Multiple sclerosis (MS) is a chronic, inflammatory demyelinating disease of central nervous system with complex etiopathogenesis that impacts young adults (Lee et al., 2015), and MS impacts younger and middle aged character and leads to a range of disabilities that can alter their daily routines (Yara et al, 2010). Although, the exact cause of MS is still undetermined, the disease is mediated by adaptive immunity through the infiltration of T cells into the central nervous system (Bjelobaba et al, 2017). MS causes the Focal neurological symptomsand biochemical changes in the molecular level and the variation of neural cells such as loss or alteration of sensation, motor function, visible signs such as blurred vision or transient blindness, disturbance of conjugate eye movements, bladder and bowel dysfunction and cognitive impairment (Induruwa et al, 2012 and Jafarzadeh et al, 2014). Autoimmune diseases (ADs) are chronic conditions initiated by way of the loss of immunological tolerance to self-antigens (TodorovicDilas et al, 2011). It is a heterogeneous group of disorders in which more than one modification in the immune system can be specific to a particular tissue or organ or might also be systemic, non-specific, involving multiple tissues or organs (Ray et al, 2012). One possible cause behind this is a lack of understanding of pathogenic mechanisms driving progressive multiple sclerosis. Due to the indolent nature of symptom progression, current disease criteria used to signify the course of disease (Lublin et al, 2014) indicate diagnosis is generally retrospective and based totally on history of gradual worsening. Clearly, diagnosis is primary based on clinical judgment, as there is no fully reliable diagnostic test (Ontaneda et al, 2015). In latest years, the elements involved in the etiology of the disease have also included oxidative stress (OS), which is described as an imbalance between the generation of reactive oxygen species (ROS) and the mechanisms that are responsible for their elimination, andthe imbalance between OS agents and antioxidants leads to OS activating the inflammatory process (Phaniendra et al, 2015). In the absence of enough antioxidant defenses, ROS can reason oxidative damage to macromolecules resulting in oxidation of lipids, proteins and deoxyribonucleic acid (DNA) (Griffiths, 2002). Some reseach report that ROS play a main role in myelin phagocytosis (Ghabaee et al, 2010 and Tasset et al, 2012). The inflammatory response gives rise to the manufacturing of both ROS and Reactive Biochem. Cell. Arch. Vol. 19, No. 1, pp. 31-35, 2019 www.connectjournals.com/bca ISSN 0972-5075 Nitrogen Species RNS through monocyte interactions with brain endothelium; ROS manufacturing induces cytoskeletal rearrangements, loss of blood-brain blood BBB integrity, tight-junction alteration and the extravasation of leukocytes into the central nervous system (Van et al, 2011; Witherick et al, 2011). Aim of study The aim of this study focuses on determination 8-H2-dG, MDA and PON1 in multiple sclerosis disease and finds the relationship between newly marker 8-H-2-dG with MDA and PON1. MATERIALS AND METHODS Subjects This study was performed on 25 female patients with age (25-35) years who diagnosed by physicians as a multiple sclerosis in Misan governorate. The patients compared with 25 apparently healthful in the identic rangel of age. In this study sample was collected five mL of venous bloods, placed in to plain tubes until coagulation was performed. Serum was separated from blood cells by centrifugation 4000 r.p.m. Assay method Determination of serum of 8-H-2-dG This assay that can be used for quantification of 8- H-2-dG in urine, cell culture, plasma and other sample matrices. The ELISA utilize an 8-H-2-dG coated plate and HRP- conjugated antibody or detection which allows for any assay range of 0.94-60 ng/mL, with sensitivity of 0.59 ng/mL. Determination of MDA The concentration of MDA,which is the consequence of lipid peroxidation and a marker of oxidative stress, was measured using thiobarbiturc acid. Determination of PON1 The quantitive sandwich enzyme immunoassay (ELISA) technique was employed for determination of PON1.