Heavy metals are defined as metals with relatively high density and atomic weight, and their various applications have raised serious concerns about the environmental impacts and potential human health effects. Chromium is an important heavy metal that is involved in biological metabolism, but Cr exposure can induce a severe impact on occupational workers or public health. In this study, we explore the toxic effects of Cr exposure through three exposure routes: dermal contact, inhalation, and ingestion. We propose the underlying toxicity mechanisms of Cr exposure based on transcriptomic data and various bioinformatic tools. Our study provides a comprehensive understanding of the toxicity mechanisms of different Cr exposure routes by diverse bioinformatics analyses.

Endocrine-disrupting chemicals (EDCs) impair growth and development. While EDCs can occur naturally in aquatic ecosystems, they are continuously introduced through anthropogenic activities such as industrial effluents, pharmaceutical production, wastewater, and mining. To elucidate the chronic toxicological effects of endocrine-disrupting chemicals (EDCs) on aquatic organisms, we collected experimental data from a standardized chronic exposure test using Daphnia magna (D. magna), individuals of which were exposed to a potential EDC, trinitrotoluene (TNT). The chronic toxicity effects of this compound were explored through differential gene expression, gene ontology, network construction, and putative adverse outcome pathway (AOP) proposition. Our findings suggest that TNT has detrimental effects on the upstream signaling of Tcf/Lef, potentially adversely impacting oocyte maturation and early development. This study employs diverse bioinformatics approaches to elucidate the gene-level toxicological effects of chronic TNT exposure on aquatic ecosystems. The results provide valuable insights into the molecular mechanisms of the adverse impacts of TNT through network construction and putative AOP proposition.

Freshwater cladocerans such as Daphnia magna (D. magna) are keystone grazers whose hormone-regulated life history traits make them sensitive sentinels of endocrine-disrupting chemicals (EDCs). The organophosphate flame-retardant tris(2-butoxyethyl) phosphate (TBOEP) and perfluoroethylcyclohexane sulfonate (PFECHS) now co-occur at ng L⁻¹–µg L⁻¹ in surface waters, yet their chronic sub-lethal impacts on invertebrate endocrine networks remain unclear. We analysed two publicly available 21-day microarray datasets (TBOEP: GSE55132; PFECHS: GSE75607) using gene ontology enrichment, STRING protein interaction networks, Drosophila phenotype mapping, and KEGG (Kyoto Encyclopaedia of Genes and Genomes)-anchored frameworks to build putative adverse outcome pathways (AOPs) for D. magna. Differentially expressed genes were clustered into functional modules and hub nodes were ranked by degree and betweenness. TBOEP suppressed moulting and growth, altering 1157 genes enriched for metabolism and membrane processes; hubs VRK1, MIB2, and adenylosuccinate synthetase formed a muscle anatomical development sub-network. PFECHS down-regulated vitellogenin and shifted 879 genes dominated by oxidative-stress and glutathione-metabolism signatures; central nodes UBC9, eIF4A-III, Tra-2α, and HDAC1 linked meiotic-cycle, oogenesis, and cyclic-compound binding. Despite chemical dissimilarity, both compounds converged on Wnt-signalling nodes—TBOEP via presenilin-1, and PFECHS via CK1ε/CK2—thereby reducing TCF/LEF-dependent transcription. Predicted outcomes include impaired oocyte maturation, reduced fecundity, and stunted body size, consistent with observed decreases in length and vitellogenin protein. Our network analysis, based on high-dose, sub-lethal exposures used in the underlying microarray studies, indicates that TBOEP- and PFECHS-induced perturbations can destabilise endocrine, developmental, and metabolic pathways in D. magna without overt lethality, and highlights Wnt-centred key events and hub genes as candidate biomarkers to be evaluated in future low-dose studies that use environmentally realistic exposure scenarios. Hub genes and Wnt-mediated key events emerge as sensitive biomarkers for monitoring mixed EDC exposure.