Implication of reactive oxygen species and mitochondrial dysfunction in the early stages of plant programmed cell death induced by ultraviolet-C overexposure.

摘要: Recent studies have suggested that ultraviolet-C (UV-C) overexposure induces programmed cell death (PCD) in Arabidopsis thaliana (L.) Heynh, and this process includes participation of caspase-like proteases, DNA laddering as well fragmentation the nucleus. To investigate possible early signal events, we used microscopic observations to monitor vivo behaviour mitochondria, production localization reactive oxygen species (ROS) during protoplast PCD induced by UV-C. A quick burst ROS was detected when protoplasts were kept continuous light after UV-C exposure, which restricted chloroplasts adjacent mitochondria. Pre-incubation with ascorbic acid (AsA, antioxidant molecule) or 3-(3, 4-dichlorophenyl)-1, 1-dimethylurea (DCMU, an inhibitor photosynthetic electron transport) decreased partially protected from PCD. mitochondrial transmembrane potential (MTP) loss occurred prior death; thereafter, mitochondria irregularly clumped around aggregated other places within cytoplasm, movement concomitantly blocked. Pre-treatment permeability transition pores (MPTP), cyclosporine (CsA), effectively retarded decrease MTP reduced percentage undergoing overexposure. Our results suggest changes distribution mobility play important roles UV-induced plant PCD, is good accordance what has been reported many types apoptotic death, both animals plants.