Abstract:
:Aluminium has been implicated in various neurodegenerative diseases but exact mechanism of action is still not known. Mitochondria being a major site of reactive oxygen species production are considered to be target of oxidative stress and it seems that the oxidative damage to mitochondrial proteins may underlie the pathogenesis of aluminium induced neurodegeneration. Thus, the present study was undertaken to reveal the effects of chronic aluminium exposure (10mg/kg b.wt, intragastrically for 12 weeks) on the oxidative damage to mitochondrial proteins in male albino Wistar rats. Chronic aluminium exposure resulted in decrease in the activity of mitochondrial superoxide dismutase (MnSOD) and aconitase in different regions of rat brain suggesting increased oxidative stress. This decrease in MnSOD activity in turn might be responsible for the increased protein oxidation as observed in our study. All these processes taken together may cause increased oxidative damage to mitochondrial proteins in general. By taking the advantage of recent immunochemical probe for oxidatively modified proteins, we identified MnSOD to be susceptible to oxidative damage in aluminium treated animals. The quantitative RT-PCR analysis for Lon protease, a protease involved in the removal of oxidatively modified proteins from mitochondria, showed decreased mRNA expression suggesting increased oxidative damage and decreased removal of mitochondrial proteins. The identification of specific proteins as targets of oxidative damage may provide new therapeutic measures to reverse the effects of aluminium induced neurodegeneration.
journal_name
Toxicologyjournal_title
Toxicologyauthors
Kumar V,Bal A,Gill KDdoi
10.1016/j.tox.2008.10.009subject
Has Abstractpub_date
2009-01-31 00:00:00pages
117-23issue
3eissn
0300-483Xissn
1879-3185pii
S0300-483X(08)00468-Xjournal_volume
255pub_type
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