Iron, selenium and glutathione peroxidase activity are elevated in sporadic motor neuron disease

Ince, Paul G.; Shaw, Pamela J.; Candy, J.M.; Mantle, David; Tandon, Lav; Ehmann, W. D.; Markesbery, William R.

doi:10.1016/0304-3940(94)90213-5

Cited by 94 publications

(42 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Alterations in antioxidant enzymes have been reported previously in patients with SALS (Ince et al, 1994;Przedborski et al, 1996a,b). An increase in protein carbonyl groups was found in SALS spinal cord (Shaw et al, 1995).…”

Section: Fig 3 Ohmentioning

confidence: 84%

Evidence of Increased Oxidative Damage in Both Sporadic and Familial Amyotrophic Lateral Sclerosis

Se²,

La³

et al. 1997

Journal of Neurochemistry

708

406

View full text Add to dashboard Cite

Some cases of autosomal dominant familial amyotrophic lateral sclerosis (FALS) are associated with mutations in the gene encoding Cu/Zn superoxide dismutase (SOD1), suggesting that oxidative damage may play a role in ALS pathogenesis. To further investigate the biochemical features of FALS and sporadic ALS (SALS), we examined markers of oxidative damage to protein, lipids, and DNA in motor cortex (Brodmann area 4), parietal cortex (Brodmann area 40), and cerebellum from control subjects, FALS patients with and without known SOD mutations, SALS patients, and disease controls (Pick's disease, progressive supranuclear palsy, diffuse Lewy body disease). Protein carbonyl and nuclear DNA 8-hydroxy-2 '-deoxyguanosine (OH 8dG) levels were increased in SALS motor cortex but not in FALS patients. Malondialdehyde levels showed no significant changes. Immunohistochemical studies showed increased neuronal staining for hemeoxygenase-1, malondialdehydemodified protein, and OH8dG in both SALS and FALS spinal cord. These studies therefore provide further evidence that oxidative damage may play a role in the pathogenesis of neuronal degeneration in both SALS and FALS.

show abstract

Section: Fig 3 Ohmentioning

confidence: 84%

Evidence of Increased Oxidative Damage in Both Sporadic and Familial Amyotrophic Lateral Sclerosis

Se²,

La³

et al. 1997

Journal of Neurochemistry

708

406

View full text Add to dashboard Cite

show abstract

“…Increased levels of iron were reported in the spinal cord from ALS subjects (206) and may possibly correlate with increased levels of oxidative damage through the induction of Fenton chemistry. Fe accumulation may be due to its increased uptake by its specific transporter, lactoferrin, which is reportedly increased in ALS-affected motor neurons (246).…”

Section: Fe Homeostasis In Alsmentioning

confidence: 97%

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Butterfield

Perluigi

Reed

et al. 2012

Antioxidants & Redox Signaling

156

142

View full text Add to dashboard Cite

Several studies demonstrated that oxidative damage is a characteristic feature of many neurodegenerative diseases. The accumulation of oxidatively modified proteins may disrupt cellular functions by affecting protein expression, protein turnover, cell signaling, and induction of apoptosis and necrosis, suggesting that protein oxidation could have both physiological and pathological significance. For nearly two decades, our laboratory focused particular attention on studying oxidative damage of proteins and how their chemical modifications induced by reactive oxygen species/reactive nitrogen species correlate with pathology, biochemical alterations, and clinical presentations of Alzheimer's disease. This comprehensive article outlines basic knowledge of oxidative modification of proteins and lipids, followed by the principles of redox proteomics analysis, which also involve recent advances of mass spectrometry technology, and its application to selected age-related neurodegenerative diseases. Redox proteomics results obtained in different diseases and animal models thereof may provide new insights into the main mechanisms involved in the pathogenesis and progression of oxidativestress-related neurodegenerative disorders. Redox proteomics can be considered a multifaceted approach that has the potential to provide insights into the molecular mechanisms of a disease, to find disease markers, as well as to identify potential targets for drug therapy. Considering the importance of a better understanding of the cause/effect of protein dysfunction in the pathogenesis and progression of neurodegenerative disorders, this article provides an overview of the intrinsic power of the redox proteomics approach together with the most significant results obtained by our laboratory and others during almost 10 years of research on neurodegenerative disorders since we initiated the field of redox proteomics. Antioxid. Redox Signal. 17, 1610-1655.

show abstract

“…Kurlander and Patten [12] found elevated selenium in the anterior horn cells of only one of 7 motor neuron disease patients, but in 3 of 12 controls. In a larger study, Ince et al [52] report significantly elevated levels of selenium in the lumbar spine of ALS patients, where there is also significantly elevated selenium-dependent glutathione peroxidase activity. Increased lumbar spine selenium levels appear to be independent of duration of disease, disease severity, and L 4 segment lower motor neuron count, suggesting that its accumulation is unlikely to be a consequence of disease progression, but rather an earlier event in the course of the disease [53] .…”

Section: Seleniummentioning

confidence: 99%

The Association of Exposure to Lead, Mercury, and Selenium and the Development of Amyotrophic Lateral Sclerosis and the Epigenetic Implications

et al. 2010

View full text Add to dashboard Cite

Metal exposures are an intriguing potential culprit in the cause of sporadic amyotrophic lateral sclerosis (ALS). For one, there are numerous case reports linking different metals to an ALS phenotype. Furthermore, some investigators have demonstrated higher levels of certain metals in the blood, bone, cerebrospinal fluid, urine, or spinal cords of patients with ALS compared to controls. There are also many case-control studies looking at the possible association of certain metals with the development of ALS. We have reviewed the relevant literature regarding metal exposures and the risk of developing ALS. We found that many different metals have been implicated as having a role in ALS, but there is more literature investigating the role of lead than any other metal. Despite many studies, the role, if any, of this metal in the pathogenesis of ALS remains unclear. Similarly, other metals either have inconclusive, conflicting, or insufficient results in order to make a definitive conclusion. One explanation for these findings is that metal exposures alone are insufficient for the development of ALS. Perhaps an interaction between the metal exposure and an individual’s genetic makeup is required to produce epigenetic changes that ultimately lead to ALS.

show abstract

Iron, selenium and glutathione peroxidase activity are elevated in sporadic motor neuron disease

Cited by 94 publications

References 13 publications

Evidence of Increased Oxidative Damage in Both Sporadic and Familial Amyotrophic Lateral Sclerosis

Evidence of Increased Oxidative Damage in Both Sporadic and Familial Amyotrophic Lateral Sclerosis

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

The Association of Exposure to Lead, Mercury, and Selenium and the Development of Amyotrophic Lateral Sclerosis and the Epigenetic Implications

Contact Info

Product

Resources

About