Effects of atrazine on tissue damage, physiological and biochemical changes and transcriptome in marine medaka (Oryzias melastigma).
Atrazine (ATZ), a widely used triazine herbicide frequently detected in aquatic environments, poses ecological risks, yet its toxicity mechanisms in estuarine/marine organisms remain unclear. The present study employed juvenile Oryzias melastigma (marine medaka) as the model organism, and the 96-h median lethal concentration (LC50) of ATZ was determined to be 31.65 mg/L. Juvenile marine medaka were exposed to 0, 0.09, 0.36, 1.07, and 3.28 mg/L ATZ for 30 days. Histopathology revealed severe gill alterations (hyperplasia, apical enlargement, disintegration of the lamellae and filament congestion) and hepatic injuries (sinusoidal dilation, cytoplasmic vacuolization, acidophilic body formation and nuclear pyknosis). Biochemically, ATZ altered Na+-K+-ATPase and Ca2+-ATPase activities in the gills, reduced the activity of catalase (CAT) in the liver. ATZ at concentrations of 0.09 and 0.36 mg/L could markedly decrease the activity of total superoxide dismutase (T-SOD), and increase the malondialdehyde (MDA) content in medaka liver. Additionally, ATZ exposure upregulated the expression levels of ucp-2 and decreased the expression levels of cox-2, ccl20, il-1β, cat and sod. Transcriptome results showed 1,078 differentially expressed genes (DEGs) in the liver, with 436 upregulated and 642 downregulated DEGs. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that ATZ exposure disturbed the expression of genes associated with the HIF-1 and PI3K-Akt signaling pathways, suggesting that ATZ may induce hypoxia, oxidative damage and apoptosis. These results corroborate the histological and enzymatic evidence, providing insights into the toxicological impacts and mechanisms of chronic ATZ exposure in estuarine and marine fish.