ArticleFree radical biology & medicine2009
Mechanisms of stress resistance in Snell dwarf mouse fibroblasts: enhanced antioxidant and DNA base excision repair capacity, but no differences in mitochondrial metabolism.
Article in Free radical biology & medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Impacts of Naphthenic Acids (NAs) Exposure on Soil Bacterial Community and Antibiotic Resistance Genes (ARGs) Dissemination.Current microbiology · 2025Article
- Balancing DNA repair to prevent ageing and cancer.Experimental cell research · 2021Review
- Mouse models of growth hormone deficiency.Reviews in endocrine & metabolic disorders · 2021Review
- Healthful aging mediated by inhibition of oxidative stress.Ageing research reviews · 2020Review
- Article
- Cap-independent mRNA translation is upregulated in long-lived endocrine mutant mice.Journal of molecular endocrinology · 2019Article
- Chemically induced carcinogenesis in rodent models of aging: assessing organismal resilience to genotoxic stressors in geroscience research.GeroScience · 2019Review
- Article
- Article
- IGF-1 deficiency in a critical period early in life influences the vascular aging phenotype in mice by altering miRNA-mediated post-transcriptional gene regulation: implications for the developmental origins of health and disease hypothesis.Age (Dordrecht, Netherlands) · 2016Article
- Reduced growth hormone signaling and methionine restriction: interventions that improve metabolic health and extend life span.Annals of the New York Academy of Sciences · 2016Review
- Longevity and skeletal muscle mass: the role of IGF signalling, the sirtuins, dietary restriction and protein intake.Aging cell · 2015Review
- Reductions in serum IGF-1 during aging impair health span.Aging cell · 2014Article
- Longevity of insulin receptor substrate1 null mice is not associated with increased basal antioxidant protection or reduced oxidative damage.Age (Dordrecht, Netherlands) · 2013Article
- Links between growth hormone and aging.Endokrynologia Polska · 2013Review
- Free radical production, antioxidant capacity, and oxidative stress response signatures in fibroblasts from Lewis dwarf rats: effects of life span-extending peripubertal GH treatment.The journals of gerontology. Series A, Biological sciences and medical sciences · 2011Article
- Single-gene mutations and healthy ageing in mammals.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2011Review
- Mammalian models of extended healthy lifespan.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2011Review
- Antioxidant enzyme activities are not broadly correlated with longevity in 14 vertebrate endotherm species.Age (Dordrecht, Netherlands) · 2010Article
- Nrf2 signaling, a mechanism for cellular stress resistance in long-lived mice.Molecular and cellular biology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Dermal fibroblasts from long-lived Snell dwarf mice can withstand a variety of oxidative and non-oxidative stressors compared to normal littermate controls. Here, we report differences in the levels and activities of intracellular antioxidant and DNA repair enzymes between normal and Snell dwarf mice fibroblasts cultured under a variety of conditions, including: 3% and 20% ambient O(2); the presence and absence of serum; and the addition of an exogenous oxidative stress. The only significant difference between normal and dwarf cells cultured in complete medium, at 20% O(2), was an approximately 40% elevation of glutathione peroxidase (GPx) activity in the mutant cells. Serum deprivation elicited increases in GPx in both genotypes, but these activities remained higher in dwarf mouse cells. Dwarf mouse cells deprived of serum and challenged with exposure to paraquat or hydrogen peroxide showed a generally greater upregulation of catalase and DNA base excision repair enzymes. As these toxins can interact with mitochondria to increase mitochondrial ROS production, we explored whether there were differences in mitochondrial metabolism between normal and dwarf mouse cells. However, neither mitochondrial content nor the apparent mitochondrial membrane potential differed between genotypes. Overall, the results suggest that superior hydrogen peroxide metabolism and a marginally greater DNA base excision repair capacity contribute to the stress resistance phenotype of Snell dwarf mouse fibroblasts.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.