Paraoxonase 1 activity in multiple sclerosis patients during mitoxantrone therapy

Jamróz-Wiśniewska, Anna; Bełtowski, Jerzy; Stelmasiak, Zbigniew; Bartosik-Psujek, Halina

doi:10.1111/ane.12000

Cited by 5 publications

(3 citation statements)

References 19 publications

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“…It should be borne in mind that mitoxantrone is potentially associated with an increased level of OS but on the other hand, the study demonstrated that mitoxantrone did not have an effect on the activity of paraoxonase 1 (an enzyme that protects the cell from OS) [160]. …”

Section: The Relationship Between Immunomodulatory Therapy Os Anmentioning

confidence: 99%

New Insights into the Role of Oxidative Stress Mechanisms in the Pathophysiology and Treatment of Multiple Sclerosis

Adamczyk

Adamczyk-Sowa

2016

Oxidative Medicine and Cellular Longevity

120

100

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Multiple sclerosis (MS) is a multifactorial disease of the central nervous system (CNS) characterized by an inflammatory process and demyelination. The etiology of the disease is still not fully understood. Therefore, finding new etiological factors is of such crucial importance. It is suspected that the development of MS may be affected by oxidative stress (OS). In the acute phase OS initiates inflammatory processes and in the chronic phase it sustains neurodegeneration. Redox processes in MS are associated with mitochondrial dysfunction, dysregulation of axonal bioenergetics, iron accumulation in the brain, impaired oxidant/antioxidant balance, and OS memory. The present paper is a review of the current literature about the role of OS in MS and it focuses on all major aspects. The article explains the mechanisms of OS, reports unique biomarkers with regard to their clinical significance, and presents a poorly understood relationship between OS and neurodegeneration. It also provides novel methods of treatment, including the use of antioxidants and the role of antioxidants in neuroprotection. Furthermore, adding new drugs in the treatment of relapse may be useful. The article considers the significance of OS in the current treatment of MS patients.

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Section: The Relationship Between Immunomodulatory Therapy Os Anmentioning

confidence: 99%

New Insights into the Role of Oxidative Stress Mechanisms in the Pathophysiology and Treatment of Multiple Sclerosis

Adamczyk

Adamczyk-Sowa

2016

Oxidative Medicine and Cellular Longevity

120

100

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“…Mitoxantrone has previously been shown to similarly induce oxidative stress of nucleated cells [8,86,87,88]. On the other hand, mitoxantrone may strengthen the antioxidative defence [89,90]. The latter effect presumably requires expression of the respective proteins, an effect not possible in erythrocytes.…”

Section: Discussionmentioning

confidence: 99%

Mitoxantrone-Induced Suicidal Erythrocyte Death

Arnold

Bissinger

Läng

2014

Cell Physiol Biochem

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Background/Aims: Mitoxantrone, a cytotoxic drug used for the treatment of malignancy and multiple sclerosis, is at least in part effective by triggering apoptosis. Similar to apoptosis of nucleated cells, erythrocytes may enter eryptosis, a type of suicidal cell death. Hallmarks of eryptosis are cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signalling involved in eryptosis include Ca²⁺-entry, ceramide formation and oxidative stress. Methods: Cell volume was estimated from forward scatter, phosphatidylserine-exposure from annexin V binding, formation of reactive oxidant species (ROS) from 2′,7′-dichlorodihydrofluorescein-diacetate fluorescence, and ceramide abundance from binding of fluorescent antibodies in flow cytometry. Results: A 48 hours exposure to mitoxantrone was followed by significant decrease of forward scatter (≥ 5 μg/ml mitoxantrone) and increase of annexin-V-binding (≥ 10 μg/ml mitoxantrone), effects paralleled by significant increases of ROS formation (25 μg/ml mitoxantrone) and ceramide abundance (25 μg/ml mitoxantrone). The effect of mitoxantrone was not significantly modified by nominal absence of extracellular Ca²⁺ but significantly blunted by the antioxidant N-acetylcysteine (1 mM). Conclusions: Mitoxantrone triggers cell membrane scrambling, an effect not requiring entry of extracellular Ca²⁺ but at least partially due to formation of ROS and ceramide.

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“…However, this increase was less significant compared with untreated RRMS patients or SPMS patients treated with mitoxantrone (103). It should be borne in mind that mitoxantrone is associated with an increased level of OS (104). On the other hand, the study demonstrated that mitoxantrone did not have an effect on the activity of paraoxonase 1 (a type of enzyme that protects cells from OS) (104).…”

Section: The Relationship Between Immunomodulatory Therapy Os and Amentioning

confidence: 99%

Novel Approaches of Oxidative Stress Mechanisms in the Multiple Sclerosis Pathophysiology and Therapy

Adamczyk

Niedziela

Adamczyk-Sowa

2017

Multiple Sclerosis: Perspectives in Treatment and Pathogenesis

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Abstract:It is suspected that the development of multiple sclerosis (MS) can be affected by oxidative stress (OS). In the acute phase of the disease, OS is responsible for initiating inflammation, whereas in the chronic phase it sustains neurodegenerative process. Redox processes in MS are related to dysregulation of axonal bioenergetics, cerebral iron accumulation, mitochondrial dysfunction, impaired oxidant/antioxidant balance, and OS memory. This chapter gives an overview of the role of OS in MS.

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Paraoxonase 1 activity in multiple sclerosis patients during mitoxantrone therapy

Abstract: Mitoxantrone therapy does not influence PON1 activity.

Cited by 5 publications

References 19 publications

New Insights into the Role of Oxidative Stress Mechanisms in the Pathophysiology and Treatment of Multiple Sclerosis

New Insights into the Role of Oxidative Stress Mechanisms in the Pathophysiology and Treatment of Multiple Sclerosis

Mitoxantrone-Induced Suicidal Erythrocyte Death

Novel Approaches of Oxidative Stress Mechanisms in the Multiple Sclerosis Pathophysiology and Therapy

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