I saw this ..
Link: http://www.ncbi.nlm....t_uids=15721990
Free Radic Biol Med. 2005 Mar 15;38(6):796-805. Related Articles, Links
Tissue-specific changes of mitochondrial functions in aged rats: Effect of a long-term dietary treatment with N-acetylcysteine.
Cocco T, Sgobbo P, Clemente M, Lopriore B, Grattagliano I, Di Paola M, Villani G.
Department of Medical Biochemistry & Biology, University of Bari, Piazza G. Cesare, 70124 Bari, Italy.
The understanding of the involvement of mitochondrial oxidative phosphorylation (OXPHOS) in the aging process has often been biased by the different methodological approaches as well as the choice of the biological material utilized by the various groups. In the present paper, we have carried out a detailed analysis of several bioenergetic parameters and oxidative markers in brain and heart mitochondria from young (2 months) and old (28 months) rats. This analysis has revealed an age-related decrease in respiratory fluxes in brain but not in heart mitochondria. The age-related decrease in respiratory rate (-43%) by NAD-dependent substrates was associated with a consistent decline (-40%) of complex I activity in brain mitochondria. On the other hand, heart mitochondria showed an age-related decline of complex II activity. Both tissues showed, however, an age-associated accumulation of oxidative damage. We have then performed the same analysis on old (28 months) rats subjected to a long-term (16 months) diet containing the antioxidant N-acetylcysteine (NAC). The treated old rats showed a slight brain-specific improvement of mitochondrial energy production efficiency, mostly with NAD-dependent substrates, together with a decrease in carbonyl protein content and an increase in the amount of protein thiols of brain cytosolic fraction. A full recovery of complex II activity was detected in heart mitochondria from NAC-treated old rats. The present work documents the marked tissue specificity of the decline of bioenergetic functions in isolated mitochondria from aged rats and provides the first data on the effects of a long-term treatment with N-acetylcysteine.
PMID: 15721990 [PubMed - as supplied by publisher]
combined with the epilepsy drug reported in nature to extend the lifespan of c. elegans
http://www.nature.co.../050110-16.html
and this..
FASEB J. 2004 Mar;18(3):598-9. Epub 2004 Jan 20. Related Articles, Links
Overexpression of the small mitochondrial Hsp22 extends Drosophila life span and increases resistance to oxidative stress.
Morrow G, Samson M, Michaud S, Tanguay RM.
Laboratory of Cell and Developmental Genetics, CREFSIP and Department Medicine, Universite Laval, Ste-Foy, Quebec, Canada.
Heat shock proteins (Hsp) are involved in protein folding, transport and stress resistance. Studies reporting an increased mRNA level of hsp genes in aged Drosophila suggest that expression of Hsp might be beneficial in preventing damages induced by aging. Because oxidative damage is often observed in aged organisms and mitochondria are sensitive to reactive oxygen species, we tested the hypothesis that increased levels of a small Hsp localized in mitochondria, Hsp22 of Drosophila melanogaster, could protect mitochondrial proteins and influence the aging process. We demonstrate that a ubiquitous or a targeted expression of Hsp22 within motorneurons increases the mean life span by more than 30%. Hsp22 shows beneficial effects on early-aging events since the premortality phase displays the same increase as the mean lifespan. Moreover, flies expressing Hsp22 in their motorneurons maintain their locomotor activity longer as assessed by a negative geotaxis assay. The motorneurons-targeted expression of Hsp22 also significantly increases flies' resistance to oxidative injuries induced by paraquat (up to 35%) and thermal stress (39% at 30 degrees C and 23% at 37 degrees C). These observations establish Hsp22 as a key player in cell-protection mechanisms against oxidative injuries and aging in Drosophila and corroborate the pivotal role of mitochondria in the process of aging.
PMID: 14734639 [PubMed - indexed for MEDLINE]
and I found another recent reference that I can't seem to locate about mitochondria in neuronal fly cells extends lifespan... maybe someone else will come across it and post it..
It may be that protecting nerves from stimulation might help longevity overall..
