DNA repair in human fibroblasts, as reflected by host-cell reactivation of a transfected UV-irradiated luciferase gene, is not related to donor age

Effect of Amalaki rasayana on DNA damage and repair in randomized aged human individuals

“…Our findings have shown that there was no difference in the gap filling capacity between rasayana and placebo administered aged individuals as well as between young and aged subjects. Consistent with this, Merkle et al (2004) have demonstrated no significant differences in UV-induced DNA repair measured by host cell reactivation between skin fibroblast cell lines of five old donors (84 -94 years old) and five young donors (17-26 years old). Similarly, T lymphocytes from young and aged subjects irradiated with graded doses of gamma rays (200 -800 rads) and then stimulated with PHA, cultured for 72 h showed minor differences in UDS between these two age groups (Licastro et al, 1982).…”

Higher DNA repair activity is related with longer replicative life span in mammalian embryonic fibroblast cells

“…DNA repair of pyrimidine dimers was not declined during cellular aging in vitro (Christiansen et al 2000). Analysis of host-cell reactivation (HCR) of UV-irradiated reporter gene-containing plasmid vectors also showed no significant difference between the young and old age groups (Merkle et al 2004). But other report observed a significant decrease with aging in the repair rates of both thymine dimers and photoproducts in UV-irradiated human dermal fibroblasts derived from donors (Goukassian et al 2000).…”

Recombinant Viral Vectors for Investigating DNA Damage Responses and Gene Therapy of Xeroderma Pigmentosum

“…This technique facilitates the identification of the complementation group of a given patient, being particularly useful in cases of CS, TTD and some XP patients such as XP-E that present a normal UDS after UV treatment (Carreau et al, 1995b). Recent data using the HCR assay has shown that the CS proteins are essential for the reversion of oxidated lesions (Pitsikas et al, 2005;Spivak & Hanawalt, 2006;Leach & Rainbow, 2011) and evidence obtained with HCR suggests that, unlike what was previously shown with UDS assays, DNA repair capacity in fibroblasts does not decrease with aging (Merkle et al, 2004). This reduction may however be cell type-specific and DNA repair pathway-specific since blood cells repair capacity decreases approximately 0.6% per year of age (Moriwaki et al, 1996).…”

“…If the cell is able to remove the lesions from the plasmid, the reporter gene will be expressed. Different DNA repair rates can be addresses by differences on the amount of gene reporter expression at a certain time (Merkle et al, 2004). A schematic representation of HCR is shown in Figure 6.…”