Takako Ueda

Protective effect of dipyridamole against lethality and lipid peroxidation in liver and spleen of the ddY mouse after whole-body irradiation

The effects of dipyridamole on radiation damage in the mouse were investigated. Dipyridamole (i.p. 2 mg/mouse) administered 1 h before exposure, protected against gamma-irradiation. Pretreatment significantly decreased the death rate at 30 days from 89 to 33% (p<0.001) after 9 Gy whole-body irradiation. LD50 at 30 days was increased from 6.67 to 7.65 Gy in the dipyridamole pretreated group. The level of thiobarbituric acid reactive substances (TBARS) in the liver and spleen, a measure of free radical initiated liver peroxidation, increased 155, 193, 195, and 236% of control (without irradiation) in liver, and 132, 146, 168, and 276% of control (without irradiation) in spleen on days 2, 4, 7, and 10 after 9 Gy of whole-body irradiation respectively. The TBARS levels in both liver and spleen 2 days after irradiation were reduced to 73 +/- 7 and 60 +/- 19% respectively after dipyridamole treatment (2 mg/mouse, i.p. injection 1 h before exposure). In electron microscopic studies, mitochondria and endoplasmic reticulum in the irradiated mouse liver were swollen, but otherwise appeared normal after dipyridamole treatment. These results suggest that dipyridamole has a protective effect on animal survival 30 days after 60Co gamma-irradiation and inhibits lipid peroxidation - which is thought to play a part in the radiation injury in mouse liver and spleen.

Retinal hazard from blue light emitting diode

PURPOSE To compare the effect of exposure time from a blue(460 nm) light emitting diode(LED) on the morphology of the outer retina and determine conditions where damage occurs. MATERIALS AND METHODS Young adult rhesus monkeys were anesthetized, and received blue LED exposure from a modified slit-lamp. A 3 mm beam of 0.85 mW was imaged onto the retina through a lens positioned before the cornea and exposure damage was determined at time intervals for 12 to 90 min. Fundus photography, fluorescein angiography(FAG), retinal tomography(HRT), and s-cone electororetinogram(S-ERG) were recorded at baseline, 2, and 30 days. RESULTS Two days after 40 min exposure, there was a grey, discolored region, which was over-fluorescent in FAG, and an incresse in HRT and S-ERG corresponding to the site which was exposed to LED light. In histological examination at 30 days, the LED had caused produced a marked disruption of the disks of photoreceptor cells, damaged retinal pigment epithelium(RPE) apical villi, and a loss of RPE melanin after 90 min exposure. CONCLUSION A threshold level was found around 40 min. This morphological damage may impair function and continuous exposure to blue light is potentially dangerous to vision.

Ultraviolet Action Spectrum for Cell Killing of Primary Porcine Lens Epithelial Cells

Ultraviolet Action Spectrum for Cell Killing of Primary Porcine Lens Epithelial Cells: Tsutomu OKUNO, et al. Human Engineering and Risk Management Research Group, National Institute of Occupational Safety and Health, Japan—

UV-B and lipid hydroperoxides promote conjunctival epithelial cell migration

Abstract The idea that sunlight itself may be a major risk factor in certain eye diseases has been widely accepted. Peroxides or radicals arising from UV irradiation may induce factors leading to cell migration. To clarify this relationship further, we have examined the effects of UV radiation and lipid hydroperoxides on cell migration of conjunctival epithelial cells in culture from palpebral, fornical and bulbar regions. The cell migration from each region was enhanced by UV-B irradiation at 50 mJ/cm 2 and linoleic acid hydroperoxide (LHP) at 10 −7 M concentration. In contrast, cell migration was suppressed by UV-B irradiation at 100 mJ/cm 2 and LHP at 10 −5 M. Both UV-B and LHP induced cell migration was also suppressed by a vitamin E and C conjugated antioxidant (EPC-K1) which has radical scavenging activity. These data suggest that reactive oxygen intermediates play a prominent role in cell migration.