Nitric oxide, superoxide and peroxynitrite: Putative mediators of NMDA-induced cell death in cerebellar granule cells

Lafon-Cazal, Mireille; Culcasi, Marcel; Gaven, Florence; Pietri, Sylvia; Bockaert, Joël

doi:10.1016/0028-3908(93)90020-4

Cited by 183 publications

(72 citation statements)

References 43 publications

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“…Glutamate mediated neurotoxicity by NMDA receptors involves calcium (Ca 2+ ) entry into cells (Butterfield and Pocernich, 2003; Tanović and Alfaro, 2006). Intracellular Ca 2+ influx affected activation of the neuronal nNOS and ROS formation (Lafon-Cazal et al ., 1993; Randall and Thayer, 1992). NO overproduction by nNOS activation and the increased formation of ROS induced neuronal cell death (Reynolds and Hastings, 1995).…”

Section: Disscusionmentioning

confidence: 99%

Neuroprotective Effect of Steamed and Fermented Codonopsis lanceolata

Weon

Yun

Lee

et al. 2014

Biomolecules & Therapeutics

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Codonopsis lanceolata has been used as an herbal medicine for several lung inflammatory diseases, such as asthma, tonsillitis, and pharyngitis. Previously, we showed the neuroprotective effect of steamed and fermented C. lanceolata (SFC) in vitro and in vivo. In the current study, the treatment of HT22 cells with SFC decreased glutamate-induced cell death, suggesting that SFC protected HT22 cells from glutamate-induced cytotoxicity. Based on these, we sought to elucidate the mechanisms of the neuro-protective effect of SFC by measuring the oxidative stress parameters and the expression of Bax and caspase-3 in HT22 cells. SFC reduced contents of ROS, Ca2+ and NO. Moreover, SFC restored contents of glutathione and glutathione reductase as well as inhibited Bax and caspase-3 activity in HT22 cells. These results indicate that steamed and fermented C. lanceolata (SFC) extract protected HT22 cells by anti-oxidative effect and inhibition of the expression of Bax and caspase-3.

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Section: Disscusionmentioning

confidence: 99%

Neuroprotective Effect of Steamed and Fermented Codonopsis lanceolata

Weon

Yun

Lee

et al. 2014

Biomolecules & Therapeutics

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“…Death of neuronal cells via this oxidative pathway is attributed to increased calcium influx that drives NOS production, and ultimately RNS formation (Dykens et al, 1987;Dawson et al, 1991;Coyle and Puttfarcken, 1993;Lafon-Cazal et al, 1993a;1993b;Lipton et al, 1993;Puttfarcken et al, 1993;Schinder et al, 1996;White and Reynolds, 1996;Ha and Park, 2006). Deficits in calcium homeostasis are clearly implicated in excitotoxininduced cell death in the auditory system (Harada et al, 1994;Puel et al, 1994), and production of NOS is part of the cochlear response to stress (Hess et al, 1999;Hanson et al, 2003;Ohinata et al, 2003;Yamane et al, 2004;Chen et al, 2005).…”

Section: Glutamate Excitotoxicitymentioning

confidence: 99%

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

et al. 2007

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Recent research has shown the essential role of reduced blood flow and free radical formation in the cochlea in noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant late formation 7-10 days following noise exposure, and one mechanism underlying noise-induced reduction in cochlear blood flow has finally been identified. These new insights have led to the formulation of new hypotheses regarding the molecular mechanisms of NIHL; and, from these, we have identified interventions that prevent NIHL, even with treatment onset delayed up to 3 days post-noise. It is essential to now assess the additive effects of agents intervening at different points in the cell death pathway to optimize treatment efficacy. Finding safe and effective interventions that attenuate NIHL will provide a compelling scientific rationale to justify human trials to eliminate this single major cause of acquired hearing loss.

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“…Entry of calcium through the NMDA receptor subtype is considered to contribute to the induction of excitotoxic neuronal death. Increases in intracellular calcium level induce the activity of several intracellular enzymatic processes involved in the degradation of cell components, such as endonucleases, phopholipases, and proteases (Lafon-Cazal et al 1993;Mattson 2007). Calpains are calcium-activated cysteine proteases involved in physiological and pathological processes (Oliver et al 1989;del Cerro et al 1990;Denny et al 1990;Vanderklish et al 1996) and are involved in necrotic cell death through the degradation of several substrates essential for cell survival, including enzymes, transcription factors, receptors, transporters, channels, and cytoskeletal proteins such as spectrin (Wang 2000;Goll et al 2003).…”

Section: Electrical Cell Stimulationmentioning

confidence: 99%