• Korean Journal of Weed Science
• /
• v.12 no.2
• /
• pp.132-143
• /
• 1992

The study was conducted to find out synergistic effects by interaction on the basis on anatomical changes between paddy rice and weed species by mixture use of oxyfluorfen and bensulfuron at 0, $10^{-6}$ and $10^{-4}$M, respectively. Tissues were sampled at 72 hrs after soaking treatment and prepared for light microscopic examination and sectioned longitudinally and transversely stem into $8{\mu}m$ thick. As the results of microscopic examination, the major response of treated plant involved rupture and constrict in mesophyll cells and epidermal cells, and shrinks in bundle sheath cells by oxyfluorfen and disorganization and swelling in meristems by bensulfuron. Anatomical changes in rice was the least affected by even high concentration and two herbicide mixtures, whereas Echinochloa crus-galli was severely disorganized in meristem regions and ruptured in epidermal cells by mixture use. Monochoria vaginalis was completely ruptured by any treatment concentrations and mixtures. Scirpus juncoides was considerably tolerant to both herbicides and their mixture and was similar to those that occur in rice. Perennial weed, Sagittaria pigmaea was observed vacuolation, non-nucleation of cell, and irregular cell layering but in mixture injury was slight. Cyperus serotinus was severely shrunk and ruptured by mixture treatment. Eventually anatomical variations in all weed species was shown synergistic effect by use of herbicide mixtures.

• Tuberculosis and Respiratory Diseases
• /
• v.60 no.4
• /
• pp.451-463
• /
• 2006

Background : Reactive oxygen species (ROS) take center stage as executers in ventilator-induced lung injury (VILI). The protein with DNA-damage scanning activity, poly (ADP-ribose) polymerase-1 (PARP1), signals DNA rupture and participates in base-excision repair. Paradoxically,overactivation of PARP1 in response to massive genotoxic injury such as ROS can induce cell death through ${\beta}$ -nicotinamide adenine dinucleotide ($NAD^+$) depletion, resulting in inflammation. The purpose of this study is to investigate the role of PARP1 and the effect of its inhibitor in VILI. Methods : Forty-eight male C57BL/6 mice were divided into sham, lung protective ventilation(LPV), VILI, and PARP1 inhibitor (PJ34)+VILI (PJ34+VILI) groups. Mechanical ventilator setting for the LPV group was $PIP\;15cmH_2O$ + $PEEP\;3cmH_2O$ + RR 90/min + 2 hours. The VILI and PJ34+VILI groups were ventilated on a setting of $PIP\;40cmH_2O$ + $PEEP\;0cmH_2O$ + RR 90/min + 2 hours. As a PARP1 inhibitor for the PJ34+VILI group, 20 mg/Kg of PJ34 was treated intraperitoneally 2 hours before mechanical ventilation. Wet-to-dry weight ratio and acute lung injury (ALI) score were measured to determine the degree of VILI. PARP1 activity was evaluated by using an immunohistochemical method utilizing biotinylated NAD. Myeloperoxidase (MPO) activity and the concentration of inflammatory cytokines such as tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 were measured in bronchoalveolar lavage fluid (BALF). Results : In the PJ34+VILI group, PJ34 pretreatment significantly reduced the degree of lung injury, compared with the VILI group (p<0.05). The number of cells expressing PARP1 activity was significantly increased in the VILI group, but significantly decreased in the PJ34+VILI group (p=0.001). In BALF, MPO activity, $TNF-{\alpha}$, $IL-1{\beta}$, and IL-6 were also significantly lower in the PJ34+VILI group (all, p<0.05). Conclusion : PARP1 overactivation plays a major role in the mechanism of VILI. PARP1 inhibitor prevents VILI, and decreases MPO activity and inflammatory cytokines.