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Nitrosative stress in primary glial cultures after induction of the inducible isoform of nitric oxide synthase (i-NOS).
Toxicology. 2000 Aug 07; 148(2-3):133-42.T

Abstract

Primary glial cultures are able to express the inducible isoform of nitric oxide synthase (i-NOS) upon stimulation by bacterial lipopolysaccharides (LPS) and gamma-interferon (gamma-IfN). Immunocytochemical studies revealed, that under our experimental conditions i-NOS is expressed exclusively by the microglial cells and not in the astrocytes. Nitric oxide (NO) formation represents an oxidative load for the microglial cells, as observed by the oxidation rate of the ROS- and peroxynitrite indicator dichloro-dihydrofluorescein (DCF-H) in these cells. However, cell viability was not affected by the nitric oxide formation, indicating some form of protection against the higher oxidative load. Upregulation of Mn-SOD in the mitochondria in the course of the induction of i-NOS and, compared to the astrocytes, higher GSH levels in the microglial cells probably explain the resistance of the cultures against nitrosative stress. Increased SOD-activities in the mitochondria could lower the superoxide concentration in this organelle and may prevent an oxidative and/or nitrosative damage via a decreased peroxynitrite formation. The higher GSH-levels in the microglial cells of unstimulated cultures represents a buffer which, under the conditions of i-NOS catalyzed NO-formation, prevents a decline of the microglial GSH-levels below that of the astrocytes.

Authors+Show Affiliations

Institute for Medical Neurobiology, Otto-von-Guericke University Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany. heiko.noack@medizin.uni-halle.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

10962132

Citation

Noack, H, et al. "Nitrosative Stress in Primary Glial Cultures After Induction of the Inducible Isoform of Nitric Oxide Synthase (i-NOS)." Toxicology, vol. 148, no. 2-3, 2000, pp. 133-42.
Noack H, Possel H, Chatterjee S, et al. Nitrosative stress in primary glial cultures after induction of the inducible isoform of nitric oxide synthase (i-NOS). Toxicology. 2000;148(2-3):133-42.
Noack, H., Possel, H., Chatterjee, S., Keilhoff, G., & Wolf, G. (2000). Nitrosative stress in primary glial cultures after induction of the inducible isoform of nitric oxide synthase (i-NOS). Toxicology, 148(2-3), 133-42.
Noack H, et al. Nitrosative Stress in Primary Glial Cultures After Induction of the Inducible Isoform of Nitric Oxide Synthase (i-NOS). Toxicology. 2000 Aug 7;148(2-3):133-42. PubMed PMID: 10962132.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitrosative stress in primary glial cultures after induction of the inducible isoform of nitric oxide synthase (i-NOS). AU - Noack,H, AU - Possel,H, AU - Chatterjee,S, AU - Keilhoff,G, AU - Wolf,G, PY - 2000/8/30/pubmed PY - 2000/10/14/medline PY - 2000/8/30/entrez SP - 133 EP - 42 JF - Toxicology JO - Toxicology VL - 148 IS - 2-3 N2 - Primary glial cultures are able to express the inducible isoform of nitric oxide synthase (i-NOS) upon stimulation by bacterial lipopolysaccharides (LPS) and gamma-interferon (gamma-IfN). Immunocytochemical studies revealed, that under our experimental conditions i-NOS is expressed exclusively by the microglial cells and not in the astrocytes. Nitric oxide (NO) formation represents an oxidative load for the microglial cells, as observed by the oxidation rate of the ROS- and peroxynitrite indicator dichloro-dihydrofluorescein (DCF-H) in these cells. However, cell viability was not affected by the nitric oxide formation, indicating some form of protection against the higher oxidative load. Upregulation of Mn-SOD in the mitochondria in the course of the induction of i-NOS and, compared to the astrocytes, higher GSH levels in the microglial cells probably explain the resistance of the cultures against nitrosative stress. Increased SOD-activities in the mitochondria could lower the superoxide concentration in this organelle and may prevent an oxidative and/or nitrosative damage via a decreased peroxynitrite formation. The higher GSH-levels in the microglial cells of unstimulated cultures represents a buffer which, under the conditions of i-NOS catalyzed NO-formation, prevents a decline of the microglial GSH-levels below that of the astrocytes. SN - 0300-483X UR - https://www.unboundmedicine.com/medline/citation/10962132/Nitrosative_stress_in_primary_glial_cultures_after_induction_of_the_inducible_isoform_of_nitric_oxide_synthase__i_NOS__ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0300483X00002043 DB - PRIME DP - Unbound Medicine ER -