Auto-catalytic ceria nanoparticles offer neuroprotection to adult rat spinal cord neurons

Das, Mainak; Patil, Swanand; Bhargava, Neelima; Kang, Jung-Fong; Riedel, Lisa; Seal, Sudipta; Hickman, James J.

doi:10.1016/j.biomaterials.2006.11.036

Cited by 680 publications

(506 citation statements)

References 33 publications

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“…35 In addition, nanoceria improved the function and survival of rat spinal cord neurons exposed to H 2 O 2 . 47 Furthermore, nanoceria protected HT22 cells, a hippocampal neuronal cell line, from glutamate-induced cell death. 48 CeO 2 nanoparticles also seem to be protective in the eye.…”

Section: Discussionmentioning

confidence: 99%

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

et al. 2014

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Evidence indicates that nitrosative stress and mitochondrial dysfunction participate in the pathogenesis of Alzheimer's disease (AD). Amyloid beta (Ab) and peroxynitrite induce mitochondrial fragmentation and neuronal cell death by abnormal activation of dynamin-related protein 1 (DRP1), a large GTPase that regulates mitochondrial fission. The exact mechanisms of mitochondrial fragmentation and DRP1 overactivation in AD remain unknown; however, DRP1 serine 616 (S616) phosphorylation is likely involved. Although it is clear that nitrosative stress caused by peroxynitrite has a role in AD, effective antioxidant therapies are lacking. Cerium oxide nanoparticles, or nanoceria, switch between their Ce 3 þ and Ce 4 þ states and are able to scavenge superoxide anions, hydrogen peroxide and peroxynitrite. Therefore, nanoceria might protect against neurodegeneration. Here we report that nanoceria are internalized by neurons and accumulate at the mitochondrial outer membrane and plasma membrane. Furthermore, nanoceria reduce levels of reactive nitrogen species and protein tyrosine nitration in neurons exposed to peroxynitrite. Importantly, nanoceria reduce endogenous peroxynitrite and Ab-induced mitochondrial fragmentation, DRP1 S616 hyperphosphorylation and neuronal cell death.

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Section: Discussionmentioning

confidence: 99%

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

et al. 2014

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“…There are two methods by which living systems remove hydroxyl radicals: blocking hydroxyl radical initiation by antioxidant enzymes (SOD, glutathione peroxidase and catalase) or breaking the hydroxyl radical chain reaction using nonenzymatic antioxidants. 49 Hickman and co-workers 53 found that ultrafine CeONP (2-5 nm) with mixed valence states had a significant neuroprotective effect on H 2 O 2 -treated adult spinal cord model systems designed to prevent oxidative injury. As H 2 O 2 provides a source of hydroxyl radicals, which have a major role in oxidative injury, Hickman and coworkers 53 proposed that the protective effect of CeONP on the spinal cord involved its free-radical scavenging effect.…”

Section: Hydroxyl Radical Scavengingmentioning

confidence: 99%

Cerium oxide nanoparticle: a remarkably versatile rare earth nanomaterial for biological applications

2014

NPG Asia Mater

854

650

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“…In in vivo rat studies, the nanoparticles (0.1-1 mM) were injected into the vitreous humor of both eyes and shown to prevent loss of vision due to the light-induced degeneration of photoreceptor cells (60). Cerium oxide nanoparticle (at nanomolar levels) proved beneficial in an in vitro cell model of adult rat spinal cord neuroprotection (78). These nanoparticles (3-5 nm) can also protect normal tissue against radiation-induced damage; CeO 2 nanoparticles prevented the onset of radiation-induced pneumonitis when delivered (IP or IV) to athymic nude mice exposed to high doses of radiation in a study using amifostine as a positive control (63).…”

Section: Other Compoundsmentioning

confidence: 99%

Superoxide Dismutase Mimics: Chemistry, Pharmacology, and Therapeutic Potential

Batinić‐Haberle

Rebouças

Spasojević

2010

Antioxidants & Redox Signaling

459

689

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Oxidative stress has become widely viewed as an underlying condition in a number of diseases, such as ischemia-reperfusion disorders, central nervous system disorders, cardiovascular conditions, cancer, and diabetes. Thus, natural and synthetic antioxidants have been actively sought. Superoxide dismutase is a first line of defense against oxidative stress under physiological and pathological conditions. Therefore, the development of therapeutics aimed at mimicking superoxide dismutase was a natural maneuver. Metalloporphyrins, as well as Mn cyclic polyamines, Mn salen derivatives and nitroxides were all originally developed as SOD mimics. The same thermodynamic and electrostatic properties that make them potent SOD mimics may allow them to reduce other reactive species such as peroxynitrite, peroxynitrite-derived CO 3 _ À , peroxyl radical, and less efficiently H 2 O 2 . By doing so SOD mimics can decrease both primary and secondary oxidative events, the latter arising from the inhibition of cellular transcriptional activity. To better judge the therapeutic potential and the advantage of one over the other type of compound, comparative studies of different classes of drugs in the same cellular and=or animal models are needed. We here provide a comprehensive overview of the chemical properties and some in vivo effects observed with various classes of compounds with a special emphasis on porphyrin-based compounds. Antioxid. Redox Signal. 13, 877-918.

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Auto-catalytic ceria nanoparticles offer neuroprotection to adult rat spinal cord neurons

Cited by 680 publications

References 33 publications

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

Cerium oxide nanoparticle: a remarkably versatile rare earth nanomaterial for biological applications

Superoxide Dismutase Mimics: Chemistry, Pharmacology, and Therapeutic Potential

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