Gramine-induced growth inhibition, oxidative damage and antioxidant responses in freshwater cyanobacterium Microcystis aeruginosa.Aquat Toxicol. 2009 Feb 19; 91(3):262-9.AT
In recent years, the exploration and development of the effective methods of treatment and prevention to algal blooms, especially Microcystis aeruginosa blooms has been an important issue in the field of water environment protection. Allelochemicals (natural plant toxins) are considered promising sources of algicides to control algal blooms. The objective of this study is to determine the inhibitory effects and potential mechanisms of a well-known allelochemical gramine (N,N-dimethyl-3-amino-methylindole) on bloom-forming cyanobacterium M. aeruginosa. The results showed that this indole alkaloid effectively inhibited the growth of M. aeruginosa. The effective concentration causing a 50% inhibition at 3 d (EC(50, 3 d)) increased with the initial algal density (IAD) increasing. When IAD increased from 5x10(4) to 5x10(5)cellsmL(-1), the values of EC(50, 3 d) increased from 0.5 to 2.1mgL(-1). In the cells of M. aeruginosa, gramine caused an obvious increase in the level of reactive oxygen species (ROS). The lipid-peroxidation product malondialdehyde (MDA) increased significantly in gramine-treated cells. The effects of gramine on enzymatic and non-enzymatic antioxidants were in different manners. The activity of superoxide dismutase (SOD) was decreased after gramine exposure. The catalase (CAT) activity was increased after 4h but decreased from 60h. Both the contents and the regeneration rates of ascorbic acid (AsA) and reduced glutathione (GSH) were increased after 4h of exposure to gramine. However, only GSH content was still increased after 40h of exposure. These results suggested that the activation of antioxidants in M. aeruginosa played an important role to resist the stress from gramine at initial time, the inactivation of SOD is crucial to the growth inhibition of M. aeruginosa by gramine, and the phytotoxicity of gramine on M. aeruginosa may be due to oxidative damage via oxidation of ROS.
