Swimming Exercise and Transient Food Deprivation in Caenorhabditis elegans Promote Mitochondrial Maintenance and Protect Against Chemical-Induced Mitotoxicity.

Loading...
Thumbnail Image

Date

2018-05-29

Journal Title

Journal ISSN

Volume Title

Repository Usage Stats

124
views
28
downloads

Citation Stats

Attention Stats

Abstract

Exercise and caloric restriction improve health, including reducing risk of cardiovascular disease, neurological disease, and cancer. However, molecular mechanisms underlying these protections are poorly understood, partly due to the cost and time investment of mammalian long-term diet and exercise intervention studies. We subjected Caenorhabditis elegans nematodes to a 6-day, twice daily swimming exercise regimen, during which time the animals also experienced brief, transient food deprivation. Accordingly, we included a non-exercise group with the same transient food deprivation, a non-exercise control with ad libitum access to food, and a group that exercised in food-containing medium. Following these regimens, we assessed mitochondrial health and sensitivity to mitochondrial toxicants. Exercise protected against age-related decline in mitochondrial morphology in body-wall muscle. Food deprivation increased organismal basal respiration; however, exercise was the sole intervention that increased spare respiratory capacity and proton leak. We observed increased lifespan in exercised animals compared to both control and transiently food-deprived nematodes. Finally, exercised animals (and to a lesser extent, transiently food-deprived animals) were markedly protected against lethality from acute exposures to the mitotoxicants rotenone and arsenic. Thus, swimming exercise and brief food deprivation provide effective intervention in C. elegans, protecting from age-associated mitochondrial decline and providing resistance to mitotoxicant exposures.

Department

Description

Provenance

Subjects

Citation

Published Version (Please cite this version)

10.1038/s41598-018-26552-9

Publication Info

Hartman, Jessica H, Latasha L Smith, Kacy L Gordon, Ricardo Laranjeiro, Monica Driscoll, David R Sherwood and Joel N Meyer (2018). Swimming Exercise and Transient Food Deprivation in Caenorhabditis elegans Promote Mitochondrial Maintenance and Protect Against Chemical-Induced Mitotoxicity. Scientific reports, 8(1). 10.1038/s41598-018-26552-9 Retrieved from https://hdl.handle.net/10161/17077.

This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.

Scholars@Duke

Sherwood

David R. Sherwood

Jerry G. and Patricia Crawford Hubbard Professor

The Sherwood lab is interested in understanding mechanisms that drive dynamic cellular behaviors underlying normal development and human disease. We study 1) How cells invade into tissues, 2) How stem cells interact with their niches, and 3) How cells control and interact with extracellular matrix. Our lab primarily examines C. elegans development, in which simple cellular complexity, amenability to genetics/genomics/transgenics/molecular perturbations, and evolutionary comparisons facilitates powerful insights. One particular emphasis of our work is live-cell imaging, where we watch cellular behaviors and cell-extracellular matrix interactions unfold in real-time to understand their regulation and function.  Cell invasion, stem cell regulation, and cell-matrix interactions are fundamental to development, regeneration, cancer, and aging.  Our work aims to advance our understanding of these fascinating processes and positively influence human health.

Meyer

Joel Meyer

Professor of Environmental Genomics in the Division of Environmental Sciences and Policy

Dr. Meyer studies the effects of toxic agents and stressors on human and wildlife health. He is particularly interested in understanding the mechanisms by which environmental agents cause DNA damage, the molecular processes that organisms employ to protect prevent and repair DNA damage, and genetic differences that may lead to increased or decreased sensitivity to DNA damage. Mitochondrial DNA damage and repair, as well as mitochondrial function in general, are a particular focus. He studies these effects in the nematode Caenorhabditis elegans, in cell culture, and collaboratively in other laboratory model organisms as well as in human populations in the USA and globally.


Unless otherwise indicated, scholarly articles published by Duke faculty members are made available here with a CC-BY-NC (Creative Commons Attribution Non-Commercial) license, as enabled by the Duke Open Access Policy. If you wish to use the materials in ways not already permitted under CC-BY-NC, please consult the copyright owner. Other materials are made available here through the author’s grant of a non-exclusive license to make their work openly accessible.