Phytotoxic effects of the cyanobacterial neurotoxin anatoxin-a: Morphological, physiological and biochemical responses in aquatic macrophyte, Ceratophyllum demersum

Anatoxin-a is one of the common and major cyanobacterial neurotoxins acting as a powerful agonist at nicotinic acetylcholine receptors (nAChR). In recent years, the toxin has become the focus of public attention, due to the mass development of cyanobacteria (cyanobacterial blooms) in freshwater bodies triggered by eutrophication and climate change. Anatoxin-a is suspected to have a distinct toxic mechanism depending on physiological and nervous systems in exposed organisms. The numerous researches have been actively conducted with respect to the toxic effects of anatoxin-a on mammals; however, little research has aimed at its possible effects on aquatic plants, wherein well-structured nervous system is absent with the lack of various components of the acetylcholine mechanism. In this study, submerged macrophyte Ceratophyllum demersum (C demersum) was adopted to examine the effects of anatoxin-a on morphological (growth), physiological (photosynthetic pigment contents) and biochemical (hydrogen peroxide level, biotransformation and antioxidative enzymes) responses in the aquatic plant at environmentally relevant concentrations (0.005, 0.05, 0.5, 5 and 50 mu g/L). The significant elevation of antioxidative enzymes in parallel with increased formation of hydrogen peroxide appeared from 0.5 mu g/L of anatoxin-a. In the measurement of photosynthetic pigments, the decrease in chlorophyll a content was detected at 5 and 50 mu g/L, whereas the increase in carotenoids/total chlorophyll was observed from 0.05 mu g/L. Accordingly, the alteration in growth was manifested in the presence of 5 and 501 mu g/L of anatoxin-a. The results clearly indicate that anatoxin-a can disrupt homeostasis of C demersum through induction of oxidative stress; furthermore this aquatic plant possesses effective defense mechanisms to cope with low concentrations of anatoxin-a. (C) 2013 Elsevier Ltd. All rights reserved.