Oxidative Stress and Inflammation Interdependence in Multiple Sclerosis.

Rodica Padureanu,Gabriela Olaru,Anca Oana Docea,Raluca Elena Sandu,Carmen Valeria Albu,Daniela Calina,Radu Razvan Mititelu,Vlad Padureanu,Ana-Maria Buga,Manuela Violeta Bacanoiu,Ramona Denise Malin

doi:10.3390/jcm8111815

Abstract

The study aims to explore the oxidative status related to inflammation in peripheral blood of stable relapsing-remitting multiple sclerosis (MS) patients with low disability. In this study, 31 people were included and divided into two groups: an MS group in which 16 relapsing-remitting MS patients with a low disability level (age 38.9 ± 7.08, EDSS median 2.5) were included and a control group that contains 15 healthy volunteers of similar age to the MS group. Thiobarbituric acid reactive substances (TBARS), protein carbonyl level (PCO), total antioxidant capacity (TAC) as oxidative stress markers, neutrophil/lymphocyte ratio (NLR), and erythrocyte sedimentation rate (ESR) were analyzed in the peripheral blood sample of the healthy and the MS patients to establish the oxidative stress/inflammatory level using conventional plasma markers. In this study, we showed that the pro-inflammatory status of the relapse-remitting stage of diseases can be easily and accurately appreciated by NLR. An increased NLR is associated with a decreased antioxidant capacity, even in the early stage of neuronal damage. Oxidative stress associated with inflammation aggravates the functional outcome, potentiates neuronal damage, and can accelerate the progression of the disease.

Highlights

Oxidative stress involves a key pathway that contributes to many pathological processes including Multiple Sclerosis (MS) [1,2]
We found that the MS patients display a significant increase of oxidative stress markers in plasma (TBARS and protein carbonyl (PCARB)) suggesting that oxidative stress induction started in the relapsing-remitting MS subjects (RRMS) stage with a low level of irreversible neuronal damage
Enhanced protection of CNS by a sustained antioxidant capacity plays a crucial role in MS patient management to limit the irreversible neuronal damage

Summary

Introduction

Oxidative stress involves a key pathway that contributes to many pathological processes including Multiple Sclerosis (MS) [1,2]. A balance between reactive oxygen species (ROS) production and antioxidant defence is crucial to prevent any structural damage to the CNS. It is well known that ROS production is necessary for neuronal cell stability, modulation of synaptic plasticity and brain functions (e.g., apoptosis, synaptic plasticity-related pathway including cognition, immune system) but the border between necessary and harmful processes is still very sensitive [5,6]. When the level of ROS increases in the cells, the capacity of the body to produce antioxidant molecules in a sufficient proportion is crucial to prevent the oxidative stress damage [9,10]

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