Butiá fruit extract ( Butia eriospatha ) protects against oxidative damage and increases lifespan on Caenorhabditis elegans

2020 ◽  
Vol 44 (3) ◽  
Author(s):  
Andréia Limana Tambara ◽  
Élen Cristiane Silveira ◽  
Ana Thalita Gonçalves Soares ◽  
Willian Goulart Salgueiro ◽  
Cristiane de Freitas Rodrigues ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Fruit Extract

Knock-down of transcription factor skinhead-1 exacerbates arsenite-induced oxidative damage in Caenorhabditis elegans

BioMetals ◽  
2021 ◽  
Author(s):  
Yijie Mao ◽  
Ling Yao ◽  
Xuejun Jiang ◽  
Golamaully Sumayyah ◽  
Zhen Zou ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Knock Down

scholarly journals Increased life span from overexpression of superoxide dismutase in Caenorhabditis elegans is not caused by decreased oxidative damage

2011 ◽  
Vol 51 (8) ◽  
pp. 1575-1582 ◽  
Author(s):  
Filipe Cabreiro ◽  
Daniel Ackerman ◽  
Ryan Doonan ◽  
Caroline Araiz ◽  
Patricia Back ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Life Span

Mitochondrial Complex I Function Affects Halothane Sensitivity in Caenorhabditis elegans 

2004 ◽  
Vol 101 (2) ◽  
pp. 365-372 ◽  
Author(s):  
Ernst-Bernhard Kayser ◽  
Phil G. Morgan ◽  
Margaret M. Sedensky
Keyword(s):  
Caenorhabditis Elegans ◽  
Oxidative Phosphorylation ◽  
Oxidative Damage ◽  
Adenosine Triphosphate ◽  
Complex I ◽  
Volatile Anesthetics ◽  
Mitochondrial Proteins ◽  
Wild Type ◽  
Complex Ii ◽  
C Elegans

Background : The gene gas-1 encodes a subunit of complex I of the mitochondrial electron transport chain in Caenorhabditis elegans. A mutation in gas-1 profoundly increases sensitivity of C. elegans to volatile anesthetics. It is unclear which aspects of mitochondrial function account for the hypersensitivity of the mutant. Methods : Oxidative phosphorylation was determined by measuring mitochondrial oxygen consumption using electron donors specific for either complex I or complex II. Adenosine triphosphate concentrations were determined by measuring luciferase activity. Oxidative damage to mitochondrial proteins was identified using specific antibodies. Results : Halothane inhibited oxidative phosphorylation in isolated wild-type mitochondria within a concentration range that immobilizes intact worms. At equal halothane concentrations, complex I activity but not complex II activity was lower in mitochondria from mutant (gas-1) animals than from wild-type (N2) animals. The halothane concentrations needed to immobilize 50% of N2 or gas-1 animals, respectively, did not reduce oxidative phosphorylation to identical rates in the two strains. In air, adenosine triphosphate concentrations were similar for N2 and gas-1 but were decreased in the presence of halothane only in gas-1 animals. Oxygen tension changed the sensitivity of both strains to halothane. When nematodes were raised in room air, oxidative damage to mitochondrial proteins was increased in the mutant animal compared with the wild type. Conclusions : Rates of oxidative phosphorylation and changes in adenosine triphosphate concentrations by themselves do not control anesthetic-induced immobility of wild-type C. elegans. However, they may contribute to the increased sensitivity to volatile anesthetics of the gas-1 mutant. Oxidative damage to proteins may be an important contributor to sensitivity to volatile anesthetics in C. elegans.

scholarly journals Proteostasis collapse is a driver of cell aging and death

2019 ◽  
Vol 116 (44) ◽  
pp. 22173-22178 ◽  
Author(s):  
Mantu Santra ◽  
Ken A. Dill ◽  
Adam M. R. de Graff
Keyword(s):  
Caenorhabditis Elegans ◽  
Oxidative Damage ◽  
Life Span ◽  
Protein Function ◽  
Tipping Point ◽  
Cell Aging ◽  
Molecular Processes ◽  
Increased Temperature ◽  
Oxidant Concentration

What molecular processes drive cell aging and death? Here, we model how proteostasis—i.e., the folding, chaperoning, and maintenance of protein function—collapses with age from slowed translation and cumulative oxidative damage. Irreparably damaged proteins accumulate with age, increasingly distracting the chaperones from folding the healthy proteins the cell needs. The tipping point to death occurs when replenishing good proteins no longer keeps up with depletion from misfolding, aggregation, and damage. The model agrees with experiments in the worm Caenorhabditis elegans that show the following: Life span shortens nonlinearly with increased temperature or added oxidant concentration, and life span increases in mutants having more chaperones or proteasomes. It predicts observed increases in cellular oxidative damage with age and provides a mechanism for the Gompertz-like rise in mortality observed in humans and other organisms. Overall, the model shows how the instability of proteins sets the rate at which damage accumulates with age and upends a cell’s normal proteostasis balance.

Pitaya fruit extract ameliorates the healthspan on copper‐induced toxicity of Caenorhabditis elegans

2022 ◽  
Author(s):  
Wagner Antonio Tamagno ◽  
Wallace Santini ◽  
Amanda Santos ◽  
Carla Alves ◽  
Denise Bilibio ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Fruit Extract

scholarly journals Protective Effect and Mechanism of Fruit Extract of Aegle marmelos Against Amyloid-β Toxicity in a Transgenic Caenorhabditis elegans

2020 ◽  
Vol 15 (7) ◽  
pp. 1934578X2093351
Author(s):  
Roongpetch Keowkase ◽  
Nattanon Kijmankongkul ◽  
Wanapong Sangtian ◽  
Sireethorn Poomborplab ◽  
Chatpiti Santa-ardharnpreecha ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Amyloid Β ◽  
The Elderly ◽  
Potential Candidate ◽  
Aegle Marmelos ◽  
Antioxidative Effect ◽  
Fruit Extract ◽  
Aβ Oligomers ◽  
C Elegans

Alzheimer’s disease (AD) is the most common form of dementia found in the elderly. AD is caused by the accumulation of toxic proteins including amyloid-β (Aβ). The purpose of this study was to investigate the effect of fruit extract of Aegle marmelos against Aβ toxicity in Caenorhabditis elegans. The fruit of A. marmelos has been used in a traditional Thai herb formula in fatigue patients recovering from illnesses such as fever and diarrhea. We used a transgenic C. elegans strain CL4176, which expresses the human Aβ42, to investigate the effects and the mechanisms of action of the extracts against Aβ toxicity. The extract of A. marmelos significantly delayed Aβ-induced paralysis. Aegle marmelos lost the ability to delay Aβ-induced paralysis in worms fed with daf-16 ribonucleic acid interference (RNAi) bacteria, but not in worms fed with hsf-1 and skin-1 RNAi bacteria. These results indicated that daf-16 transcription factor was required for A. marmelos-mediated delayed paralysis. Aegle marmelos enhanced the level of daf-16 gene. Taken together, these results indicated that A. marmelos reduced Aβ toxicity via the DAF-16-mediated cell signaling pathway. In addition, A. marmelos reduced toxic Aβ oligomers. Aegle marmelos also displayed antioxidative effect in in vivo as it enhanced resistance to paraquat-induced oxidative stress in wild type worms. All of the results suggested that A. marmelos can protect against Aβ-induced toxicity and can be a potential candidate for the prevention or treatment of AD.

Sign in / Sign up

Export Citation Format

Share Document