Intoxication and biochemical responses of freshwater snail Bellamya aeruginosa to ethylbenzene

No acute toxic data of ethylbenzene on gastropod is available in literature. In the present study, the acute toxicity of ethylbenzene was assessed on a freshwater snail Bellamya aeruginosa, which was exposed to ethylbenzene concentration from 1 to 100 mg/L for 96 h. No mortality occurred, but a manifestation of intoxication (distress syndrome) was observed in part of exposed snails, and meanwhile, another part was moved normally. The distress syndrome showed clear dose- and time-dependent effects, and the 96-h EC₅₀ value for distress syndrome was 13.3 mg/L in snail. The biochemical responses induced by ethylbenzene to the snail, including acetylcholinesterase (AChE) in the whole body and superoxide dismutase (SOD), catalase (CAT), glutathione S-transferases (GST), and reduced glutathione (GSH) in the hepatopancreas, were evaluated both for distressed snail and moved snail. The AChE activity of distressed snail was all inhibited more than 45 %, and the inhibition of AChE activity in the moved snail was all less than 30 % and more than 20 %, demonstrating that ethylbenzene exerted nervous toxicity to both distressed snail and moved snail. Meanwhile, the difference for AChE activity between the two different response snails was significant. Among the antioxidant biomarkers (SOD, CAT, GST, and GSH), only GST displayed significant difference between the distressed snail and moved snail. However, the activities of enzymes (SOD, CAT, and GST) in the moved snail were greater than those in the distressed snail, no matter significantly or insignificantly, which indicated that the ability of antioxidant defense in the distressed snail was weaker than that in the moved snail. The findings here reported manifest that ethylbenzene exerted nervous toxicity to snail, and the snail with intoxication response (distress syndrome) presented larger inhibition on AChE activity and weaker antioxidant ability in comparison with the moved snail.