Dopamine promotes cathepsin B-mediated amyloid precursor protein degradation by reactive oxygen species-sensitive mechanism in neuronal cell

Mitoquinone (MitoQ) is a mitochondrial reactive oxygen species scavenger that is characterized by high bioavailability. Prior studies have demonstrated its neuroprotective potential. Indeed, the release of reactive oxygen species due to damage to mitochondrial components plays a pivotal role in the pathogenesis of several neurodegenerative diseases. The present study aimed to examine the impact of the inflammation platform activation on the neuronal cell line (DAOY) treated with specific inflammatory stimuli and whether MitoQ addition can modulate these deregulations. DAOY cells were pre-treated with MitoQ and then stimulated by a blockade of the cholesterol pathway, also called mevalonate pathway, using a statin, mimicking cholesterol deregulation, a common parameter present in some neurodegenerative and autoinflammatory diseases. To verify the role played by MitoQ, we examined the expression of genes involved in the inflammation mechanism and the mitochondrial activity at different time points. In this experimental design, MitoQ showed a protective effect against the blockade of the mevalonate pathway in a short period (12 h) but did not persist for a long time (24 and 48 h). The results obtained highlight the anti-inflammatory properties of MitoQ and open the question about its application as an effective adjuvant for the treatment of the autoinflammatory disease characterized by a cholesterol deregulation pathway that involves mitochondrial homeostasis.

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Cadmium induction of reactive oxygen species activates the mTOR pathway, leading to neuronal cell death

Free Radical Biology and Medicine ◽

10.1016/j.freeradbiomed.2010.12.032 ◽

2011 ◽

Vol 50 (5) ◽

pp. 624-632 ◽

Cited By ~ 153

Author(s):

Long Chen ◽

Baoshan Xu ◽

Lei Liu ◽

Yan Luo ◽

Hongyu Zhou ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Cell Death ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Reactive Oxygen ◽

Mtor Pathway ◽

Oxygen Species

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Low-DoseAronia melanocarpaConcentrate Attenuates Paraquat-Induced Neurotoxicity

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/5296271 ◽

2016 ◽

Vol 2016 ◽

pp. 1-11 ◽

Cited By ~ 6

Author(s):

A. J. Case ◽

D. Agraz ◽

I. M. Ahmad ◽

M. C. Zimmerman

Keyword(s):

Reactive Oxygen Species ◽

Hydrogen Peroxide ◽

Cell Death ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Reactive Oxygen ◽

High Dose ◽

Low Doses ◽

Oxygen Species ◽

High Doses

Herbicides containing paraquat may contribute to the pathogenesis of neurodegenerative disorders such as Parkinson’s disease. Paraquat induces reactive oxygen species-mediated apoptosis in neurons, which is a primary mechanism behind its toxicity. We sought to test the effectiveness of a commercially available polyphenol-richAronia melanocarpa(aronia berry) concentrate in the amelioration of paraquat-induced neurotoxicity. Considering the abundance of antioxidants in aronia berries, we hypothesized that aronia berry concentrate attenuates the paraquat-induced increase in reactive oxygen species and protects against paraquat-mediated neuronal cell death. Using a neuronal cell culture model, we observed that low doses of aronia berry concentrate protected against paraquat-mediated neurotoxicity. Additionally, low doses of the concentrate attenuated the paraquat-induced increase in superoxide, hydrogen peroxide, and oxidized glutathione levels. Interestingly, high doses of aronia berry concentrate increased neuronal superoxide levels independent of paraquat, while at the same time decreasing hydrogen peroxide. Moreover, high-dose aronia berry concentrate potentiated paraquat-induced superoxide production and neuronal cell death. In summary, aronia berry concentrate at low doses restores the homeostatic redox environment of neurons treated with paraquat, while high doses exacerbate the imbalance leading to further cell death. Our findings support that moderate levels of aronia berry concentrate may prevent reactive oxygen species-mediated neurotoxicity.

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Vitamin D, reactive oxygen species and calcium signalling in ageing and disease

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2015.0434 ◽

2016 ◽

Vol 371 (1700) ◽

pp. 20150434 ◽

Cited By ~ 38

Author(s):

Michael J. Berridge

Keyword(s):

Reactive Oxygen Species ◽

Vitamin D ◽

Neuronal Cell Death ◽

Memory Loss ◽

Neuronal Cell ◽

Reactive Oxygen ◽

Cardiac Cells ◽

Amyloid Formation ◽

Oxygen Species ◽

Age Related

Vitamin D is a hormone that maintains healthy cells. It functions by regulating the low resting levels of cell signalling components such as Ca 2+ and reactive oxygen species (ROS). Its role in maintaining phenotypic stability of these signalling pathways depends on the ability of vitamin D to control the expression of those components that act to reduce the levels of both Ca 2+ and ROS. This regulatory role of vitamin D is supported by both Klotho and Nrf2. A decline in the vitamin D/Klotho/Nrf2 regulatory network may enhance the ageing process, and this is well illustrated by the age-related decline in cognition in rats that can be reversed by administering vitamin D. A deficiency in vitamin D has also been linked to two of the major diseases in man: heart disease and Alzheimer's disease (AD). In cardiac cells, this deficiency alters the Ca 2+ transients to activate the gene transcriptional events leading to cardiac hypertrophy and the failing heart. In the case of AD, it is argued that vitamin D deficiency results in the Ca 2+ landscape that initiates amyloid formation, which then elevates the resting level of Ca 2+ to drive the memory loss that progresses to neuronal cell death and dementia. This article is part of the themed issue ‘Evolution brings Ca 2+ and ATP together to control life and death’.

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