Severe oxidative damage in multiple sclerosis lesions coincides with enhanced antioxidant enzyme expression
Autor: | Thierry Hazes, Gerty Schreibelt, J. van Horssen, P. van der Valk, H.E. de Vries, Joost A. R. Drexhage, Christine D. Dijkstra |
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Přispěvatelé: | Molecular cell biology and Immunology, Division 6, Pathology, Neuroscience Campus Amsterdam 2008 |
Rok vydání: | 2008 |
Předmět: |
Adult
Male Leukocyte migration Multiple Sclerosis medicine.disease_cause Biochemistry Antioxidants Superoxide dismutase Lesion Immunoenzyme Techniques Superoxide Dismutase-1 Physiology (medical) medicine Humans Aged chemistry.chemical_classification Aged 80 and over Reactive oxygen species biology Superoxide Dismutase Multiple sclerosis Macrophages Brain Middle Aged medicine.disease Catalase Cell biology Heme oxygenase Oxidative Stress chemistry Astrocytes Case-Control Studies biology.protein Female medicine.symptom Oxidative stress Heme Oxygenase-1 Immunity infection and tissue repair [NCMLS 1] |
Zdroj: | Free Radical Biology and Medicine, 45, 1729-37 Free Radical Biology and Medicine, 45(12), 1729-1737. Elsevier Inc. van Horssen, J, Schreibelt, G, Drexhage, J, Hazes, T, Dijkstra, C D, van der Valk, P & de Vries, H E 2008, ' Severe oxidative damage in multiple sclerosis lesions coincides with enhanced antioxidant enzyme expression ', Free Radical Biology and Medicine, vol. 45, no. 12, pp. 1729-1737 . https://doi.org/10.1016/j.freeradbiomed.2008.09.023 Free Radical Biology and Medicine, 45, 12, pp. 1729-37 |
ISSN: | 0891-5849 |
DOI: | 10.1016/j.freeradbiomed.2008.09.023 |
Popis: | Contains fulltext : 71055.pdf (Publisher’s version ) (Closed access) Reactive oxygen species (ROS) and subsequent oxidative damage may contribute to the formation and persistence of multiple sclerosis (MS) lesions by acting on distinct pathological processes. ROS initiate lesion formation by inducing blood-brain barrier disruption, enhance leukocyte migration and myelin phagocytosis, and contribute to lesion persistence by mediating cellular damage to essential biological macromolecules of vulnerable CNS cells. Relatively little is known about which CNS cell types are affected by oxidative injury in MS lesions. Here, we show the presence of extensive oxidative damage to proteins, lipids, and nucleotides occurring in active demyelinating MS lesions, predominantly in reactive astrocytes and myelin-laden macrophages. Oxidative stress can be counteracted by endogenous antioxidant enzymes that confer protection against oxidative damage. Here, we show that antioxidant enzymes, including superoxide dismutase 1 and 2, catalase, and heme oxygenase 1, are markedly upregulated in active demyelinating MS lesions compared to normal-appearing white matter and white matter tissue from nonneurological control brains. Particularly, hypertrophic astrocytes and myelin-laden macrophages expressed an array of antioxidant enzymes. Enhanced antioxidant enzyme production in inflammatory MS lesions may reflect an adaptive defense mechanism to reduce ROS-induced cellular damage. |
Databáze: | OpenAIRE |
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