Exposure to tebufenpyrad interrupts histo-architecture and fatty acid compositions of carpet shell clam <i>Ruditapes decussatus</i>

Tebufenpyrad (TUBF) is classified as a pyrazole acaricide and insecticide and is extensively utilized in greenhouse environments in several countries. Nevertheless, limited data exists regarding the potential reproductive toxicity of TUBF, particularly in non-target species. In this study, the fatty acid (FA) composition, the histopathology aspects, and redox status were assessed in the digestive gland of the clam <i>Ruditapes decussatus</i> following short-term exposure (96 h) to a series of concentrations (50, 100, and 200 µgL^-1) of TUBF. Our findings indicated that TUBF induced oxidative stress, as evidenced by elevated levels of hydrogen peroxide (H₂O₂), malondialdehyde (MDA), and lipid peroxides (LOOH) in the treated groups. TUBF was also found to disrupt the enzymatic (catalase) and non-enzymatic (reduced glutathione) antioxidant defense systems. Additionally, TUBF was found to disrupt the FA composition. Overall, alterations in saturated (SFA), monounsaturated (MUFA), and polyunsaturated (PUFA) fatty acids, including certain essential FAs (such as LA, ARA, EPA, and DHA), exhibited differential compensatory/adaptive processes in <i>R. decussatus</i> depending on the concentration of TUBF. Furthermore, both examined organs showed various histological impairments, such as lipofuscin accumulation, infiltrative inflammations, and changes in digestive tubules, which provide additional evidence of TUBF toxic effects.