title: The impact of detoxifying and repair gene polymorphisms on oxidative stress in ischemic stroke.
abstract: Stroke is a multifactorial disease caused by the combination of certain risk factors and genetic factors. There are possible risk factors having important role in the pathogenesis of stroke. The most important environmental factors are cigarette smoking and oxidative stress which have different sources. GST (M1, T1, P1) have major roles in detoxification of the products of oxidative stress and they are polymorphic. DNA damages can also be repaired by repair enzymes such as OGG1 and XRCC1 which are highly polymorphic and have pivotal roles in repair systems. In the present study, we investigated that polymorphisms in genes involved in detoxification and DNA-repair pathways might modify the individual's risk for ischemic stroke. Furthermore, the products of oxidative stress and antioxidant capacity were measured and the impact of gene polymorphism on them was evaluated. Our data showed that OGG1 Ser326Cys and XRCC1 Arg399Gln gene polymorphisms had impacts on the development of stroke.
authors.affiliation: Clinics of Neurology, Ankara Numune Hospital, Ankara, Turkey.
authors.forename: Gürdal
authors.initials: G
authors.lastname: Orhan
authors.affiliation: Department of Toxicology, Faculty of Pharmacy, Gazi University, 06330, Ankara, Turkey.
authors.forename: Aylin
authors.initials: A
authors.lastname: Elkama
authors.affiliation: Clinics of Neurology, Ankara Numune Hospital, Ankara, Turkey.
authors.forename: Semra Öztürk
authors.initials: SÖ
authors.lastname: Mungan
authors.affiliation: Clinics of Neurology, Ankara Numune Hospital, Ankara, Turkey.
authors.forename: Esra
authors.initials: E
authors.lastname: Eruyar
authors.affiliation: Department of Toxicology, Faculty of Pharmacy, Gazi University, 06330, Ankara, Turkey. bensuka@gmail.com.
authors.forename: Bensu
authors.initials: B
authors.lastname: Karahalil
mesh_terms: D000975:Antioxidants / Q000378:metabolism; D002545:Brain Ischemia / Q000150:complications; D016022:Case-Control Studies; D045647:DNA Glycosylases / Q000235:genetics*; D004252:DNA Mutational Analysis; D004268:DNA-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005838:Genotype; D005982:Glutathione Transferase / Q000235:genetics; D006801:Humans; D006912:Hydroxyquinolines / Q000097:blood; D008297:Male; D018384:Oxidative Stress / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D017382:Reactive Oxygen Species / Q000097:blood*; D012307:Risk Factors; D018709:Statistics, Nonparametric; D020521:Stroke / Q000209:etiology / Q000235:genetics* / Q000503:physiopathology; D014421:Turkey; D000076105:X-ray Repair Cross Complementing Protein 1
chemical_list: D000975:Antioxidants; D045647:DNA Glycosylases; D004268:DNA-Binding Proteins; D005982:Glutathione Transferase; D006912:Hydroxyquinolines; D017382:Reactive Oxygen Species; D000076105:X-ray Repair Cross Complementing Protein 1; C000619371:XRCC1 protein, human; C056147:8-hydroxyquinoline glucuronide; C413545:glutathione S-transferase T1; C479058:oxoguanine glycosylase 1, human
keywords: 8-OHdGua; GSTs gene polymorphism; OGG1; RFLP; ROS; Stroke; XRCC1; XRCC1 activity