Microglial activation and cell death induced by the mitochondrial toxin 3-nitropropionic acid: in vitro and in vivo studies

Ryu, Jae K.; Nagai, Atsushi; Kim, Jean; Lee, Min C.; McLarnon, James G.; Kim, Seung Up

doi:10.1016/s0969-9961(03)00002-0

Cited by 73 publications

(50 citation statements)

References 42 publications

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“…Similarly to what it had been demonstrated for complex I inhibitors, it has been shown that 3-NP causes the activation of both a human microglia cell line and rodents microglial cells [65].…”

Section: DI Filippo Et Al / Mitochondria and Neuroinflammationsupporting

confidence: 57%

Mitochondria and the Link Between Neuroinflammation and Neurodegeneration

Filippo

Chiasserini

Tozzi

et al. 2010

JAD

124

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Abstract. The innate immune response is thought to exert a dichotomous role in the brain. Indeed, although molecules of the innate immune response can promote repair mechanisms, during neuroinflammatory processes many harmful mediators are also released. Signs of neuroinflammation and neurodegeneration represent a ubiquitous pathological finding during the course of several different neurological diseases. Interestingly, it has been proposed that mitochondria may exert a crucial role in the pathogenesis of both inflammatory and neurodegenerative central nervous system disorders. In this review, we describe the mechanisms by which neuroinflammation and mitochondrial impairment may synergistically trigger a vicious cycle ultimately leading to neuronal death. In particular, we describe the close relationship existing among neuroinflammation, neurodegeneration, and mitochondrial impairment in three different widely-diffused neurological diseases in which these pathogenetic events coexist, namely multiple sclerosis, Parkinson's disease, and Alzheimer's disease.

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Section: DI Filippo Et Al / Mitochondria and Neuroinflammationsupporting

confidence: 57%

Mitochondria and the Link Between Neuroinflammation and Neurodegeneration

Filippo

Chiasserini

Tozzi

et al. 2010

JAD

124

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“…Regardless of astrocyte activation, whether microwave electromagnetic fields acted on astrocytes in the caudateputamen is not known. Treatment by 3-NP has also been shown to affect nnicroglia [Pubill et al, 2001;Ryu et al, 2003] and endothelial cells [Hamilton & Gould, 1987;Mogami et al, 2002], which are also possible sites of microwave action and interaction in our study. In addition, isolated neurons are affected by exposure to 3-NP Nasr et al, 2003].…”

Section: Microwave-3-np Resultssupporting

confidence: 64%

Services to Operate and Maintain a Microwave Research Laboratory

Akyel¹

2004

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Supplementary Notes (i.e., report contains color photos, report contains appendix in non-print form, etc.) 12a. Distribution/Availability Statement (check one)Approved for public release; distribution unlimited Due to growing concerns for the health and safety of military and civilian personnel exposed to radiofrequency radiation (RFR), a series of research have been performed at the U.S. Army Medical Research Detachment, Microwave Bioeffects Branch at Brooks City-Base, Texas. The research has been concentrated on neurotoxic effects of high peak power but low average power RFR, Interaction between neurotoxin and RFR on manifestation of neurotoxic effects, effects of high power RFR on hippocampus, biological hazards of ultrawide-band (UWB) pulses on cardiovascular function and cell systems, cytotoxic effect of nanosecond high-intensity electric pulses, finite difference time domain techniques for RFR dosimetry, role of ambient temperature on manifestation of RFR induced biological effects, design fabrication and testing a circularly polarized 1.25 GHz waveguide exposure system, and formulate a research plan for body borne and helmet mounted antennas. Majority of results falls in "thermal" effect, albeit, the threshold was at lower magnitude than that previously envisioned. A model is devised to demonstrate the additive effect of RFR to thermal "stress" from ambient environment. On the other hand, some of the observed effects cannot be easily explained by the "thermal" mechanism. They were effects of UWB pulses and nanosecond high power electric pulses.14. Subject Terms (keywords previously assigned to proposal abstract or terms which apply to this award) high peak power pulsed microwaves, ultra-wide-band pulses, neural, Behavior, cardiovascular, cytotoxicity, neurotoxin, genotoxicity References 33Appendices 39 INTRODUCTIONThe following report summarizes the performance of McKesson BioServices Corporation (MBS) staff at the Walter Reed Army Institute of Research (WRAIR), U.S. Army Medical Research Detachment (USAMRD), Microwave Bioeffects Branch at Brooks City-Base, Texas under the contracts DAMD17-94-4069 and DAMD17-94-E-0001. MBS has nine years contract with the U.S. Army Medical Research and Acquisition Activity (USAMRAA) to operate and maintain Microwave Bioeffects Branch, a Government-owned Contractor-operated (GOCO) facility. Reports summarized the base three years (May 21, 1994 -May 20, 1997) (DTIC STINET ADA 351987, http://handle.dtic.mi 1/100.2/ADA351978\ the first option years (May 21, 1997 -May 20, 1999) (DTIC STINET AD A3 67478, http://handle.dfic.mi1/100.2/ADA367478;) and the second opfions years (May 21 1999 -May 20, 2001, DTIC STINET ADA392971, http://handle.dfic.mi1/100.2/ADA39297n were previously filed with the U.S. Army Medical Research and Materiel Command, Fort Detrick, Maryland in June 1997, May 1999and May 2001. The present report covers the efforts of MBS staff during the third opfion years (May 21 2001 -May 20, 2003 and extensions (May 21, 2003 -May 31, 2004 of the aforementioned contrac...

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“…Free-floating sections (40 m serial coronal sections) were processed for immunostaining as described previously (Ryu et al, 2003). To ensure striatal sections were matched between groups, anatomical landmarks provided by the brain atlas (Paxinos and Watson, 1998) were used for tissue selection.…”

Section: Methodsmentioning

confidence: 99%

Modulation of the Purinergic P2X₇Receptor Attenuates Lipopolysaccharide-Mediated Microglial Activation and Neuronal Damage in Inflamed Brain

Choi

Ryu²,

Kim³

et al. 2007

J. Neurosci.

151

118

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We investigated the involvement and roles of the ionotropic purinergic receptor P2X 7 R in microglia in mediating lipopolysaccharide (LPS)-induced inflammatory responses and neuronal damage in rat striatum. A detailed in vivo study showed that LPS injection into striatum markedly increased the expression of P2X 7 R in microglia compared with control (saline)-injected animals. Additionally, LPS injection upregulated a broad spectrum of proinflammatory mediators, including inducible nitric oxide synthase (nitric oxide production marker), 3-nitrotyrosine (peroxynitrite-mediated nitration marker), 4-hydroxynonenal (lipid peroxidation marker), and 8-hydroxy-2Ј-deoxyguanosine (oxidative DNA damage marker), and reduced neuronal viability. The P2X 7 R antagonist oxidized ATP (oxATP) was effective in attenuating expressions of all inflammatory mediators and in addition inhibited LPS-induced activation of the cellular signaling factors p38 mitogen-activated protein kinase and transcriptional factor nuclear factor B.

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Microglial activation and cell death induced by the mitochondrial toxin 3-nitropropionic acid: in vitro and in vivo studies

Cited by 73 publications

References 42 publications

Mitochondria and the Link Between Neuroinflammation and Neurodegeneration

Mitochondria and the Link Between Neuroinflammation and Neurodegeneration

Services to Operate and Maintain a Microwave Research Laboratory

Modulation of the Purinergic P2X₇Receptor Attenuates Lipopolysaccharide-Mediated Microglial Activation and Neuronal Damage in Inflamed Brain

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Microglial activation and cell death induced by the mitochondrial toxin 3-nitropropionic acid: in vitro and in vivo studies

Cited by 73 publications

References 42 publications

Mitochondria and the Link Between Neuroinflammation and Neurodegeneration

Mitochondria and the Link Between Neuroinflammation and Neurodegeneration

Services to Operate and Maintain a Microwave Research Laboratory

Modulation of the Purinergic P2X7Receptor Attenuates Lipopolysaccharide-Mediated Microglial Activation and Neuronal Damage in Inflamed Brain

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Modulation of the Purinergic P2X₇Receptor Attenuates Lipopolysaccharide-Mediated Microglial Activation and Neuronal Damage in Inflamed Brain