scholarly journals Low-DoseAronia melanocarpaConcentrate Attenuates Paraquat-Induced Neurotoxicity

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
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.

scholarly journals Cadmium induces neuronal cell death through reactive oxygen species activated by GADD153

2013 ◽  
Vol 14 (1) ◽  
Author(s):  
Seungwoo Kim ◽  
Hyo-Soon Cheon ◽  
So-Young Kim ◽  
Yong-Sung Juhnn ◽  
Young-Youl Kim
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Methylmercury induces neuronal cell death by inducing TNF-α expression through the ASK1/p38 signaling pathway in microglia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takashi Toyama ◽  
Takayuki Hoshi ◽  
Takuya Noguchi ◽  
Yoshiro Saito ◽  
Atsushi Matsuzawa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Mouse Brain ◽  
Neuronal Cell Death ◽  
Brain Slices ◽  
Neuronal Cell ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Bv2 Cells ◽  
Tnf Α

AbstractWe recently found that tumor necrosis factor-α (TNF-α) may be involved in neuronal cell death induced by methylmercury in the mouse brain. Here, we examined the cells involved in the induction of TNF-α expression by methylmercury in the mouse brain by in situ hybridization. TNF-α-expressing cells were found throughout the brain and were identified as microglia by immunostaining for ionized calcium binding adaptor molecule 1 (Iba1). Methylmercury induced TNF-α expression in mouse primary microglia and mouse microglial cell line BV2. Knockdown of apoptosis signal-regulating kinase 1 (ASK1), an inflammatory cytokine up-regulator that is responsible for reactive oxygen species (ROS), decreased methylmercury-induced TNF-α expression through decreased phosphorylation of p38 MAP kinase in BV2 cells. Suppression of methylmercury-induced reactive oxygen species (ROS) by antioxidant treatment largely abolished the induction of TNF-α expression and phosphorylation of p38 by methylmercury in BV2 cells. Finally, in mouse brain slices, the TNF-α antagonist (WP9QY) inhibited neuronal cell death induced by methylmercury, as did the p38 inhibitor SB203580 and liposomal clodronate (a microglia-depleting agent). These results indicate that methylmercury induces mitochondrial ROS that are involved in activation of the ASK1/p38 pathway in microglia and that this is associated with induction of TNF-α expression and neuronal cell death.

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

2016 ◽  
Vol 371 (1700) ◽  
pp. 20150434 ◽  
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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