 35 patients were included in the study. Patients formed in two groups as VPA (n=17) and CBZ (n=18) treatment. Blood samples were obtained before AED therapy and at the 3rd. month of therapy. At the 3rd. month, patients had significantly higher ADMA levels (VPA: p=0,002, KBZ: p=0,024) in both groups. In VPA group, pHcy (p=0,005) and VitB-12 (p=0,001) levels were significantly higher. In CBZ group folate levels were significantly lower (p=0,006). Our data suggest that these two AEDs exhibit their antiepileptic effects by lowering the NO levels in CNS and increased ADMA and pHcy levels indicate high atherosclerotic risk. Decreased folate levels in CBZ group, may cause malfunction in metabolic processes that folate is used as a cofactor.
Özet (Çeviri)
Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS) enzyme. Elevations in plasma ADMA (pADMA) contribute to vascular pathophysiology observed in atherosclerosis. So it is important to keep pADMA levels under control. Generation of free ADMA by sequence of complex events reveals DDAH enzyme, which selectively degrades ADMA, as a target for controlling ADMA levels. In this study developing the method of DDAH enzyme activity (DDAHea) measurement, measuring serum/erythrocyte DDAHea and researching if it is a risk factor for CAD has been aimed. Firstly HPLC method of ADMA measurement was developed then DDAHea was determined by a decrease in the level of ADMA during incubation. This decrease was seen after incubation in erythrocyte samples but similar change wasn?t seen in serum samples and absence of DDAHea in serum was concluded. Then erythrocyte DDAHea (eDDAHea), erythrocyte ADMA (eADMA), pADMA and plasma total homocysteine (ptH) levels were measured in CAD patients (n=40) and 40 patients with normal coronary angiography. According to eDDAHea there weren?t significant difference between groups but pADMA and ptH levels were significantly high in CAD patients. No correlation between eDDAHa and pADMA levels was seen. But a significant negative correlation between eDDAHea and eADMA levels was determined. Our study is the first showing that there is no DDAHea in serum and measuring eDDAHa in a disease group. According to our results eDDAHea is influential on eADMA levels but it hasn?t got any place in regulating pADMA levels and it can not be evaluated as a risk factor for CAD. In addition to this the existence of significant difference in pADMA and ptH levels between two groups, which are likely about total cholesterol, age, gender and smoking status, supported both ADMA and homocysteine as independent CAD risk factors.
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