Arsenite exposure accelerates aging process regulated by the transcription factor DAF-16/FOXO in Caenorhabditis elegans

Yu, Chun; How, Chun Ming; Liao, Vivian Hsiu‐Chuan

doi:10.1016/j.chemosphere.2016.01.004

Cited by 31 publications

(12 citation statements)

References 47 publications

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“…Previous investigations provided convincing evidence that FoxO transcription factors play positive regulatory roles in the stress resistance and lifespan of C. elegans (Hesp, Smant, & Kammenga, 2015;Yu, How, & Liao, 2016). Thus, we speculate that Bxdaf-16-2b gene plays a positive role in responses to botanical pesticides and that the other three IIS pathway genes profiled participate in the defence responses of B. xylophilus.…”

Section: (B) (A)supporting

confidence: 51%

Molecular characterization and functional analysis of daf‐16‐2b gene in the pine wood nematode, Bursaphelenchus xylophilus

Wang

Wen

et al. 2019

Forest Pathology

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The Forkhead box O transcription factor DAF-16 is an important downstream transcription factor in the well-conserved insulin signalling (IIS) pathway in Caenorhabditis elegans. The nuclear localization of DAF-16 can activate a series of genes that mediate oxidative stress, heat shock, xenobiotic responses, innate immunity, metabolism and autophagy. In this study, a Bxdaf-16-2b gene encoding 510 amino acids was

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Section: (B) (A)supporting

confidence: 51%

Molecular characterization and functional analysis of daf‐16‐2b gene in the pine wood nematode, Bursaphelenchus xylophilus

Wang

Wen

et al. 2019

Forest Pathology

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“…More importantly with regard to the relevance of our study, nematodes display some of the lowest sensitivity to arsenic yet observed, with a previously reported 24 h LC 50 value of 1.3 mM arsenite (Liao and Yu, 2005;Tseng et al, 2007), although here we report a slightly higher 24 h LC 50 value of $5 mM ( Supplementary Figure 6). Reduced sensitivity to arsenite is further demonstrated by the fact that only chronic, lifelong exposure to !100 mM ($7.5 ppm) arsenite reduce nematode lifespan ($10 to 15%) (Yu et al, 2016), whereas chronic exposure to much lower concentrations (10-150 ppb) of arsenite are associated with increased mortality rates in humans (Argos et al, 2010). Reduced sensitivity is likely, in part, due to the nematode's cuticle, a collagenous barrier that has been shown to limit the absorption of a variety of toxicants, including: bisphenol A (Watanabe et al, 2005), oligomycin (Luz et al, 2015a), and drugs such as nicotine and ivermectin (Partridge et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

From the Cover: Arsenite Uncouples Mitochondrial Respiration and Induces a Warburg-like Effect inCaenorhabditis elegans

Luz

Godebo

Bhatt³

et al. 2016

Toxicol. Sci.

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Millions of people worldwide are chronically exposed to arsenic through contaminated drinking water. Despite decades of research studying the carcinogenic potential of arsenic, the mechanisms by which arsenic causes cancer and other diseases remain poorly understood. Mitochondria appear to be an important target of arsenic toxicity. The trivalent arsenical, arsenite, can induce mitochondrial reactive oxygen species production, inhibit enzymes involved in energy metabolism, and induce aerobic glycolysis in vitro, suggesting that metabolic dysfunction may be important in arsenic-induced disease. Here, using the model organism Caenorhabditis elegans and a novel metabolic inhibition assay, we report an in vivo induction of aerobic glycolysis following arsenite exposure. Furthermore, arsenite exposure induced severe mitochondrial dysfunction, including altered pyruvate metabolism; reduced steady-state ATP levels, ATP-linked respiration and spare respiratory capacity; and increased proton leak. We also found evidence that induction of autophagy is an important protective response to arsenite exposure. Because these results demonstrate that mitochondria are an important in vivo target of arsenite toxicity, we hypothesized that deficiencies in mitochondrial electron transport chain genes, which cause mitochondrial disease in humans, would sensitize nematodes to arsenite. In agreement with this, nematodes deficient in electron transport chain complexes I, II, and III, but not ATP synthase, were sensitive to arsenite exposure, thus identifying a novel class of gene-environment interactions that warrant further investigation in the human populace.

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“…The three kinds of nematodes were cultured and treated as described above. The intestinal lipofuscin deposition was measured as described previously with modifications [ 38 ]. The autofluorescence of intestinal lipofuscin was measured at day-5 and day-7 adulthood using an epifluorescence microscope (Leica, Wetzlar, Germany) with excitation/emission wavelength of 350 ± 25/460 ± 25 nm.…”

Section: Methodsmentioning

confidence: 99%

Spermidine inhibits neurodegeneration and delays aging via the PINK1-PDR1-dependent mitophagy pathway in C. elegans

Yang

Zhang²,

Dai

et al. 2020

Aging

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Aging is the primary driver of various diseases, including common neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Currently there is no cure for AD and PD, and the development of novel drug candidates is demanding. Spermidine is a small anti-aging molecule with elimination of damaged mitochondria via the process of mitophagy identified as a molecular mechanism of action. Here, we show that spermidine inhibits memory loss in AD worms and improves behavioral performance, e.g., locomotor capacity, in a PD worm model, both via the PINK1-PDR1-dependent mitophagy pathway. Additionally, spermidine delays accelerated aging and improves healthspan in the DNA repair-deficient premature aging Werner syndrome (WS) worm model. While possible intertwined interactions between mitophagy/autophagy induction and DNA repair by spermidine are to be determined, our data support further translation of spermidine as a possible therapeutic intervention for such diseases.

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Arsenite exposure accelerates aging process regulated by the transcription factor DAF-16/FOXO in Caenorhabditis elegans

Cited by 31 publications

References 47 publications

Molecular characterization and functional analysis of daf‐16‐2b gene in the pine wood nematode, Bursaphelenchus xylophilus

Molecular characterization and functional analysis of daf‐16‐2b gene in the pine wood nematode, Bursaphelenchus xylophilus

From the Cover: Arsenite Uncouples Mitochondrial Respiration and Induces a Warburg-like Effect inCaenorhabditis elegans

Spermidine inhibits neurodegeneration and delays aging via the PINK1-PDR1-dependent mitophagy pathway in C. elegans

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