Hydrogen peroxide induces neurite degeneration: Prevention by tocotrienols

Fukui, Koji; Takatsu, Hirokatsu; Koike, Takao; Urano, Shiro

doi:10.3109/10715762.2011.567984

Cited by 44 publications

(49 citation statements)

References 42 publications

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“…These results indicate that axonal beading occurs in hippocampal neurons of vitamin E-deficient and normal old mice, extending our previous findings from cultured models (16,17). It is possible that axonal degeneration relates to changes in the CRMP-2 expression.…”

Section: Discussionsupporting

confidence: 77%

“…Urano et al reported that a large number of synaptic vesicles had accumulated in synapses of aged rats and young rats exposed to reactive oxygen species (15). Previously, we reported that treatment of cerebellar granule neurons with a low concentration of hydrogen peroxide induced axon and dendrite degeneration, but not cell death (16,17). However, these data were from cultured models, and axonal condition in living tissues…”

mentioning

confidence: 46%

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Vitamin E Deficiency Induces Axonal Degeneration in Mouse Hippocampal Neurons

Fukui

Kawakami

Honjo

et al. 2012

J Nutr Sci Vitaminol

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SummarySeveral lines of evidence demonstrate the relationship between vitamin E deficiency and cognitive dysfunction in rodent models, but little is known about the underlying mechanisms. In this study, we found axonal injury in the hippocampal CA1 region of vitamin E-deficient and normal old mice using immunohistochemical assay. The number of cells in the hippocampal CA1 region of vitamin E-deficient mice and normal old mice was significantly lower than in normal young mice. It is well known that collapsin response mediator protein (CRMP)-2 plays a crucial role in the maintenance of axonal conditions. The expressions of CRMP-2 in the cerebral cortex and hippocampus of vitamin E-deficient mice were significantly lower than both the regions of normal ones. In normal old mice, the expression of CRMP-2 in the cerebral cortex was significantly lower than in the normal ones. In addition, the appearance of microtubule-associated protein (MAP)-light chain 3 (LC3), a major index of autophagy, was higher in the cerebral cortex and hippocampus of vitamin E-deficient mice than in normal young and old mice. These results indicate that axonal degeneration is induced in living tissues, but not cultured cells, and that changes in CRMP-2 and MAP-LC3 may underlie vitamin E-deficiency-related axonal degeneration.

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Section: Discussionsupporting

confidence: 77%

mentioning

confidence: 46%

Vitamin E Deficiency Induces Axonal Degeneration in Mouse Hippocampal Neurons

Fukui

Kawakami

Honjo

et al. 2012

J Nutr Sci Vitaminol

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“…In recent years, evidence has accumulated for a role of reactive oxygen metabolites as a mediator of tissue injury in several animal models (Özdemir et al 2010;Fukui et al 2011;Sato et al 2011). Although the exact mechanisms of free-radical generation are still not completely understood, it is postulated that the antioxidant glutathione (GSH) depletion by the intestinal parasites may be a trigger for the production of reactive oxygen species (ROS) (Cam et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Protective effect of Azadirachta indica extract against Eimeria papillata-induced coccidiosis

et al. 2012

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Coccidiosis in poultry is caused by protozoan parasites of the genus Eimeria, which is responsible for worldwide economic losses. The methanolic extract of Azadirachta indica (neem) leaves was used in vivo for its pharmacological, antioxidant, and anticoccidial properties. Four groups of mice were investigated. The first group was inoculated only with sterile saline and served as the control group. The second group was treated by oral gavage with neem extract (500 mg/kg) daily for 4 days. The third and fourth groups were infected with 10(3) sporulated oocysts of Eimeria papillata. The fourth group was also treated once daily with neem extract for 4 days. Paraffin sections from the jejunum as well as jejunal homogenate were prepared for the histopathological and biochemical investigations, respectively. The data showed that mice infected with E. papillata revealed an output of 6.5 × 10(5) ± 29,753 oocysts per gram feces on day 4 postinoculation. This output is significantly decreased to 2.7 × 10(5) ± 37,341 oocysts in neem-treated mice. Infection with E. papillata induced marked histopathological alterations in the jejunum in the form of inflammation, vacuolation of the epithelium, and destruction of some villi. Also, the neem extract greatly diminished body weight loss of infected mice. Moreover, the number of goblet cells stained with Alcian blue within the infected villi was significantly lowered (P ≤ 0.05). In addition, E. papillata enhanced lipid peroxidation and nitric oxide production in both serum and jejunum with concomitant reduction in glutathione. Neem induced marked improvements in all of the studied parameters as well as the histopathological features of the jejunum. Our study revealed that neem as a natural product has protective effects against E. papillata-induced coccidiosis.

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“…Thus by modulating ROS, LIF could also influence differentiation. Given the reduction of ROS in LIF þ cultures, it was important to address whether the observed neuroprotective effect extends to ROS induced by extrinsic factors as may be encountered in a hostile niche upon transplantation or in disease [58][59][60][61]. H 2 O 2 is often generated in cells in response to a hostile environment and has widely been used to induce ROS in a variety of neuronal cells [60,61].…”

Section: Reduced Apoptosis Correlated To Reduction In Caspases and Rosmentioning

confidence: 99%

Neurotrophic Effects of Leukemia Inhibitory Factor on Neural Cells Derived from Human Embryonic Stem Cells

et al. 2012

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Various growth factor cocktails have been used to proliferate and then differentiate human neural progenitor (NP) cells derived from embryonic stem cells (ESC) for in vitro and in vivo studies. However, the cytokine leukemia inhibitory factor (LIF) has been largely overlooked. Here, we demonstrate that LIF significantly enhanced in vitro survival and promoted differentiation of human ESC-derived NP cells. In NP cells, as well as NP-derived neurons, LIF reduced caspase-mediated apoptosis and reduced both spontaneous and H 2 O 2 -induced reactive oxygen species in culture. In vitro, NP cell proliferation and the yield of differentiated neurons were significantly higher in the presence of LIF. In NP cells, LIF enhanced cMyc phosphorylation, commonly associated with self-renewal/proliferation. Also, in differentiating NP cells LIF activated the phosphoinositide 3-kinase and signal transducer and activator of transcription 3 pathways, associated with cell survival and reduced apoptosis. When differentiated in LIF 1 media, neurite outgrowth and ERK1/2 phosphorylation were potentiated together with increased expression of gp130, a component of the LIF receptor complex. NP cells, pretreated in vitro with LIF, were effective in reducing infarct volume in a model of focal ischemic stroke but LIF did not lead to significantly improved initial NP cell survival over nontreated NP cells. Our results show that LIF signaling significantly promotes human NP cell proliferation, survival, and differentiation in vitro. Activated LIF signaling should be considered in cell culture expansion systems for future human NP cell-based therapeutic transplant studies.

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Hydrogen peroxide induces neurite degeneration: Prevention by tocotrienols

Cited by 44 publications

References 42 publications

Vitamin E Deficiency Induces Axonal Degeneration in Mouse Hippocampal Neurons

Vitamin E Deficiency Induces Axonal Degeneration in Mouse Hippocampal Neurons

Protective effect of Azadirachta indica extract against Eimeria papillata-induced coccidiosis

Neurotrophic Effects of Leukemia Inhibitory Factor on Neural Cells Derived from Human Embryonic Stem Cells

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