By P. E. Slagboom, D. L. Knook (auth.), Suresh I. S. Rattan, Olivier Toussaint (eds.)
Esteemed researchers from various eu laboratories supply cutting-edge experiences on biology and getting old, besides guidance for destiny investigations. They hide such matters in molecular gerontological examine as rules of gene expression from DNA to RNA to useful proteins, foundation of assorted age-associated ailments, genetic law of growing older and toughness, and various mechanisms of safeguard and service. different contributions review new applied sciences, together with transgenic organisms, and using dietary and chemical modulators of growing older and lifespan.
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13. , and Goldstein, S. (1980) Loss of reiterated DNA sequences during serial passage of human diploid fibroblasts. Cell, 21,739-749. 14. H. (1994) Telomeres: no end in sight. Cell, 77, 621-623. 15. , and Greider, C. W. (1990) Telomeres shorten during ageing of human fibroblasts. Nature, 345, 458-460. 16. , and Bacchetti, S. (1992) Telomere shortening associated with chromosome instability is arrested in immortal cells which express telomerase activity. , II, 1921-1929. 17. , Gupta, J.. , and Bacchetti, S.
Burkle ii). Efficient anti-oxidative defences will prevent at least some ROI from damaging DNA. To some extent, cells are protected against the damaging effects of ROI by means of nonenzymatic and enzymatic antioxidant activities through which oxidants are detoxified before they can damage cellular macromolecules. Among the enzymatic antioxidants are superoxide dismutases (SOD), catalase, and gluthathione peroxidases. Experimentally, in at least one system, the critical impact of these enzymes for the ageing rate has already been demonstrated: Orr & Sohaeo reported on transgenic Drosophila melanogaster strains carrying an additional gene copy for the Drosophila cytosolic copper/zinc SOD and catalase, respectively.
A lot of data have accumulated which show an age-dependent increase of chromosomal damages and instabilities in a broad sense 2•3: For instance, it has long been known that in mouse liver the number ofhepatocytes with chromosomal abnormalities increased with age 4 . Likewise, an increased frequency of structural and numerical chromosomal abnormalities was recorded in lymphocytes from elderly humans 5 •6. Besides, complete or partial loss of specific chromosomes is a characteristic feature of malignant tumor cells and plays an important role in tumor formation and progression, through the loss of growth control genes ("tumor suppressor genes,,7,8).