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Summary: The physiological effects of Cd and Cu have been highlighted in several studies over the last years. At the cellular level, oxidative stress has been reported as a common mechanism in both stress situations. Nevertheless, because of differences in their redox-related properties, the origin of the stress and regulation of these effects can be very different. Our results show a specific Cd-related induction of NADPH oxidases, whereas both metals induced lipid peroxidation via the activation of lipoxygenases. With respect to the antioxidative defense system, metal-specific patterns of superoxide dismutases (SODs) were detected, whereas gene expression levels of the H2O2-quenching enzymes were equally induced by both metals. Because monometallic exposure is very unusual in real-world situations, the metal-specific effects were compared with the mechanisms induced when the plants are exposed to both metals simultaneously. Combined exposure to Cd and Cu enhanced some of the effects that were induced when only one metal was applied to the medium. Other specific monometallically induced effects, such as a copper zinc superoxide dismutase (CSD2) downregulation due to Cd, were also sustained in a multipollution context, irrespective of the other monometallic effects. Furthermore, specific multipollution effects were unravelled, as iron superoxide dismutase 1 (FSD1) upregulation in the leaves was significant only when both Cu and Cd were applied. Additional relationships between these treatments and the common and specific stress induction mechanisms are discussed. [Copyright &y& Elsevier]

Abstract: Oxidative stress has been shown to be of great importance in the toxicity of several metals (copper, zinc, …). In this study, the relationship of cadmium phytotoxicity and antioxidative reactions in bean (Phaseolus vulgaris L.) plants was investigated. Eleven-day-old seedlings were exposed to an environmentally realistic concentration of cadmium (2 µM CdSO4). Several biochemical and physiological parameters were influenced even by these low concentrations. At the biochemical level, the antioxidative defence mechanism was significantly activated after 24 h of cadmium exposure. Some enzymes able of quenching reactive oxygen species (syringaldazine peroxidase, EC 1.11.1.7; guaiacol peroxidase, EC 1.11.1.7) as well as enzymes important in the reduction of NAD(P)+ (isocitrate dehydrogenase, EC 1.1.1.42; malic enzyme, EC 1.1.1.40) were significantly elevated by cadmium exposure. Furthermore, the ascorbate–glutathione cycle appeared to be a very important mechanism against cadmium-induced oxidative stress. In leaves, significant increases of ascorbate peroxidase (EC 1.11.1.11) and glutathione reductase (EC 1.6.4.2) and significant changes in the ascorbate and glutathione pool were observed. Morphological and other biochemical parameters (lipid peroxidation) were significantly enhanced 48 h after the start of the cadmium exposure. At the end of the experiment (72 h after the start of the metal treatment), even visual effects, such as chlorosis, were observed. The present data indicate that cadmium, like other metals, induces cellular redox disequilibrium suggesting that an environmentally realistic concentration of cadmium can cause oxidative stress. [Copyright &y& Elsevier]

Abstract: When aiming to evaluate the environmental impact of uranium contamination, it is important to unravel the mechanisms by which plants respond to uranium stress. As oxidative stress seems an important modulator under other heavy metal stress, this study aimed to investigate oxidative stress related responses in Arabidopsis thaliana exposed to uranium concentrations ranging from 0.1 to 100 μM for 1, 3 and 7 days. Besides analyzing relevant reactive oxygen species-producing and -scavenging enzymes at protein and transcriptional level, the importance of the ascorbate–glutathione cycle under uranium stress was investigated. These results are reported separately for roots and leaves in two papers: Part I dealing with responses in the roots and Part II unraveling responses in the leaves and presenting general conclusions. Results of Part I indicate that oxidative stress related responses in the roots were only triggered following exposure to the highest uranium concentration of 100 μM. A fast oxidative burst was suggested based on the observed enhancement of lipoxygenase (LOX1) and respiratory burst oxydase homolog (RBOHD) transcript levels already after 1 day. The first line of defense was attributed to superoxide dismutase (SOD), also triggered from the first day. The enhanced SOD-capacity observed at protein level corresponded with an enhanced expression of iron SOD (FSD1) located in the plastids. For the detoxification of H2O2, an early increase in catalase (CAT1) transcript levels was observed while peroxidase capacities were enhanced at the later stage of 3 days. Although the ascorbate peroxidase capacity and gene expression (APX1) increased, the ascorbate/dehydroascorbate redox balance was completely disrupted and shifted toward the oxidized form. This disrupted balance could not be inverted by the glutathione part of the cycle although the glutathione redox balance could be maintained. [Copyright &y& Elsevier]

Abstract: The cellular redox balance seems an important modulator under heavy metal stress. While for other heavy metals these processes are well studied, oxidative stress related responses are also known to be triggered under uranium stress but information remains limited. This study aimed to further unravel the mechanisms by which plants respond to uranium stress. Seventeen-day-old Arabidopsis thaliana seedlings, grown on a modified Hoagland solution under controlled conditions, were exposed to 0, 0.1, 1, 10 and 100 μM uranium for 1, 3 and 7 days. While in Part I of this study oxidative stress related responses in the roots were discussed, this second Part II discusses oxidative stress related responses in the leaves and general conclusions drawn from the results of the roots and the leaves will be presented. As several responses were already visible following 1 day exposure, when uranium concentrations in the leaves were negligible, a root-to-shoot signaling system was suggested in which plastids could be important sensing sites. While lipid peroxidation, based on the amount of thiobarbituric acid reactive compounds, was observed after exposure to 100 μM uranium, affecting membrane structure and function, a transient concentration dependent response pattern was visible for lipoxygenase initiated lipid peroxidation. This transient character of uranium stress responses in leaves was emphasized by results of lipoxygenase (LOX2) and antioxidative enzyme transcript levels, enzyme capacities and glutathione concentrations both in time as with concentration. The ascorbate redox balance seemed an important modulator of uranium stress responses in the leaves as in addition to the previous transient responses, the total ascorbate concentration and ascorbate/dehydroascorbate redox balance increased in a concentration and time dependent manner. This could represent either a slow transient response or a stable increase with regard to plant acclimation to uranium stress. [Copyright &y& Elsevier]

Abstract: The leaf proteome of 3-week-old Arabidopsis thaliana seedlings exposed for 1 week to low, environmentally realistic Cd concentrations was investigated. The data indicated that at 1μMCd, A. thaliana plants adapted their metabolism to cope with the Cd exposure. As a result, only moderate protein changes were observed. However, at 10μMCd, severe stress was indicated by growth reduction and chlorosis of rosette leaves at the macroscopic level and by lipid peroxidation and enhanced peroxidase activity at the cellular level. Of the 730 reproducible proteins among all gels, 21 were statistically upregulated in response to Cd. These proteins can be functionally grouped into 5 classes: proteins involved in (1) oxidative stress response, (2) photosynthesis and energy production, (3) protein metabolism, (4) gene expression and finally, (5) proteins with various or unknown function. In order to provide greater insight into the mechanisms induced on Cd exposure, a working model is proposed. [Copyright &y& Elsevier]