Cadmium toxicity of rice leaves is mediated through lipid peroxidation

Oxidative stress, in relation to toxicity of detached rice leaves, caused by excess cadmium was investigated. Cd content in CdCl2-treated detached rice leaves increased with increasing duration of incubation in the light. Cd toxicity was followed by measuring the decrease in chlorophyll and protein. CdCl2 was effective in inducing toxicity and increasing lipid peroxidation of detached rice leaves under both light and dark conditions. These effects were also observed in rice leaves treated with CdSO4, indicating that the toxicity was indeed attributed to cadmium ions. Superoxide dismutase (SOD), ascorbate peroxidase (APOD), and glutathione reductase (GR) activities were reduced by excess CdCl2 in the light. The changes in catalase and peroxidase activities were observed in CdCl2-treated rice leaves after the occurrence of toxicity in the light. Free radical scavengers reduced CdCl2-induced toxicity and at the same time reduced CdCl2-induced lipid peroxidation and restored CdCl2-decreased activities of SOD, APOD, and GR in the light. Metal chelators (2,2'-bipyridine and 1,10-phenanthroline) reduced CdCl2 toxicity in rice leaves in the light. The reduction of CdCl2 toxicity by 2,2'-bipyridine (BP) is closely associated with a decrease in lipid peroxidation and an increase in activities of antioxidative enzymes. Furthermore, BP-reduced toxicity of detached rice leaves, induced by CdCl2, was reversed by adding Fe2+ or Cu2+, but not by Mn2+ or Mg2+. Reduction of CdCl2 toxicity by BP is most likely mediated through chelation of iron. It seems that toxicity induced by CdCl2 may require the participation of iron.