Journal ArticleDOI
Neurotoxic potential of iron oxide nanoparticles in the rat brain striatum and hippocampus
Jie Wu,Tingting Ding,Jiao Sun +2 more
Reads0
Chats0
TLDR
In vitro studies demonstrate that Fe(3)O(4)-NPs may decrease neuron viability, trigger oxidative stress, and activate JNK- and p53-mediated pathways to regulate the cell cycle and apoptosis, and suggest that environmental exposure to Fe( 3)O (4)- NPs may play a role in the development of neurodegenerative diseases.Abstract:
It has recently been reported that iron oxide nanoparticles (Fe 3 O 4 -NPs, 30 nm) have the ability to translocate directly from the olfactory nerve to the brain The striatum and hippocampus are important structures in the brain and are associated with the development of Parkinson's and Alzheimer's diseases Therefore, it is critical to evaluate Fe 3 O 4 -NPs and their potential to confer striatum and hippocampus neurotoxicity This study focuses on the effects of Fe 3 O 4 -NPs on the striatum and hippocampus, including oxidative injury and the accumulation and retention of Fe 3 O 4 -NPs This study also explores the molecular mechanism of oxidative damage in dopaminergic neurons; we were able to assess the neurotoxic effects of Fe 3 O 4 -NPs by incubating dopaminergic neurons with radioactive Fe 3 O 4 -NPs A regional distribution of Fe 3 O 4 -NPs was observed in rat brains after the particles were intranasally instilled for seven days The particles were found to be deposited at particularly high concentrations in the rat striata and hippocampi Over half of the Fe 3 O 4 -NPs were retained in the striata for a minimum of 14 days, and may have induced oxidative damage to the region However, no injuries were observed in the hippocampi These in vitro studies demonstrate that Fe 3 O 4 -NPs may decrease neuron viability, trigger oxidative stress, and activate JNK- and p53-mediated pathways to regulate the cell cycle and apoptosis These results also suggest that environmental exposure to Fe 3 O 4 -NPs may play a role in the development of neurodegenerative diseasesread more
Citations
More filters
Journal ArticleDOI
Metals, oxidative stress and neurodegeneration: a focus on iron, manganese and mercury.
TL;DR: This review focuses on the neurodegenerative mechanisms and effects of Fe, Mn and Hg, addressing the main sources of exposure to these metals, their transport mechanisms into the brain, and therapeutic modalities to mitigate their neurotoxic effects.
Journal ArticleDOI
The plastic brain: neurotoxicity of micro- and nanoplastics
TL;DR: The combined data, although fragmentary, indicate that exposure to micro- and nanoplastics can induce oxidative stress, potentially resulting in cellular damage and an increased vulnerability to develop neuronal disorders.
Journal ArticleDOI
Tau-Targeted Multifunctional Nanocomposite for Combinational Therapy of Alzheimer's Disease.
Qing Chen,Yang Du,Kai Zhang,Zeyu Liang,Jinquan Li,Hao Yu,Ren Rong,Jin Feng,Zhiming Jin,Fangyuan Li,Jihong Sun,Min Zhou,Qinggang He,Xiaolian Sun,Hong Zhang,Hong Zhang,Mei Tian,Mei Tian,Daishun Ling +18 more
TL;DR: It is demonstrated that these nanocomposites can relieve the AD symptoms by mitigating mitochondrial oxidative stress, suppressing tau hyperphosphorylation, and preventing neuronal death both in vitro and in vivo.
Journal ArticleDOI
Iron oxide nanoparticles may damage to the neural tissue through iron accumulation, oxidative stress, and protein aggregation
TL;DR: IONPs depending on their properties can lead to iron accumulation, oxidative stress and protein aggregation in the neural cells, which can be toxic for the cell.
Journal ArticleDOI
Are iron oxide nanoparticles safe? Current knowledge and future perspectives.
Vanessa Valdiglesias,Natalia Fernández-Bertólez,Gözde Kiliç,Carla Costa,Solange Costa,Sónia Fraga,Maria João Bessa,Eduardo Pásaro,João Paulo Teixeira,Blanca Laffon +9 more
TL;DR: It is shown that influence of nanoparticle surface coating, size, or dose, and of other experimental factors such as treatment time or cell type, has been demonstrated to be important for ION in vitro toxicity manifestation.
References
More filters
Journal ArticleDOI
A model for p53-induced apoptosis
Kornelia Polyak,Kornelia Polyak,Yong Xia,Jay L. Zweier,Kenneth W. Kinzler,Bert Vogelstein,Bert Vogelstein +6 more
TL;DR: Examination of transcripts induced by p53 expression before the onset of apoptosis stimulated additional biochemical and pharmacological experiments suggesting that p53 results in apoptosis through a three-step process: the transcriptional induction of redox-related genes; the formation of reactive oxygen species; and the oxidative degradation of mitochondrial components, culminating in cell death.
Journal Article
Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo
Toshiyuki Miyashita,Stanislaw Krajewski,Maryla Krajewska,Hong Gang Wang,Hsueh Kung Lin,Dan A. Liebermann,Barbara Hoffman,John C. Reed +7 more
TL;DR: It is demonstrated that a temperature-sensitive p53 induces temperature-dependent decreases in the expression of the apoptosis-suppressing gene bcl-2 in the murine leukemia cell M1, while simultaneously stimulating increases in theexpression of bax, a gene which encodes a dominant-inhibitor of the Bcl-1 protein.
Journal ArticleDOI
Carbon nanotubes: a review of their properties in relation to pulmonary toxicology and workplace safety.
Ken Donaldson,Robert Aitken,Lang Tran,Vicki Stone,Rodger Duffin,Gavin A. Forrest,Andrew J. Alexander +6 more
TL;DR: The toxicological paradigms applicable to the toxicity of inhaled CNT are set out, building on the toxicological database on nanoparticles (NP) and fibers, and the current paradigm for fiber toxicology is discussed.
Journal ArticleDOI
Translocation of inhaled ultrafine manganese oxide particles to the central nervous system.
Alison Elder,Robert Gelein,Vanessa D. Silva,Tessa Feikert,Lisa A. Opanashuk,Janet M. Carter,Russell M. Potter,Andrew D. Maynard,Yasuo Ito,Jacob N. Finkelstein,Günter Oberdörster +10 more
TL;DR: The olfactory neuronal pathway is efficient for translocating inhaled Mn oxide as solid UFPs to the central nervous system and that this can result in inflammatory changes.
Journal ArticleDOI
The apoptotic effect of nanosilver is mediated by a ROS- and JNK-dependent mechanism involving the mitochondrial pathway in NIH3T3 cells
TL;DR: It is shown that nanosilver is cytotoxic, inducing apoptosis in NIH3T3 fibroblast cells, and the first evidence for a molecular mechanism of nanosSilver cytotoxicity is provided, showing that nanOSilver acts through ROS and JNK to induce apoptosis via the mitochondrial pathway.