Life-long reduction in MnSOD activity results in increased DNA damage and higher incidence of cancer but does not accelerate aging.

By H. Van Remmen, Y. Ikeno, Michelle L. Hamilton, M. Pahlavani, N. Wolf, S. Thorpe, N. L. Alderson, J. Baynes, C. Epstein, Ting-Ting Huang and 3 more. Physiological Genomics, 2003

758 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d788199c6a8a183f6e2d3e02bfc24cfa87ac3d44

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

Citations in the corpus

Overview of caloric restriction and ageing. (2005, background): “Van Remmen et al. (2003) found that in mice deficient in Mn-superoxide dismutase, the increased oxidative stress/damage does not affect life span and other age-sensitive parameters.”
Trends in oxidative aging theories. (2007, background): “It will be especially interesting to determine whether oxidative damage is elevated in the heterozygote , and if tumor burden is increased as in the Prxd1 +/− and Sod2 +/− mice [212] [229].”
Redox Regulation of Cell Survival (2008, neutral): “Heterozygous SOD2 (cid:4) / (cid:2) mice, which exhibited a 50% reduction in SOD levels, appeared normal but had mitochondrial oxidative damage and decreased mitochondrial membrane potential (312).”
Reactive Species and Antioxidants. Redox Biology Is a Fundamental Theme of Aerobic Life (2006, background): “EvenMnSOD (1/2) heterozygous mice, which at first seem normal, show increased mitochondrial oxidative damage as they age, as well as increased nuclear oxidative DNA damage and elevated cancer rates (Van Remmen et al., 2003).”
The hallmarks of aging. (2013, background): “Similarly unexpected, genetic manipulations in mice that increase mitochondrial ROS and oxidative damage do not accelerate aging (Van Remmen et al., 2003; Zhang et al., 2009), mice with increased antioxidant defenses do not present an extended life- span (Pérez et al., 2009), and, finally, genetic…”
A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine (2005, background): “A role for mitochondrial ROS in cancer is supported by the observations that mice heterozygous for the MnSOD knock-out locus have a 100% increase in cancer incidence (226), many types of tumors have reduced MnSOD, transformation of certain tumors with the MnSOD cDNA can reverse the malignant phenoty”
Oxidative Stress, Mitochondrial Dysfunction, and Aging (2011, background): “Mice heterozygous for superoxide dismutase 2 (Sod2+/−) have reduced manganese SOD (MnSOD) activity, increased oxidative damage, but normal lifespan [63].”