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 inCdCl₂-treated detached rice leaves increased with increasingdurationof incubation in the light. Cd toxicity was followed by measuring the decreasein chlorophyll and protein. CdCl₂ was effective in inducing toxicityand increasing lipid peroxidation of detached rice leaves under both light anddark conditions. These effects were also observed in rice leaves treated withCdSO₄, indicating that the toxicity was indeed attributed to cadmiumions. Superoxide dismutase (SOD), ascorbate peroxidase (APOD), and glutathionereductase (GR) activities were reduced by excess CdCl₂ in the light.The changes in catalase and peroxidase activities were observed inCdCl₂-treated rice leaves after the occurrence of toxicity in thelight. Free radical scavengers reduced CdCl₂-induced toxicity and atthe same time reduced CdCl₂-induced lipid peroxidation and restoredCdCl₂-decreased activities of SOD, APOD, and GR in the light. Metalchelators (2,2-bipyridine and 1,10-phenanthroline) reducedCdCl₂ toxicity in rice leaves in the light. The reduction ofCdCl₂ toxicity by 2,2-bipyridine (BP) is closely associatedwith a decrease in lipid peroxidation and an increase in activities ofantioxidative enzymes. Furthermore, BP-reduced toxicity of detached riceleaves,induced by CdCl₂, was reversed by adding Fe²⁺ orCu²⁺, but not by Mn²⁺ or Mg²⁺.Reduction of CdCl₂ toxicity by BP is most likely mediated throughchelation of iron. It seems that toxicity induced by CdCl₂ mayrequire the participation of iron.