Inhibition of the mitochondrial respiratory components (Complex I and Complex III) as stimuli to induce oxidative damage in Oryza sativa L. under thiocyanate exposure.

Repression of the electron transport in mitochondria can result in an increase of reactive oxygen species (ROS) in plant cells. This study was to clarify inhibition of the mitochondrial respiratory components (Complex I and Complex III) as stimuli to induce oxidative damage in Oryza sativa L. under exogenous SCN exposure with special emphasis on lipid peroxidation, protein modification, and DNA damage at the biochemical and molecular levels. Our results showed that enzymatic activity and gene expression of cytochrome c reductase (Complex III) in roots and shoots of rice seedlings were significantly repressed by SCN exposure, where significant inhibition of NADH dehydrogenase (Complex I) was only detected in shoots, suggesting that Complex III was the main target attacked by SCN ligand in rice roots, and both components were arrested in shoots. ROS analysis in tissues indicated that SCN exposure caused significant accumulation of HO and O, increased malondialdehyde (MDA) and carbonyl content in rice materials in a dose-dependent manner. Similarly, a remarkable elevation of electrolyte leakage was observed in rice tissue samples. The comet assay indicated a positive correlation between DNA damage and external SCN exposure. In conclusion, oxidative burst generated from the inhibitions of the electron transport in mitochondria in rice seedlings under SCN exposure can cause lipid peroxidation, protein modification and DNA damage, eventually decreasing fresh weight of rice seedlings.