Thesis: Wildlife is chronically exposed to various sources of ionizing radiations, either environmental or anthropic due to nuclear energy use, which can induce several defects in organisms. In invertebrates, reproduction, which directly impacts population dynamics, was found to be the most radiosensitive individual endpoint. Understanding the underlying molecular pathways inducing this reproduction decrease can help to characterize early effects and to understand species radiosensitivity. This type of data can be structured through the AOP (Adverse Outcome Pathway) framework in order to causally link molecular initiating events to adverse outcomes at different biological levels of organization and to compare with other toxicants (exposome). This thesis aimed to decipher the molecular determinants of reproduction decrease (broodsize decrease, no observed hatching default) in the hermaphroditic soil invertebrate Caenorhabditis elegans, after chronic exposure to gamma radiations. Several pathways and biological processes were investigated (lipid metabolism, sex determination and stress-response) to determine the molecular initiating- and key- event(s) of observed reproduction decrease. A life-stage dependent approach was adopted to identify the timing of occurrence and early mechanisms of reprotoxic effects. Our results showed that reprotoxic effects are life stage dependent and intertwined with the regulation of lipid metabolism by the germline and the soma. Moreover, we showed how both gametes (spermatozoa and oocytes) are affected by different radio-induced response pathways and unevenly contribute to the broodsize decrease. These results will contribute to build an AOP scheme, to causally link the observed effects leading to reproduction decrease, and eventually improve environmental risk assessment.