Formation of nitric oxide by astrocytes has been suggested to contribute, via impairment of mitochondrial function, to the neurodegenerative process. Mitochondria under oxidative stress are thought to play a key role in various neurodegenerative disorders; therefore protection by antioxidants against oxidative stress to mitochondria may prove to be beneficial in delaying the onset or progression of these diseases. Carnosine has been recently proposed to act as antioxidant in vivo. In the present study, we demonstrate its neuroprotective effect in astrocytes exposed to LPS- and INFγ-induced nitrosative stress. Carnosine protected against nitric oxide-induced impairment of mitochondrial function. This effect was associated with decreased formation of oxidatively modified proteins and with decreased up-regulation oxidative stress-responsive genes, such as Hsp32, Hsp70 and mt-SOD. Our results sustain the possibility that carnosine might have anti-ageing effects to brain cells under pathophysiological conditions leading to degenerative damage, such as aging and neurodegenerative disorders.
|Number of pages||11|
|State||Published - Jun 2005|
Bibliographical noteFunding Information:
This work was supported by the University of Catania, Ricerca di Ateneo; by MIUR, grant N. 196(D.M. 1105/2002); and by FIRB RBNE01ZK8F(2001).
- Heme oxygenase
- Oxidative stress
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience