Chronic Exposure to Perfluorooctane Sulfonate Reduces Lifespan of Caenorhabditis elegans Through Insulin/IGF-1 Signaling

Xu, Tiantian; Li, Ping; Wu, Siyu; Li, Dan; Jing-Xuan, WU; Raley‐Susman, Kathleen M.; He, Defu

doi:10.1007/s00128-016-1808-5

Cited by 19 publications

(5 citation statements)

References 30 publications

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“…Adult nematodes were collected into tubes, and then dissolved a bleach-containing buffer (0.45 mM NaOH, 2% HClO) to release eggs. The eggs were collected and hatched on the plates with food, then synchronized for experiments (Xu et al, 2016).…”

Section: Methodsmentioning

confidence: 99%

Mutation of hop-1 and pink-1 attenuates vulnerability of neurotoxicity in C. elegans: the role of mitochondria-associated membrane proteins in Parkinsonism

Lei

Song

et al. 2018

Experimental Neurology

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Mitochondrial dysfunction is considered as a critical mechanism in the pathogenesis of Parkinson's disease (PD). Increasing evidence supports the notion of mitochondria-associated membranes (MAMs) in mitochondrial dysfunction; yet little is known about the role of MAMs-related proteins in the pathogenesis of PD. Herein we exposed the nematode Caenorhabditis elegans to 0.5-10.0 μM rotenone (RO) or 0.2-1.6 mM paraquat (PQ) for 3 days. Our results showed that both RO and PQ induced similar Parkinsonism including motor deficits and dopaminergic degeneration. RO/PQ caused mitochondrial damages characterized by the increase of vacuole areas and autophagy vesicles, but the decrease of mitochondrial cristae. RO/PQ-impacted mitochondrial function was also demonstrated by the decrease of ATP level and mitochondrial membrane potential. Additionally, the attachment or surrounding of endoplasmic reticulum to the damaged mitochondria indicates ultrastructural alterations in MAMs. Using fluorescently labeled transgenic nematodes, we further found that the expression of tomm-7 and genes of Complex I, II and III was reduced, whereas the expression of pink-1 was increased in the exposed animals. To determine MAMs in toxicity toward PD, we investigated the mutants of hop-1 and pink-1, encoding presenilin and PTEN-induced putative kinase 1 (PINK1) in mitochondria-associated membranes, respectively. Results demonstrated that the mutation of both hop-1 and pink-1 reduced the vulnerability of lethal, behavioral, and mitochondrial toxicity induced by RO/PQ. These findings suggest that presenilin and PINK1 play important roles in the RO/PQ-induced neurotoxicity through the mechanisms involved in mitochondria-associated membranes.

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Section: Methodsmentioning

confidence: 99%

Mutation of hop-1 and pink-1 attenuates vulnerability of neurotoxicity in C. elegans: the role of mitochondria-associated membrane proteins in Parkinsonism

Lei

Song

et al. 2018

Experimental Neurology

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“…Nematodes were maintained on nematode growth medium (NGM) plates seeded with E. coli OP50 at 20°C (Brenner, ). According to previous methods (Chen et al, ; Xu et al, ), adult animals were collected into tubes by washing plates with M9 buffer and then dissolved in bleaching solution (0.45 M NaOH, 2% HClO) to collect eggs. The eggs were hatched on the plates with food and then synchronized for experiments.…”

Section: Methodsmentioning

confidence: 99%

“…Previous works have used the level of GFP expression as an indicator of neurodegeneration (Settivari et al, 2009;Harrison et al, 2013;Li et al, 2016). However, gene expression can be altered, upregulated or downregulated, in the absence of overt structural damage (Harrison et al, 2013;Xu et al, 2016). Indeed, a previous report demonstrated manganese-dependent downregulation of gene expression within 30 min, long before observable neurodegeneration was evident (Settivari et al, 2009).…”

Section: Neural Damagesmentioning

confidence: 99%

Chronic exposure to graphene-based nanomaterials induces behavioral deficits and neural damage inCaenorhabditis elegans

et al. 2017

J. Appl. Toxicol.

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Nanomaterials of graphene and its derivatives have been widely applied in recent years, but whose impacts on the environment and health are still not well understood. In the present study, the potential adverse effects of graphite (G), graphite oxide nanoplatelets (GO) and graphene quantum dots (GQDs) on the motor nervous system were investigated using nematode Caenorhabditis elegans as the assay system. After being characterized using TEM, SEM, XPS and PLE, three nanomaterials were chronically exposed to C. elegans for 6 days. In total, 50-100 mg l GO caused a significant reduction in the survival rate, but G and GDDs showed low lethality on nematodes. After chronic exposure of sub-lethal dosages, three nanomaterials were observed to distribute primarily in the pharynx and intestine; but GQDs were widespread in nematode body. Three graphene-based nanomaterials resulted in significant declines in locomotor frequency of body bending, head thrashing and pharynx pumping. In addition, mean speed, bending angle-frequency and wavelength of the crawling movement were significantly reduced after exposure. Using transgenic nematodes, we found high concentrations of graphene-based nanomaterials induced down-expression of dat-1::GFP and eat-4::GFP, but no significant changes in unc-47::GFP. This indicates that graphene-based nanomaterials can lead to damages in the dopaminergic and glutamatergic neurons. The present data suggest that chronic exposure of graphene-based nanomaterials may cause neurotoxicity risks of inducing behavioral deficits and neural damage. These findings provide useful information to understand the toxicity and safe application of graphene-based nanomaterials. Copyright © 2017 John Wiley & Sons, Ltd.

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“…44 Previous studies have shown that environmental pollutants could reduce lifespan through affecting insulin signaling. 45,46 We found that 1 and 10 μg/L 6-PPDQ upregulated akt-1, age-1, daf-2, and akt-2 expressions (Figure 2A). Meanwhile, expressions of daf-16 and DAF-16::GFP were downregulated after 6-PPDQ exposure (Figure 2A,B).…”

Section: -Ppdq Shortened Lifespan Of Nematodes and Affected Physiolog...mentioning

confidence: 88%

Exposure to 6-PPD Quinone at Environmentally Relevant Concentrations Inhibits Both Lifespan and Healthspan in C. elegans

Hua,

Wang

2023

Environ. Sci. Technol.

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Chronic Exposure to Perfluorooctane Sulfonate Reduces Lifespan of Caenorhabditis elegans Through Insulin/IGF-1 Signaling

Cited by 19 publications

References 30 publications

Mutation of hop-1 and pink-1 attenuates vulnerability of neurotoxicity in C. elegans: the role of mitochondria-associated membrane proteins in Parkinsonism

Mutation of hop-1 and pink-1 attenuates vulnerability of neurotoxicity in C. elegans: the role of mitochondria-associated membrane proteins in Parkinsonism

Chronic exposure to graphene-based nanomaterials induces behavioral deficits and neural damage inCaenorhabditis elegans

Exposure to 6-PPD Quinone at Environmentally Relevant Concentrations Inhibits Both Lifespan and Healthspan in C. elegans

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