Time sequence of cancer occurrence. Implications in low level radiation risk assessment

Mewissen, D.J.; Rust, John H.; Ugarte, Araceli; Harem, D.J

doi:10.1016/s0764-4469(99)80043-2

Cited by 1 publication

(1 citation statement)

References 9 publications

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“…The husbandry conditions used in our studies were optimal as shown by the long lifespans of the WT mice used in these studies, e.g., the mean and maximum survivals of more than 30 and 40 months, respectively, which is as long if not longer than the lifespans of similar inbred mice reported by other laboratories, including the aging colony maintained by the NIA [11, 16]. For example, data published by Jackson's Laboratory show that C57B6 mice have a mean and maximal lifespans of 27 and 40 months, respectively (mean lifespan approximately 3 months shorter compared to our data) [60, 61]. However, the comparisons of others parameters such as food intake, body weight, fecundity and incidence of tumors, resulted to be similar to the data coming from our animal facility [60-62].…”

Section: Discussionsupporting

confidence: 65%

Is the oxidative stress theory of aging dead?

Pérez¹,

Bokov²,

Remmen³

et al. 2009

Biochimica et Biophysica Acta (BBA) - General Subjects

532

412

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Currently, the Oxidative Stress (or Free Radical) Theory of Aging is the most popular explanation of how aging occurs at the molecular level. While data from studies in invertebrates (e.g., C. elegans and Drosophila) and rodents show a correlation between increased lifespan and resistance to oxidative stress (and in some cases reduced oxidative damage to macromolecules), direct evidence showing that alterations in oxidative damage/stress play a role in aging are limited to a few studies with transgenic Drosophila that overexpress antioxidant enzymes. Over the past eight years, our laboratory has conducted an exhaustive study on the effect of under- or overexpressing a large number and wide variety of genes coding for antioxidant enzymes. In this review, we present the survival data from these studies together. Because only one (the deletion of the Sod1 gene) of the 18 genetic manipulations we studied had an effect on lifespan, our data calls into serious question the hypothesis that alterations in oxidative damage/stress play a role in the longevity of mice.

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