title: Induction of oxidative stress and antioxidative mechanisms in Phaseolus vulgaris after Cd application.
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 microM CdSO(4)). 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.
authors.affiliation: Environmental Biology, Centre for Environmental Sciences, Limburgs Universitair Centrum, Universitaire Campus, B-3590 Diepenbeek, Belgium.
authors.forename: Karen
authors.initials: K
authors.lastname: Smeets
authors.forename: Ann
authors.initials: A
authors.lastname: Cuypers
authors.forename: Ann
authors.initials: A
authors.lastname: Lambrechts
authors.forename: Brahim
authors.initials: B
authors.lastname: Semane
authors.forename: Peter
authors.initials: P
authors.lastname: Hoet
authors.forename: André
authors.initials: A
authors.lastname: Van Laere
authors.forename: Jaco
authors.initials: J
authors.lastname: Vangronsveld
mesh_terms: D000975:Antioxidants / Q000378:metabolism; D060387:Ascorbate Peroxidases; D002104:Cadmium / Q000378:metabolism / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D007521:Isocitrate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008291:Malate Dehydrogenase / Q000378:metabolism; D018384:Oxidative Stress; D009195:Peroxidase / Q000378:metabolism; D010544:Peroxidases / Q000378:metabolism; D027805:Phaseolus / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D018515:Plant Leaves / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D013997:Time Factors
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D002104:Cadmium; D008291:Malate Dehydrogenase; D007521:Isocitrate Dehydrogenase; D010544:Peroxidases; C121048:guaiacol peroxidase; D060387:Ascorbate Peroxidases; D009195:Peroxidase; D005980:Glutathione Reductase; D005978:Glutathione; D019803:Glutathione Disulfide