The effects of exogenous antioxidants on lifespan and oxidative stress resistance in Drosophila melanogaster

Magwere, Tapiwanashe; West, Melanie; Riyahi, Kumars; Murphy, Michael P.; Smith, Robin A.J.; Partridge, Linda

doi:10.1016/j.mad.2005.12.009

Cited by 130 publications

(83 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is also consistent with studies in invertebrates (198,261). The extension of maximum life span by SOD mimetic drugs described a few years ago for C. elegans (230) has been unable to be repeated by others either for C. elegans (170) or Drosophila (214).…”

Section: B Antioxidant Defensessupporting

confidence: 89%

Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals

Hulbert¹,

Pamplona²,

Buffenstein

et al. 2007

Physiological Reviews

765

725

View full text Add to dashboard Cite

Maximum life span differences among animal species exceed life span variation achieved by experimental manipulation by orders of magnitude. The differences in the characteristic maximum life span of species was initially proposed to be due to variation in mass-specific rate of metabolism. This is called the rate-of-living theory of aging and lies at the base of the oxidative-stress theory of aging, currently the most generally accepted explanation of aging. However, the rate-of-living theory of aging while helpful is not completely adequate in explaining the maximum life span. Recently, it has been discovered that the fatty acid composition of cell membranes varies systematically between species, and this underlies the variation in their metabolic rate. When combined with the fact that 1) the products of lipid peroxidation are powerful reactive molecular species, and 2) that fatty acids differ dramatically in their susceptibility to peroxidation, membrane fatty acid composition provides a mechanistic explanation of the variation in maximum life span among animal species. When the connection between metabolic rate and life span was first proposed a century ago, it was not known that membrane composition varies between species. Many of the exceptions to the rate-of-living theory appear explicable when the particular membrane fatty acid composition is considered for each case. Here we review the links between metabolic rate and maximum life span of mammals and birds as well as the linking role of membrane fatty acid composition in determining the maximum life span. The more limited information for ectothermic animals and treatments that extend life span (e.g., caloric restriction) are also reviewed.

show abstract

Section: B Antioxidant Defensessupporting

confidence: 89%

Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals

Hulbert¹,

Pamplona²,

Buffenstein

et al. 2007

Physiological Reviews

765

725

View full text Add to dashboard Cite

show abstract

“…Among invertebrate model organisms, the importance of oxidative stress in aging has been demonstrated in studies of SOD-deficient Drosophila melanogaster and in C. elegans. In D. melanogaster, exogenous provision of antioxidants increased the lifespan of SOD-deficient flies and improved their tolerance to oxidative stress (Magwere et al, 2006). Similarly, studies in C. elegans have demonstrated that provision of antioxidants extended lifespan in oxidatively stressed but not in unstressed nematodes (Keaney et al, 2004), while others showed a direct effect of SOD/catalase mimetics in the growth medium on the lifespan of normal nematodes (Melov et al, 2000).…”

Section: Introductionmentioning

confidence: 96%

Insulin regulates aging and oxidative stress in Anopheles stephensi

Kang

Mott

Tapley

et al. 2008

Journal of Experimental Biology

View full text Add to dashboard Cite

SUMMARYObservations from nematodes to mammals indicate that insulin/insulin-like growth factor signaling (IIS) regulates lifespan. As in other organisms, IIS is conserved in mosquitoes and signaling occurs in multiple tissues. During bloodfeeding, mosquitoes ingest human insulin. This simple observation suggested that exogenous insulin could mimic the endogenous hormonal control of aging in mosquitoes, providing a new model to examine this phenomenon at the organismal and cellular levels. To this end, female Anopheles stephensi mosquitoes were maintained on diets containing human insulin provided daily in sucrose or three times weekly by artificial bloodmeal. Regardless of delivery route, mosquitoes provided with insulin at 1.7ϫ10 -4 and 1.7ϫ10 -3 ·mol·l -1 , doses 0.3-fold and 3.0-fold higher than non-fasting blood levels, died at a faster rate than controls. In mammals, IIS induces the synthesis of reactive oxygen species and downregulates antioxidants, events that increase oxidative stress and that have been associated with reduced lifespan. Insulin treatment of mosquito cells in vitro induced hydrogen peroxide synthesis while dietary supplementation reduced total superoxide dismutase (SOD) activity and manganese SOD activity relative to controls. The effects of insulin on mortality were reversed when diets were supplemented with manganese (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), a cell-permeable SOD mimetic agent, suggesting that insulin-induced mortality was due to oxidative stress. In addition, dietary insulin activated Akt/protein kinase B and extracellular signal-regulated kinase (ERK) in the mosquito midgut, suggesting that, as observed in Caenorhabditis elegans, the midgut may act as a ʻsignaling centerʼ for mosquito aging.

show abstract

“…60,61 It must be noted, however, that in another study, antioxidants failed to extend the lifespan of wild-type flies. 62 In nematodes, lowering the activity of the mitochondrial electron transport chain during development extends adult lifespan. 58 When mitochondrial respiration is decreased only during adulthood, animals have wild-type lifespan.…”

mentioning

confidence: 99%

Autophagy genes and ageing

2008

View full text Add to dashboard Cite

Ageing in divergent animal phyla is influenced by several evolutionarily conserved signalling pathways, mitochondrial activity and various environmental factors such as nutrient availability and temperature. Although ageing is a multifactorial process with many mechanisms contributing to the decline, the intracellular accumulation of damaged proteins and mitochondria is a feature common to all aged cells. Autophagy (cellular self-eating) -a lysosome-mediated catabolic process of eukaryotic cells to digest their own constituents -is a major route for the bulk degradation of aberrant cytosolic macromolecules and organelles. Indeed, genetic studies show that autophagy-related genes are required for lifespan extension in various long-lived mutant nematodes and promote survival in worms and flies exposed to prolonged starvation. These data implicate autophagy in ageing control. Furthermore, results in Drosophila demonstrate that promoting basal expression of the autophagy gene Atg8 in the nervous system extends lifespan by 50%, thereby providing evidence that the autophagy pathway regulates the rate at which the tissues age. In this review, the molecular mechanisms by which autophagy genes interact with longevity pathways in diverse organisms ranging from yeast to mammals are discussed.

show abstract

The effects of exogenous antioxidants on lifespan and oxidative stress resistance in Drosophila melanogaster

Cited by 130 publications

References 41 publications

Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals

Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals

Insulin regulates aging and oxidative stress in Anopheles stephensi

Autophagy genes and ageing

Contact Info

Product

Resources

About