1. Academic Validation
  2. Freshwater pollution: cardiotoxicity effect of perfluorooctane sulfonic acid and neonicotinoid imidacloprid mixture

Freshwater pollution: cardiotoxicity effect of perfluorooctane sulfonic acid and neonicotinoid imidacloprid mixture

  • Environ Toxicol Chem. 2025 Jan 1;44(1):136-145. doi: 10.1093/etojnl/vgae013.
Simone Palazzolo 1 Sabrina Natale 1 Fabiano Capparucci 1 Maria Giovanna Piro 1 Salvatore Cuzzocrea 1 2 Alessio Filippo Peritore 3 Rosalia Crupi 3 Domenico Britti 4
Affiliations

Affiliations

  • 1 Department of Chemical, Biological, Pharmaceutical, and Environmental Science, University of Messina, Messina, Italy.
  • 2 Link Campus University, Rome, Italy.
  • 3 Department of Veterinary Science, University of Messina, Messina, Italy.
  • 4 Department of Health Sciences, "Magna Græcia University" of Catanzaro, Catanzaro, Italy.
Abstract

Perfluorooctanesulfonate (PFOS) is a widely used chemical that accumulates in living things and the environment, especially the aquatic, over time. It is also known as a "forever chemical". Furthermore, different anthropogenic substances are rarely found individually in the environment. Some of these substances are very toxic to aquatic species, such as imidacloprid (IMI), an Insecticide belonging to the neonicotinoid family. The main objectives of this study were to investigate the effect of coexposure of these two contaminants at individual nontoxic concentration. In this study, we first analyzed different nominal concentrations of PFOS (from 0.1 to 10 μM) and IMI (from 75 to 1,000 μM) to highlight the morphological effects at 96 hr postfertilization and subsequently assessed the toxicity of mixture coexposure at both lethal and sublethal levels. Coexposure of PFOS and IMI at two individually nontoxic concentrations resulted in increased toxicity in terms of morphological alterations, accompanied by increased cell death in the pericardium. Molecular investigations confirmed the increased cardiotoxicity accompanied by cell death, showing overexpression of apoptosis-associated genes (Caspase 3, Bax, and Bcl-2.) and a dysregulation of oxidative stress-related genes (cat, sod1, and gstp2). These results suggest that IMI could potentiate PFOS cardiotoxicity on zebrafish embryo development by alteration of antioxidative balance and induced Apoptosis.

Keywords

environment; freshwater; per- and polyfluoroalkyl substances (PFAS); pesticides; pollutants.

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