Biochemical responses to the toxicity of the biocide abamectin on the freshwater snail Physa acuta

• Acute and sublethal effects of ABM to freshwater snail Physa acuta were tested.
• ABM-exposure alters the activities of SOD, CAT, AChE, and NOS in the snail.
• ABM-exposure causes lipid peroxidation in snail viscera.

The toxic effects of abamectin (ABM), an anthelmintic drug, on the snail, Physa Acuta, and the biochemical responses to the exposure stress were evaluated. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), acetylcholinesterase (AChE), and nitric oxide synthase (NOS), and the contents of malondialdehyde (MDA) were determined in snail soft tissues (head, foot, visceral mass, and the mantle) for up to 96 h of exposure to 3.4, 9.6, 19.2, or 27.4 μg L−1 of ABM. The results showed that SOD and GST activities were promoted by ABM-exposure at the earlier periods of treatment (12–48 h) while these activites were inhibited at the end of test. The tendency of CAT activity was similar to that of SOD, but it increased at the end of test. MDA levels of the snail soft tissues increased in all treatment groups, including the recovery group, indicating that lipid peroxidation occurred in snail soft tissues. ABM-exposure inhibited AChE activity. However, NOS activities increased by ABM-exposure. In addition, activities of antioxidant enzymes and AChE from the snail soft tissues resumed the normal levels after 96 h of recovery period, but MDA level did not attain the original level. This study provides information on the biochemical mechanism of ABM toxicity on the snail.