Spartina densiflora is an invasive cordgrass that is colonizing new habitats and ousting indigenous species in pro-oxidative environments like cadmium-polluted salt marshes in the Odiel estuary (Spain). The aim of our study was to characterize its antioxidative system in order to find out if the system underlies the tolerance of S. densiflora to cadmium toxicity. S. densiflora plants were firstly evaluated to ascertain its antioxidative status in the natural habitat and then they were cultured in the laboratory in unpolluted sand for 28 days. Throughout this period, plants acclimatized and oxidative stress markers reached stable low levels. Then, S. densiflora plants were exposed to cadmium concentrations (10, 100 and 1000 microM Cd) for another 28 days. Higher Cd content in leaves was related to higher level of reactive oxygen species (ROS) causing important oxidative cell damage (lipid peroxidation and lower chlorophyll content). However, S. densiflora possesses a well-organized and appropriately modulated antioxidative defense system which comprises enzymatic activities of guaiacol peroxidase (EC 1.11.1.7), catalase (EC 1.11.1.6), ascorbate peroxidase (EC 1.11.1.11) and superoxide dismutase (EC 1.15.1.1) coupled with the activation of the ascorbate cycle, including enzymatic activities of glutathione reductase (EC 1.6.4.2), dehydroascorbate reductase (EC 1.8.5.1) and monodehydroascorbate reductase (EC 1.6.5.4). This activation was sufficient to reduce Cd-induced ROS accumulation and oxidative damage caused by the lowest Cd-concentrations, but not by the highest Cd-concentration (1000 microM). Nevertheless, the antioxidant system seems to be efficient to achieve a tolerance to cadmium toxicity, allowing normal plant development, even at the presence of highest Cd concentration.

Spartina densiflora, an invader cordgrass living in polluted salt marshes of the Odiel estuary (SW Spain), was collected and cultured under controlled laboratory conditions. After acclimation to non-polluted soils for 28 days, both metabolites and enzymes activities used as indicators of oxidative stress were reduced significantly. Then, plants were exposed to 500 and 1000 ppm Fe-ethylenediamine-N,N'-2-hydroxyphenyl acetic acid (EDDHA) for 28 days. Our data demonstrate that iron content in leaves was enhanced by iron exposure. This iron increase caused an enhancement in the concentration of H2O2, hydroperoxides and lipid peroxidation, and a decrease in chlorophyll levels. Thus, iron exposure led to oxidative stress conditions. However, oxidative indicators stabilised after first 2 weeks of exposure, although the highest iron levels in leaves were reached at the end of treatments. Iron exposure induced an enhancement of catalase, ascorbate peroxidase and guaiacol peroxidase activities, together with an increase in total and oxidised ascorbate. This response may be defensive against oxidative stress and thus help to explain why cell oxidative damages were stabilised. Thus, by using a sensitive long-time protocol, iron-dependent oxidative damages may be controlled and even reverted successfully by the activation of the antioxidative defences of S. densiflora. This efficient antioxidative system, rapidly modulated in response to excess iron and other environmental stressors, may account for S. densiflora's successful adaptation to stress conditions in its habitat.