Methomyl-induced developmental and cardiovascular toxicity in zebrafish via immune response, oxidative stress, and apoptosis.

Abstract

Methomyl, a widely used carbamate pesticide, is frequently detected in aquatic ecosystems, due to its high water solubility and long environmental half-life. Although carbamate pesticides have been implicated in cardiovascular toxicity, the specific effects of methomyl on cardiovascular development remain largely unknown. In this study, we investigated the environmental and developmental effects of methomyl using Danio rerio (zebrafish) as an in vivo model. Methomyl exposure lowered cell viability and morphological abnormalities. Impaired cardiac development and disrupted vascular formation in zebrafish were confirmed using cmlc2:dsRed and fli1a:EGFP transgenic models. Furthermore, blood flow defects and erythrocyte accumulation were observed in gata1:dsRed transgenic model, suggesting compromised circulation. In addition, mpeg1:EGFP model revealed that methomyl activates the innate immune response in zebrafish. Molecular analyses revealed that methomyl exposure altered the expression of key genes involved in cardiac development, angiogenesis, and erythropoiesis, implicating oxidative stress and immune activation as potential underlying mechanisms. Human umbilical vein endothelial cells (HUVECs) were used as an in vitro model. We found that methomyl exhibited vascular toxicity in HUVECs, further supporting its role as a cardiovascular disruptor. These findings provide novel insights into the environmental and toxicological effects of methomyl and highlight its potential risk of accumulation in aquatic systems.