Effects of deleting mitochondrial Antioxidant genes on life span
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Dosyalar
Tarih
2007
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Ann N Y Acad Sci.
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Reactive oxygen species (ROS) damage biomolecules, accelerate
aging, and shorten life span, whereas antioxidant enzymes mitigate
these effects. Because mitochondria are a primary site of ROS generation
and also a primary target of ROS attack, they have become a major
focus area of aging studies. Here, we employed yeast genetics to identify
mitochondrial antioxidant genes that are important for replicative
life span. In our studies, it was found that among the known mitochondrial
antioxidant genes (TTR1, CCD1, SOD1, GLO4, TRR2, TRX3, CCS1,
SOD2, GRX5, PRX1), deletion of only three genes, SOD1 (Cu, Zn superoxide
dismutase), SOD2 (Manganese-containing superoxide dismutase),
and CCS1 (Copper chaperone), shortened the life span enormously. The
life span decreased 40% forΔsod1 mutant, 72% forΔsod2 mutant, and
50% forΔccs1 mutant. Deletion of the other genes had little or no effect
on life span.
Açıklama
Ann N Y Acad Sci., (1100), 505–0.
Anahtar Kelimeler
Aging, Antioxidant genes, Mitochondria, ROS, CCS1
Kaynak
Ann N Y Acad Sci.
WoS Q Değeri
Scopus Q Değeri
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0
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0
Künye
Ünlü, E. S., & Koç, A. (2007). Effects Of Deleting Mitochondrial Antioxidant Genes On Life Span . Ann N Y Acad Sci., (1100), 505–0.
