Effects of mercury chloride on antioxidant and inflammatory cytokines in zebrafish embryos

Abstract

AbstractIn this study, a zebrafish embryo toxicity model was employed, utilizing 24 h postfertilization (hpf) zebrafish embryos. These embryos were treated with varying concentrations of mercuric chloride for 96 h under static conditions. We assessed multiple parameters that reflected developmental abnormalities, behavioral alterations, morphological anomalies, antioxidant enzyme activities, including those of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and glutathione S‐transferase (GST), immune messenger RNA transcription levels of key factors such as tumor necrosis factor α (TNF‐α), interleukin‐1β (IL‐1β), interleukin‐6 (IL‐6), and cyclooxygenase 2 (COX‐2), as well as protein expression of TNF‐α. The results revealed that embryos exposed to higher concentrations of mercury exhibited reduced hatchability and increased rates of morphological abnormalities and mortality at 48, 72, and 96 hpf. In addition, a concentration‐dependent increase in developmental abnormalities, including cardiac edema, reduced body length, yolk sac edema, scoliosis, and bent tails, was observed. Larval behaviors, such as touch‐induced escape responses, startle reactions, and turning actions, were found to be diminished in a concentration‐dependent manner. Additionally, the activities of various antioxidative enzymes, such as SOD, CAT, and GST, exhibited an increase at higher mercury concentrations, with the exception of GPX activity, which decreased significantly in a dose‐dependent manner (p < 0.05). Pro‐inflammatory cytokine transcription levels, specifically TNF‐α, IL‐1β, IL‐6, and COX‐2, were significantly upregulated in a dose‐dependent manner in the mercuric (II) chloride (HgCl2) treatment group compared with the control group. TNF‐α protein expression was notably elevated in the larvae group treated with 300 and 400 nM HgCl2.