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Manganese neurotoxicity and the role of reactive oxygen species

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TLDR
This review focuses on all of the preceding mechanisms and the scientific studies that support them as well as providing an overview of the absorption, distribution, and excretion of Mn and the stability and transport of Mn compounds in the body.
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This article is published in Free Radical Biology and Medicine.The article was published on 2013-09-01 and is currently open access. It has received 238 citations till now. The article focuses on the topics: Manganism & Oxidative stress.

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Manganese Increases the Sensitivity of the cGAS-STING Pathway for Double-Stranded DNA and Is Required for the Host Defense against DNA Viruses

TL;DR: It is found that upon virus infection, Manganese (Mn2+) is released from organelles into the cytosol and facilitates the activation of cGAS and STING.
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ROS and diseases: role in metabolism and energy supply.

TL;DR: The opinions presented in this review interpret the researches of ROS from a different dimension that might explain the competing results of ROS introduced so far from a broader perspective.
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The role of zinc, copper, manganese and iron in neurodegenerative diseases.

TL;DR: Delineating the specific mechanisms by which metals alter redox homeostasis is essential to understand the pathophysiology of AD, PD, and MS and may provide possible new targets for their prevention and treatment of the patients affected by these NDDs.
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Mn-euvering manganese: the role of transporter gene family members in manganese uptake and mobilization in plants

TL;DR: A combination of techniques including mutant analysis and Synchrotron X-ray Fluorescence Spectroscopy can assist in identifying essential transporters of Mn, which would vastly improve understanding of plant Mn homeostasis.
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The elements of life and medicines.

TL;DR: An element-by-element journey through the periodic table is made and it is attempted to assess whether elements are essential or not, and if they are, whether there is a relevant code for them in the human genome.
References
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How mitochondria produce reactive oxygen species.

TL;DR: The description outlined here facilitates the understanding of factors that favour mitochondrial ROS production and develops better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.
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Parkinson's disease: Mechanisms and models

TL;DR: PD models based on the manipulation of PD genes should prove valuable in elucidating important aspects of the disease, such as selective vulnerability of substantia nigra dopaminergic neurons to the degenerative process.
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Redox environment of the cell as viewed through the redox state of the glutathione disulfide/glutathione couple.

TL;DR: Estimates can be used to more fully understand the redox biochemistry that results from oxidative stress, which hopefully will provide a rationale and understanding of the cellular mechanisms associated with cell growth and development, signaling, and reductive or oxidative stress.
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The mitochondrial permeability transition pore and its role in cell death.

TL;DR: Current evidence that the pore complex is involved in outer-membrane rupture and release of these proteins during programmed cell death is reviewed, along with indications that transient pore opening may provoke 'accidental' apoptosis.
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Reactive oxygen species generated at mitochondrial complex III stabilize hypoxia-inducible factor-1alpha during hypoxia: a mechanism of O2 sensing.

TL;DR: Findings reveal that mitochondria-derived ROS are both required and sufficient to initiate HIF-1α stabilization during hypoxia and that catalase abolishes hypoxic response element-luciferase expression during Hypoxia.
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