Chemical contaminants and environmental stressors induced teratogenic effect in aquatic ecosystem - A comprehensive review

Abstract

Aquatic environments, including marine and freshwater ecosystems, are vital for ecological balance and biodiversity. The rising global demand for aquaculture products necessitates increased production, with intensified aquaculture practices posing significant environmental risks. This review explores the pathways through which chemical pollutants, heavy metals, pharmaceuticals, and environmental stressors induce teratogenic effects in aquatic species. The review highlights the impact of pesticide include triazine herbicides, organophosphate and organochlorine insecticides, and carbamates on aquatic life, emphasizing their interference with endocrine systems and developmental processes. Heavy metals like mercury, lead, cadmium, arsenic, and chromium are noted for their persistence and bioaccumulative properties, disrupting cellular and hormonal functions. Pharmaceuticals, including NSAIDs, antibiotics, and chemotherapeutic agents, exert teratogenic effects by disrupting physiological and developmental pathways. Environmental stressors includes temperature fluctuations, salinity variations, pH changes, and oxygen level imbalances exacerbate the teratogenic impact of pollutants. This review highlights the importance of comprehensive environmental management and understanding these complex interactions is essential for formulating efficient strategies to safeguard the effective measures to protect aquatic ecosystems and the biodiversity.

Keywords: Aquatic ecosystem; Endocrine disruption; Oxidative damage; Pollutants; Teratogens.

Graphical abstract

Fig. 1

Main oxidative interactions of chemicals include activation of receptors (AhR, CAR, PXR), transcription factors (Nrf2, NF-κB), and enzymes (CYP450, GST), leading to ROS production and cellular oxidative stress responses.

Fig. 2

Mechanism of ROS-induced teratogenicity in aquatic species, highlighting pesticide impact, oxidative stress, and apoptosis pathways via caspase activation.

Fig. 3

Methionine cycle and methylation pathway in aquatic species, showing the roles of homocysteine, S-adenosyl methionine, and methionine synthase in DNA, protein, and lipid methylation processes.

Fig. 4

Mechanism of NSAIDs-induced epithelial damage in aquatic species, illustrating the inhibition of COX-1 and COX-2, leading to mucosal injury, impaired blood flow, and increased leukocyte adhesion.

Fig. 5

Pollutants and environmental stressors in aquatic ecosystems lead to oxidative stress, altering water quality and impacting aquatic species. Sources include industrial discharge, medical waste, pesticides, and melting glaciers, resulting in reactive oxygen species (ROS) formation and biological damage.