Ultrastructural Alterations in Melanopsis praemorsa (Linnaeus, 1758) (Gastropoda: Prosobranchia) Induced by Imidacloprid and the Protective Role of Ascorbic Acid.

Imidacloprid, a neonicotinoid pesticide widely used for controlling agricultural pests, is known to exert toxic effects on non-target aquatic organisms. This study aimed to investigate the toxicological impact of imidacloprid and the potential protective effect of an antioxidant, ascorbic acid, in the freshwater snail Melanopsis praemorsa. Eight experimental groups were established: two controls; three groups exposed to imidacloprid at concentrations of 4.016, 40.16, and 80.32 μg/L; and three groups co-exposed to imidacloprid and ascorbic acid. Test organisms were maintained under defined conditions for 21 days. Following exposure, tissues from the digestive gland, mantle, and foot were dissected and examined at the ultrastructural level using transmission electron microscopy (TEM). Imidacloprid concentrations in the test medium were quantified via LC-MS/MS analysis. Ultrastructural examination revealed pronounced cytopathological alterations in imidacloprid-exposed groups, including cytoplasmic vacuolization, disrupted mitochondrial cristae, degeneration of the rough endoplasmic reticulum and Golgi apparatus, nuclear abnormalities, necrosis, and cellular lysis. In contrast, co-treatment with ascorbic acid led to a noticeable reduction in the severity of these lesions. These findings demonstrate that imidacloprid induces significant tissue damage in Melanopsis praemorsa, while the protective effect of ascorbic acid highlights the potential of this species as a promising bioindicator for monitoring aquatic pesticide contamination.