Oxidative Modification of Blood Serum Proteins in Multiple Sclerosis after Interferon Beta and Melatonin Treatment.

Monika Adamczyk-Sowa,Paweł Sowa,Ewa Żyracka,Katarzyna Naparło,Grzegorz Bartosz,Michalina Grzesik,Izabela Sadowska-Bartosz,Sabina Galiniak

doi:10.1155/2017/7905148

Abstract

Multiple sclerosis (MS) is a disease involving oxidative stress (OS). This study was aimed at examination of the effect of melatonin supplementation on OS parameters, especially oxidative protein modifications of blood serum proteins, in MS patients. The study included 11 control subjects, 14 de novo diagnosed MS patients with the relapsing-remitting form of MS (RRMS), 36 patients with RRMS receiving interferon beta-1b (250 μg every other day), and 25 RRMS patients receiving interferon beta-1b plus melatonin (5 mg daily). The levels of N′-formylkynurenine, kynurenine, dityrosine, carbonyl groups, advanced glycation products (AGEs), advanced oxidation protein products (AOPP), and malondialdehyde were elevated in nontreated RRSM patients. N′-Formylkynurenine, kynurenine, AGEs, and carbonyl contents were decreased only in the group treated with interferon beta plus melatonin, while dityrosine and AOPP contents were decreased both in the group of patients treated with interferon beta and in the group treated with interferon beta-1b plus melatonin. These results demonstrate that melatonin ameliorates OS in MS patients supporting the view that combined administration of interferon beta-1b and melatonin can be more effective in reducing OS in MS patients than interferon beta-1b alone.

Highlights

Multiple sclerosis (MS) is one of the most widespread chronic inflammatory, demyelinating diseases of the central nervous system (CNS), which leads to damage of myelin and axons
The factors involved in the etiology of the disease have included oxidative stress (OS), which is defined as an imbalance between the generation of reactive oxygen species (ROS) and the mechanisms that are responsible for their elimination
This study was aimed at examining the effect of MEL on the OS markers in MS patients treated with interferon beta-1b, basing mainly on the oxidative modifications of serum proteins as sensitive markers of OS [14, 15]

Summary

Introduction

Multiple sclerosis (MS) is one of the most widespread chronic inflammatory, demyelinating diseases of the central nervous system (CNS), which leads to damage of myelin and axons. The exact cause of MS is unknown, it is considered that genetic predisposition, environmental factors, and abnormal immune response, consisting of delivery of cytokines from lymphocytes including Th1 and Th17 cells, contribute to the pathogenesis of this disease [1, 2]. The factors involved in the etiology of the disease have included oxidative stress (OS), which is defined as an imbalance between the generation of reactive oxygen species (ROS) and the mechanisms that are responsible for their elimination. It is suggested that the increased generation of ROS and reactive forms of nitrogen (RNS) leads to oxidative and nitrosative stress causing damage to mitochondria and myelin, oligodendrocyte apoptosis, and astrocyte dysfunction [3].

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