Effect of cardiac glycosides from Nerium indicum on feeding rate, digestive enzymes activity and ultrastructural alterations of hepatopancreas in Pomacea canaliculata.

Cardiac glycosides from Nerium indicum showed potent molluscicide activity against Pomacea canaliculata (GAS), but the toxicological mechanism is still far less understood. Effects of sublethal treatments of cardiac glycosides on feeding rate, digestive enzymes and ultrastructural alterations of the hepatopancreas in GAS were evaluated in this study. Exposure of GAS to sublethal concentrations of cardiac glycosides resulted in a significant reduction of feeding rate of GAS. The amylase, cellulose and protease activity were increase significantly at the end of 24 h followed by significant inhibition after 48 h of exposure while lipase activity was not affected significantly at the end of 24 h followed by a significant inhibition after 48 h of exposure during experimental period. The main ultrastructural alterations of hepatopancreas observed in snails under cardiac glycosides treatment comprised disruption of nuclear membrane, increased vesiculation and dilatation of endoplasmic reticulum, and vacuolization and swelling of mitochondrial compared to the untreated GAS. These results, for the first time, provide systematic evidences showing that cardiac glycosides seriously impairs the hepatopancreas tissues of GAS, resulting in inhibition of digestive enzymes activity and feeding rate and cause GAS death in the end.

Molluscicidal activity of cardiac glycosides from Nerium indicum against Pomacea canaliculata and its implications for the mechanisms of toxicity.

Cardiac glycosides from fresh leaves of Nerium indicum were evaluated for its molluscicidal activity against Pomacea canaliculata (golden apple snail: GAS) under laboratory conditions. The results showed that LC(50) value of cardiac glycosides against GAS was time dependent and the LC(50) value at 96 h was as low as 3.71 mg/L, which was comparable with that of metaldehyde at 72 h (3.88 mg/L). These results indicate that cardiac glycosides could be an effective molluscicide against GAS. The toxicological mechanism of cardiac glucosides on GAS was also evaluated through changes of selected biochemical parameters, including cholinesterase (ChE) and esterase (EST) activities, glycogen and protein contents in hepatopancreas tissues of GAS. Exposure to sublethal concentrations of cardiac glycosides, GAS showed lower activities of EST isozyme in the later stages of the exposure period as well as drastically decreased glycogen content, although total protein content was not affected at the end of 24 and 48 h followed by a significant depletion at the end of 72 and 96 h. The initial increase followed by a decline of ChE activity was also observed during the experiment. These results suggest that cardiac glycosides seriously impair normal physiological metabolism, resulting in fatal alterations in major biochemical constituents of hepatopancreas tissues of P. canaliculata.