title: Cadmium-induced oxidative stress and response of the ascorbate-glutathione cycle in Bechmeria nivea (L.) Gaud.
abstract: Bechmeria nivea (L.) Gaud. (ramie) seedlings subjected to a series of cadmium (Cd) concentrations (0, 1, 3 and 7 mg l(-1)) over a 10d period were investigated with regard to the uptake and distribution of Cd, its effect on membrane lipid and chlorophyll synthesis, and response of the ascorbate-glutathione cycle in both leaves and roots. Increased Cd level in the medium resulted in a significant enhancement of Cd concentration in tested plants, with most accumulation in roots. Ramie under Cd stress exhibited increased level of lipid peroxidation, as was evidenced by the increased malondialdehyde content (MDA, an index of lipid peroxidation) in leaves and roots. Shorter exposure to lower Cd concentrations (1 and 3 mg l(-1)) led to a stimulation of chlorophyll synthesis, while longer exposure and higher Cd concentration (7 mg l(-1)) led to a remarkable breakdown of chlorophyll, suggesting that Cd caused oxidative stress in ramie. The antioxidant system as represented by the ascorbate-glutathione pathway was clearly activated following Cd exposure. An overall increase in the metabolite levels and major constituting enzyme activities (ascorbate peroxidase APX and glutathione reductase GR) was observed in ramie treated with 1 and 3 mg l(-1) Cd throughout the entire experimental period, while prolongation of exposure to 7 mg l(-1) Cd resulted in decrease of GR activity and GSH pool in roots which may limit the operation of the whole cycle. Results suggest that Cd-induced oxidative damage in ramie is closely associated with the efficiency of its intrinsic antioxidant mechanisms and the accelerated operation of ascorbate-glutathione cycle provides ramie with enhanced Cd-stress tolerance.
authors.affiliation: College of Environmental Science and Engineering, Hunan University, Changsha 410082, China.
authors.forename: Yunguo
authors.initials: Y
authors.lastname: Liu
authors.forename: Xin
authors.initials: X
authors.lastname: Wang
authors.forename: Guangming
authors.initials: G
authors.lastname: Zeng
authors.forename: Dan
authors.initials: D
authors.lastname: Qu
authors.forename: Jiajia
authors.initials: J
authors.lastname: Gu
authors.forename: Ming
authors.initials: M
authors.lastname: Zhou
authors.forename: Liyuan
authors.initials: L
authors.lastname: Chai
mesh_terms: D000975:Antioxidants / Q000378:metabolism; D060387:Ascorbate Peroxidases; D001205:Ascorbic Acid / Q000378:metabolism; D001673:Biodegradation, Environmental; D002104:Cadmium / Q000633:toxicity*; D002734:Chlorophyll / Q000378:metabolism; D003683:Dehydroascorbic Acid / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress; D010544:Peroxidases / Q000378:metabolism; D018515:Plant Leaves / Q000187:drug effects / Q000378:metabolism; D018517:Plant Roots / Q000187:drug effects / Q000378:metabolism; D012989:Soil Pollutants / Q000633:toxicity*; D027003:Urticaceae / Q000187:drug effects* / Q000378:metabolism
chemical_list: D000975:Antioxidants; D012989:Soil Pollutants; D002104:Cadmium; D002734:Chlorophyll; D008315:Malondialdehyde; D010544:Peroxidases; D060387:Ascorbate Peroxidases; D005980:Glutathione Reductase; D005978:Glutathione; D001205:Ascorbic Acid; D019803:Glutathione Disulfide; D003683:Dehydroascorbic Acid