Triphenyl phosphate induced reproductive toxicity through the JNK signaling pathway in Caenorhabditis elegans.

Triphenyl phosphate (TPHP) is a widely used aryl organophosphate flame retardant (OPFR) that has attracted attention due to its frequent detection in the environment and living organisms. To date, the reproductive toxicity of TPHP has been investigated in organisms, but its molecular mechanisms are not fully understood. Caenorhabditis elegans (C.

Decabromodiphenyl ethane induces locomotion neurotoxicity and potential Alzheimer's disease risks through intensifying amyloid-beta deposition by inhibiting transthyretin/transthyretin-like proteins.

As a major alternative to traditional brominated flame retardants (BFRs), decabromodiphenyl ethane (DBDPE) is widely used and has been commonly detected in various environmental media and organisms. Few previous studies have focused on DBDPE-induced locomotion neurotoxicity, and the exact molecular mechanisms and related health risks remain unclear. In this study, we first analyzed the locomotion indicators of nematodes following DBDPE exposure, demonstrated that DBDPE caused locomotion neurotoxicity, and identified that a series of the transthyretin (TTR)-like genes participated in the regulation of nematode motility by transcriptomic analysis, gene transcription validation and TTR-like mutant verification.

Review of the toxicity and potential molecular mechanisms of parental or successive exposure to environmental pollutants in the model organism Caenorhabditis elegans.

Environmental pollutants such as heavy metals, nano/microparticles, and organic compounds have been detected in a wide range of environmental media, causing long-term exposure in various organisms and even humans through breathing, contacting, ingestion, and other routes. Long-term exposure to environmental pollutants in organisms or humans promotes exposure of offspring to parental and environmental pollutants, and subsequently results in multiple biological defects in the offspring. This review dialectically summarizes and discusses the existing studies using Caenorhabditis elegans (C.

Tris(1,3-dichloro-2-propyl) phosphate reduces longevity through a specific microRNA-mediated DAF-16/FoxO in an unconventional insulin/insulin-like growth factor‑1 signaling pathway.

Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) has received concerns due to its frequent detection in environmental media and biological samples. Our previous study has indicated TDCPP reduced the lifespan of Caenorhabditis elegans (C. elegans) by triggering an unconventional insulin/insulin-like growth factor signaling (IIS) pathway.