Geroprotector efficiency depends on viability of control population: life span investigation in D. melanogaster

Izmaylov, D.M.; Obukhova, L. K.

doi:10.1016/s0047-6374(96)01776-9

Cited by 21 publications

(14 citation statements)

References 19 publications

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“…Therefore, varying viability of the population from which the control and experimental groups are formed determines the geroprotective effect of melatonin. Previously we revealed a similar relationship for the geroprotector spin radical trap 4-hydroxytetramethyl-piperidine-N-oxyl [5]. The geroprotective effect of melatonin at larval stages of the insect development indirectly suggests the antioxidant mechanism of its effect.…”

Section: Resultssupporting

confidence: 58%

“…A probable mechanism of this phenomenon has been discussed previously [10]. Similar effects are exhibited by 3-hydroxypyridine [10], vitamins A and E [2,9], and 4-hydroxy-tempo [5].…”

Section: Resultssupporting

confidence: 53%

“…All experimental procedures and growth conditions have been described in detail [5]. The LS distribution in the control and experimental groups was compared by pairs using the Kolmogorov--Smirnov test.…”

Section: Methodsmentioning

confidence: 99%

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Melatonin as a geroprotector: Experiments withDrosophila melanogaster

Izmailov¹,

Obukhova²

1999

Bull Exp Biol Med

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The lifespan of D. melanogaster treated with melatonin in a concentration of 0.08% at the stage of development is studied. The geroprotective effect of melatonin is the most obvious (up to 12-18%) in comparison with controls with a short lifespan; if the controls' lifespan was relatively long, the hormone exerts negligible or toxic effect shortening the lifespan by up to 10%. Antioxidant mechanism of geroprotective effect of melatonin is discussed in light of the concept of fluctuations in the lifespan in successive D. melanogaster generations.Key Words: melatonin; lifespan; geroprotector; Drosophila melanogaster Melatonin (N-acetyl-5-methoxytryptamine), first known as a pineal hormone, attracts attention due to its numerous positive effects on biological systems of various complexity [3,13]. The efficacy of melatonin in vitro surpasses that of glutathion, mannitol, tx-tocopherol, and ascorbic acid [11,14]. Melatonin regulates circadian rhythms in live organisms [13].The geroprotective activity of melatonin has been little studied in experiments. Melatonin added to daily rations of mice during the whole life increased the mean lifespan (LS) by 25%. However, no geroprotective effect was detected after addition of the drug at the late larval stages of D. melanogaster development.All this necessitates further investigation of geroprotective properties of melatonin. We studied the LS of D. melanogaster treated with melatonin. MATERIALS AND METHODSCrystalline melatonin (Sigma) was used.Lipophilic substance dissolved in ethanol was added to ready nutrient medium cooled to 45~ For control groups, the same amount of ethanol was added into the nutrient medium (final ethanol concentration 0.1%/unit). Preliminary tests showed that this con- D. melanogaster, Canton-S wild strain, was used.All experimental procedures and growth conditions have been described in detail [5]. The LS distribution in the control and experimental groups was compared by pairs using the Kolmogorov--Smirnov test. Cot'relations between LS in the control population and the geroprotector efficacy was analyzed using Spearman's test [151. RESULTSThe LS in the control groups greatly varied: the extreme values differed by more than 40% in females and by almost 30% in males (Table 1). These results agree with previous reports on the natural fluctuations in LS of successive D. melanogaster generations [6,7].Paired differences in LS between the control and experimental groups varied: we observed a significant geroprotective effect of melatonin prolonging the LS by 10-18% and lack of the effect or even a 10% shortening of LS. For elucidating the relationship between LS in the control and experimental groups, each mean 0007-4888/99/0002-0186522.00 ~ Kluwer Academic/Plenum Publishers

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Section: Resultssupporting

confidence: 58%

“…A probable mechanism of this phenomenon has been discussed previously [10]. Similar effects are exhibited by 3-hydroxypyridine [10], vitamins A and E [2,9], and 4-hydroxy-tempo [5].…”

Section: Resultssupporting

confidence: 53%

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Melatonin as a geroprotector: Experiments withDrosophila melanogaster

Izmailov¹,

Obukhova²

1999

Bull Exp Biol Med

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“…Tempol increases the lifespan of Drosophila melanogaster (Izmaylov and Obukhova, 1996), and mice fed tempol from birth live significantly longer than controls (Mitchell et al , 2003). By lowering oxidative stress, tempol has been shown to normalize the age-related decline in dopamine receptor function (Fardoun et al , 2006).…”

Section: Pharmacologic Therapiesmentioning

confidence: 99%

Mitochondrial function in hypoxic ischemic injury and influence of aging

Ham

Raju

2017

Progress in Neurobiology

270

205

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Mitochondria are a major target in hypoxic/ischemic injury. Mitochondrial impairment increases with age leading to dysregulation of molecular pathways linked to mitochondria. The perturbation of mitochondrial homeostasis and cellular energetics worsens outcome following hypoxic-ischemic insults in elderly individuals. In response to acute injury conditions, cellular machinery relies on rapid adaptations by modulating posttranslational modifications. Therefore, post-translational regulation of molecular mediators such as hypoxia-inducible factor 1α (HIF-1α), peroxisome proliferator-activated receptor γ coactivator α (PGC-1α), c-MYC, SIRT1 and AMPK play a critical role in the control of the glycolytic-mitochondrial energy axis in response to hypoxic-ischemic conditions. The deficiency of oxygen and nutrients leads to decreased energetic reliance on mitochondria, promoting glycolysis. The combination of pseudohypoxia, declining autophagy, and dysregulation of stress responses with aging adds to impaired host response to hypoxic-ischemic injury. Furthermore, intermitochondrial signal propagation and tissue wide oscillations in mitochondrial metabolism in response to oxidative stress are emerging as vital to cellular energetics. Recently reported intercellular transport of mitochondria through tunneling nanotubes also play a role in the response to and treatments for ischemic injury. In this review we attempt to provide an overview of some of the molecular mechanisms and potential therapies involved in the alteration of cellular energetics with aging and injury with a neurobiological perspective.

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“…Sacher and Trucco also postulated that hormesis can be found only if control animals are short-lived [17] . Similarly, geroprotector efficiency depends on viability of the control population [21] . For example, for a relatively low life span in a population from which the control and experimental groups were formed, the geroprotective effect of melatonin was the most distinct; for a relatively high life span, the effect of the hormone was either not detected or appeared as a toxic reduction in life span (up to 10%) in the experimental group [22] .…”

Section: Life Extension Patterns By Anti-aging Drugs and By Hormetic mentioning

confidence: 99%

Life Extension by Anti-Aging Drugs: Hormetic Explanation?

Vaiserman¹

2008

American J. of Pharmacology and Toxicology

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A number of chemicals including antioxidants, vitamins and hormones are widely advertised as anti-aging drugs (geroprotectors). It is usually believed that life-extending capacity of geroprotectors may be attributed to their specific anti-aging mechanisms, even without solid scientific evidence. The analysis of the survival data gathered by both anti-aging and hormetic interventions demonstrates that many essential similarities exist between them. The evidence that life-extending effects of anti-aging drugs may be due to hormetic-like response is discussed in this review.

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Geroprotector efficiency depends on viability of control population: life span investigation in D. melanogaster

Cited by 21 publications

References 19 publications

Melatonin as a geroprotector: Experiments withDrosophila melanogaster

Melatonin as a geroprotector: Experiments withDrosophila melanogaster

Mitochondrial function in hypoxic ischemic injury and influence of aging

Life Extension by Anti-Aging Drugs: Hormetic Explanation?

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