Abstract
Some regions of the brain, especially the basal ganglia, are particularly susceptible to excess manganese, and excessive accumulation there may result in the neurodegenerative disorder manganism. Research efforts into the poorly understood molecular mechanisms by which elevated manganese levels in the brain could cause neuronal dysfunction and death have increased. The most popular model suggests that excess manganese causes imbalance of the mitochondrial redox activity, which may then lead to proliferation of cellular oxidative stress (OS). Such a mitochondrial event may be a key step in the demise of the affected central nervous system (CNS) cells. This chapter discusses the sources, absorption, and transportation of manganese, as well as the nature of manganese toxicities reported in humans. The chapter also addresses the mechanistic hypothesis that manganese induces OS in areas of the brain where it accumulates most, thereby leading to the onset of neurotoxicity.
Original language | English (US) |
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Title of host publication | Oxidative Stress and Neurodegenerative Disorders |
Publisher | Elsevier |
Pages | 433-450 |
Number of pages | 18 |
ISBN (Print) | 9780444528094 |
DOIs | |
State | Published - 2007 |
Externally published | Yes |
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ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
Manganese-induced oxidative stress. / Dobson, Allison W.; Aschner, Michael.
Oxidative Stress and Neurodegenerative Disorders. Elsevier, 2007. p. 433-450.Research output: Chapter in Book/Report/Conference proceeding › Chapter
}
TY - CHAP
T1 - Manganese-induced oxidative stress
AU - Dobson, Allison W.
AU - Aschner, Michael
PY - 2007
Y1 - 2007
N2 - Some regions of the brain, especially the basal ganglia, are particularly susceptible to excess manganese, and excessive accumulation there may result in the neurodegenerative disorder manganism. Research efforts into the poorly understood molecular mechanisms by which elevated manganese levels in the brain could cause neuronal dysfunction and death have increased. The most popular model suggests that excess manganese causes imbalance of the mitochondrial redox activity, which may then lead to proliferation of cellular oxidative stress (OS). Such a mitochondrial event may be a key step in the demise of the affected central nervous system (CNS) cells. This chapter discusses the sources, absorption, and transportation of manganese, as well as the nature of manganese toxicities reported in humans. The chapter also addresses the mechanistic hypothesis that manganese induces OS in areas of the brain where it accumulates most, thereby leading to the onset of neurotoxicity.
AB - Some regions of the brain, especially the basal ganglia, are particularly susceptible to excess manganese, and excessive accumulation there may result in the neurodegenerative disorder manganism. Research efforts into the poorly understood molecular mechanisms by which elevated manganese levels in the brain could cause neuronal dysfunction and death have increased. The most popular model suggests that excess manganese causes imbalance of the mitochondrial redox activity, which may then lead to proliferation of cellular oxidative stress (OS). Such a mitochondrial event may be a key step in the demise of the affected central nervous system (CNS) cells. This chapter discusses the sources, absorption, and transportation of manganese, as well as the nature of manganese toxicities reported in humans. The chapter also addresses the mechanistic hypothesis that manganese induces OS in areas of the brain where it accumulates most, thereby leading to the onset of neurotoxicity.
UR - http://www.scopus.com/inward/record.url?scp=84867311513&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84867311513&partnerID=8YFLogxK
U2 - 10.1016/B978-044452809-4/50160-5
DO - 10.1016/B978-044452809-4/50160-5
M3 - Chapter
AN - SCOPUS:84867311513
SN - 9780444528094
SP - 433
EP - 450
BT - Oxidative Stress and Neurodegenerative Disorders
PB - Elsevier
ER -