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.

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