Oxidative stress resistance as a factor in aging: evidence from an extended longevity phenotype of Drosophila melanogaster

Deepashree, S; Niveditha, S; Shivanandappa, T.; Ramesh, S. R.

doi:10.1007/s10522-019-09812-7

Cited by 35 publications

(21 citation statements)

References 64 publications

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“…There is a strong correlation between stress resistance and lifespan of C. elegans. Several studies have shown that the lifespan of C. elegans is affected by oxidative stress or high temperatures [41,42]. In order to study whether naringin affects stress resistance of C. elegans, wild-type N2 worms were pretreated with naringin, followed by oxidative stress or heat stress treatment.…”

Section: Naringin Promotes the Stress Resistance Of C Elegansmentioning

confidence: 99%

A Dihydroflavonoid Naringin Extends the Lifespan of C. elegans and Delays the Progression of Aging-Related Diseases in PD/AD Models via DAF-16

Zhu

Yuan

Zhou

et al. 2020

Oxidative Medicine and Cellular Longevity

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Naringin is a dihydroflavonoid, which is rich in several plant species used for herbal medicine. It has a wide range of biological activities, including antineoplastic, anti-inflammatory, antiphotoaging, and antioxidative activities. So it would be interesting to know if naringin has an effect on aging and aging-related diseases. We examined the effect of naringin on the aging of Caenorhabditis elegans (C. elegans). Our results showed that naringin could extend the lifespan of C. elegans. Moreover, naringin could also increase the thermal and oxidative stress tolerance, reduce the accumulation of lipofuscin, and delay the progress of aging-related diseases in C. elegans models of AD and PD. Naringin could not significantly extend the lifespan of long-lived mutants from genes in insulin/IGF-1 signaling (IIS) and nutrient-sensing pathways, such as daf-2, akt-2, akt-1, eat-2, sir-2.1, and rsks-1. Naringin treatment prolonged the lifespan of long-lived glp-1 mutants, which have decreased reproductive stem cells. Naringin could not extend the lifespan of a null mutant of the fox-head transcription factor DAF-16. Moreover, naringin could increase the mRNA expression of genes regulated by daf-16 and itself. In conclusion, we show that a natural product naringin could extend the lifespan of C. elegans and delay the progression of aging-related diseases in C. elegans models via DAF-16.

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Section: Naringin Promotes the Stress Resistance Of C Elegansmentioning

confidence: 99%

A Dihydroflavonoid Naringin Extends the Lifespan of C. elegans and Delays the Progression of Aging-Related Diseases in PD/AD Models via DAF-16

Zhu

Yuan

Zhou

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Previous studies founded a positive association between stress resistance and extended lifespan or aging in D. melanogaster [34,43,44]. In this species, the ROS defences are mediated by both immune and antioxidant response pathways.…”

Section: Suzukii Genotypes Vary In Lifespan and Response To Oxidatmentioning

confidence: 96%

“…Paraquat (N,N′-dimethyl-4,4′-bipyridinium dichloride) is one of the most widely used herbicide in the world [29,30]. Exposure to paraquat leads to the production of ROS (reactive oxygen species) and has often been used in the lab as a proxy to study oxidative stress [31][32][33][34]. Resistance to oxidative stress has been associated with extended lifespan [34][35][36], a trait possibly under selection during invasion of a new area.…”

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confidence: 99%

Phenotypic and transcriptomic responses to stress differ according to population geography in an invasive species

St.Pierre

Jaquet

Picarle

et al. 2020

Preprint

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BackgroundAdaptation to rapid environmental changes must occur within a short time scale. In this context, studies of invasive species may provide insights into the underlying mechanisms of rapid adaptation as these species have repeatedly encountered and successfully adapted to novel environmental conditions. Here we investigated how invasive and non-invasive populations of D. suzukii deal with an oxidative stress at both the phenotypic and molecular level. We also investigated the impact of transposable element insertions on the differential gene expression between genotypes in response to oxidative stress.ResultsInvasive populations lived longer in the untreated condition than non-invasive Japanese populations. As expected, lifespan was greatly reduced following exposure to paraquat, but this reduction varied among genotypes (a genotype by environment interaction, GEI) with invasive genotypes appearing more affected by exposure than non-invasive genotypes. We also performed transcriptomic sequencing of selected genotypes upon and without paraquat and detected a large number of genes differentially expressed, distinguishing the genotypes in the untreated environment. While a small core set of genes were differentially expressed by all genotypes following paraquat exposure, much of the response of each population was unique. Interestingly, we identified a set of genes presenting genotype by environment interaction (GEI). Many of these differences may reflect signatures of history of past adaptation. Transposable elements (TEs) were not activated after oxidative stress and differentially expressed (DE) genes were significantly depleted of TEs.ConclusionIn the decade since the invasion from the south of Asia, invasive populations of D. suzukii have diverged from populations in the native area regarding their genetic response to oxidative stress. This suggests that such transcriptomic changes could be involved in the rapid adaptation to local environments.

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“…The brain is particularly susceptible to oxidative damage being the most aerobically active organ in the body due to its high metabolism [34]. The brain is generally in a redox balance; however, the high production and accumulation of ROS accompanied by a reduction in the antioxidant defense system plays a key role in aging, causing damaging effects due to the large number of potential harmful intermediates that cause neuronal dysfunction [3,35]. In turn, increased oxygen radical-induced oxidative damage during aging leads to significant changes in brain mitochondrial function [29].…”

Section: Oxidative Stress: the Main Characteristic Of Normal Agingmentioning

confidence: 99%

Mitochondrial Dysfunction as a Key Event during Aging: From Synaptic Failure to Memory Loss

Jara¹,

Torres²,

Olesen³

et al. 2020

Mitochondria and Brain Disorders

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Mitochondria are important cellular organelles with key regulatory functions in energy production, oxidative balance, and calcium homeostasis. This is especially important in the brain, since neurons require a large number of functional mitochondria to supply their high energy requirement, mainly for synaptic processes. A decrease in the activity and quality of mitochondria in the brain, particularly in the hippocampus, is associated with normal aging and a large number of neurodegenerative diseases compromising memory function. Although synaptic and cognitive dysfunction is multifactorial, growing evidence demonstrates that mitochondria play a key role in these processes and suggests that maintaining mitochondrial function could prevent these age-dependent alterations. In this chapter, we will discuss the hippocampal mitochondrial dysfunction present in aging and how these defects promote age-associated synaptic damage and cognitive impairment. We will summarize evidence that shows how neurodegeneration can be accelerated or attenuated during aging by modulating mitochondrial function.

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Oxidative stress resistance as a factor in aging: evidence from an extended longevity phenotype of Drosophila melanogaster

Cited by 35 publications

References 64 publications

A Dihydroflavonoid Naringin Extends the Lifespan of C. elegans and Delays the Progression of Aging-Related Diseases in PD/AD Models via DAF-16

A Dihydroflavonoid Naringin Extends the Lifespan of C. elegans and Delays the Progression of Aging-Related Diseases in PD/AD Models via DAF-16

Phenotypic and transcriptomic responses to stress differ according to population geography in an invasive species

Mitochondrial Dysfunction as a Key Event during Aging: From Synaptic Failure to Memory Loss

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