Extension of Life-Span with Superoxide Dismutase/Catalase Mimetics

Melov, Simon; Ravenscroft, J; Malik, Sarwatt; Gill, Matthew S.; Walker, David W.; Clayton, Peter E.; Wallace, Douglas C.; Malfroy, Bernard; Doctrow, Susan R.; Lithgow, Gordon J.

doi:10.1126/science.289.5484.1567

Cited by 855 publications

(482 citation statements)

References 17 publications

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“…Cytosolic catalase was reported to be required for the life span extension of age-l, daf-2and clk-1 mutants (39). The addition of SOD / catalase mimetics into medium were shown to extend the life span of C. elegans (45). These findings suggest that oxidative damage is an important causative factor in the aging process of C. elegans.…”

Section: Life Span Extension By Short-term Exposure To Hyperoxiamentioning

confidence: 89%

Life span extensions associated with upregulation of gene expression of antioxidant enzymes in Caenorhabditis elegans; studies of mutation in the age-1, PI3 kinase homologue and short-term exposure to hyperoxia

Honda

2002

AGE

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Section: Life Span Extension By Short-term Exposure To Hyperoxiamentioning

confidence: 89%

Life span extensions associated with upregulation of gene expression of antioxidant enzymes in Caenorhabditis elegans; studies of mutation in the age-1, PI3 kinase homologue and short-term exposure to hyperoxia

Honda

2002

AGE

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“…Maintaining high levels of antioxidant enzyme activity in old age has been described in animals and is related to the diminished accumulation of damaged proteins and an increase in cell survival, delayed ageing and the onset of age-associated diseases that finally can extend the lifespan (Melov et al 2000;Vaanholt et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Total antioxidant capacity of honeybee haemolymph in relation to age and exposure to pesticide, and comparison to antioxidant capacity of seminal plasma

et al. 2015

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-Oxidative stress is defined as a disturbance in the balance between the production of reactive oxygen species and antioxidant defences. We measured total antioxidant capacity (TAC) in honeybee haemolymph and seminal plasma and analysed TAC of haemolymph in relation to age and exposure to pesticide. TAC of haemolymph increased with age of bees (1.18 vs 1.97 mM of (±)-6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox) for 1-and 30-day-old bees, respectively, P ≤0.05). Exposure to imidacloprid (IMD) affected TAC of haemolymph of 1-day-old but not 30-day-old honeybees. TAC in haemolymph of 1-day-old bees was lower in treatments with the addition of 5 and 200 ppb IMD (1.57-1.46 mM of Trolox in treated bees compared with 2.37 mM of Trolox in controls; P ≤0.05). In conclusion, antioxidant protection of honeybees seems to be related to age and may be disturbed by exposure to IMD. Older bees with higher antioxidant protection seem to be less susceptible to IMD toxicity. The toxic effect of pesticide seems to be particularly dangerous in early life stages of honeybees.Apis mellifera / total antioxidant capacity / haemolymph / ageing / pesticide

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“…ROS (superoxide anions, hydroxyl radicals, and H 2 O 2 ) are produced by di erent intracellular redox reactions, which involve molecular oxygen as the ®nal electron acceptor, and are the most recognized mediators of cell damage (Harman, 1981;Lambeth et al, 2000). In support of the free radical theory of ageing, antioxidant treatment or overexpression of antioxidant genes increase life span in invertebrates (Guarente and Kenyon, 2000;Melov et al, 2000). In mammals, instead, supporting evidence is largely correlative, mainly based on ®ndings of increased oxidative damaged DNA/proteins in aged individuals (Van Remmen and Richardson, 2001).…”

Section: Introductionmentioning

confidence: 99%

A p53-p66Shc signalling pathway controls intracellular redox status, levels of oxidation-damaged DNA and oxidative stress-induced apoptosis

et al. 2002

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Correlative evidence links stress, accumulation of oxidative cellular damage and ageing in lower organisms and in mammals. We investigated their mechanistic connections in p66Shc knockout mice, which are characterized by increased resistance to oxidative stress and extended life span. We report that p66Shc acts as a downstream target of the tumour suppressor p53 and is indispensable for the ability of stress-activated p53 to induce elevation of intracellular oxidants, cytochrome c release and apoptosis. Other functions of p53 are not in¯uenced by p66Shc expression. In basal conditions, p66Shc7/7 and p537/7 cells have reduced amounts of intracellular oxidants and oxidation-damaged DNA. We propose that steady-state levels of intracellular oxidants and oxidative damage are genetically determined and regulated by a stress-induced signal transduction pathway involving p53 and p66Shc.

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Extension of Life-Span with Superoxide Dismutase/Catalase Mimetics

Cited by 855 publications

References 17 publications

Life span extensions associated with upregulation of gene expression of antioxidant enzymes in Caenorhabditis elegans; studies of mutation in the age-1, PI3 kinase homologue and short-term exposure to hyperoxia

Life span extensions associated with upregulation of gene expression of antioxidant enzymes in Caenorhabditis elegans; studies of mutation in the age-1, PI3 kinase homologue and short-term exposure to hyperoxia

Total antioxidant capacity of honeybee haemolymph in relation to age and exposure to pesticide, and comparison to antioxidant capacity of seminal plasma

A p53-p66Shc signalling pathway controls intracellular redox status, levels of oxidation-damaged DNA and oxidative stress-induced apoptosis

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