Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 19, Pages -Publisher
MDPI
DOI: 10.3390/ijms221910277
Keywords
ionizing radiation; oxidative stress; lipids; reproduction; Caenorhabditis elegans; chronic exposure; life stage
Funding
- IRSN
- European Union Regional Developing Fund
- Region Provence Alpes Cote d'Azur
- French Ministry of Research
- CEA
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This study investigated the impact of radiation on reproduction decrease in the roundworm C. elegans using a life stage dependent approach. The results showed that reproductive defects are life stage dependent, lipids are differently regulated according to the exposure, and a proposed conceptual model of lipid signaling after radiation stress was provided.
Wildlife is chronically exposed to various sources of ionizing radiations, both environmental or anthropic, due to nuclear energy use, which can induce several defects in organisms. In invertebrates, reproduction, which directly impacts population dynamics, has been found to be the most radiosensitive endpoint. Understanding the underlying molecular pathways inducing this reproduction decrease can help in predicting the effects at larger scales (i.e., population). In this study, we used a life stage dependent approach in order to better understand the molecular determinants of reproduction decrease in the roundworm C. elegans. Worms were chronically exposed to 50 mGy center dot h(-1) external gamma ionizing radiations throughout different developmental periods (namely embryogenesis, gametogenesis, and full development). Then, in addition to reproduction parameters, we performed a wide analysis of lipids (different class and fatty acid via FAMES), which are both important signaling molecules for reproduction and molecular targets of oxidative stress. Our results showed that reproductive defects are life stage dependent, that lipids are differently misregulated according to the considered exposure (e.g., upon embryogenesis and full development) and do not fully explain radiation induced reproductive defects. Finally, our results enable us to propose a conceptual model of lipid signaling after radiation stress in which both the soma and the germline participate.
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