Revealing the photochemical damage behavior of acidified Xuan paper based on the spectroscopic investigation and principal component analysis.

In museums, there is a huge storage of Xuan paper cultural relics with profound historical and artistic significances. Exploring the photochemical damage behavior of Xuan paper that is generally in acidification, namely its damage mechanisms and laws, is crucial for the preventive lighting protection for paper cultural relics. In this study, the accelerated aging experiments in the range of visible light were conducted on Xuan paper samples with different degrees of acidification. The photochemical damage mechanisms of samples were traced, which is related with the synergistic effects of oxidation and hydrolysis reactions. It can be found that there is an effect of acidification, a long-standing material property of Xuan paper, on its damage, which further defines its preservation state in museums. On this basis, a spectral quantification method of infrared spectra combined with the principal component analysis was proposed to comprehensively analyze the photochemical damage law of Xuan paper in different preservation states. The analysis shows that the effect of acidification degree (pH values), spectra wavelength (λ), and their interaction on the damage to Xuan paper are statistically significant. Furthermore, the fitted mathematical function of pH values and λ is of great importance for evaluating photochemical damage, in order to further develop preventive lighting protection applications.

Case series of photic maculopathy associated with exposure to a plasma flash induced by a femtosecond laser.

BACKGROUND AND OBJECTIVES: Photic maculopathy resulting from laser-induced plasma flash has been rarely reported, and the corresponding mechanism of the injury is still unclear. We present a case series of three patients with bilateral macular injuries produced by exposure to the plasma radiation from femtosecond laser tightly focusing. STUDY DESIGN/MATERIALS AND METHODS: Funduscopic findings were accompanied mainly by optical coherence tomography (OCT) investigation of the macula during the follow-up period. RESULTS: All patients shared similar clinical symptoms soon after the initial injury, including reduced visual acuity and central scotomas. It was acutely characterized by foveolar yellowish faceted lesions upon fundus examination. The main OCT finding in the acute stage was a hyper-reflective area involving all foveolar retinal layers without retinal edema. Repeat OCT evaluation during the latter stages revealed that the retinal changes were reversible, but delineated mild pathology at the outer foveal retina. This retinal structural recovery was accompanied by improvements in visual acuity and central scotomas as well. CONCLUSIONS: Prolonged viewing of a plasma flash induced by a focused femtosecond laser without eye protection may produce persistent damage to the retina. We believe that a photochemical process similar to the mechanism of a solar burn or welder's maculopathy may cause retinal damage in this case series.

[Retinoprotective effects of Retinalamin studied in an experimental model of photochemical damage to rabbit retinas]. / Issledovanie retinoprotektornykh effektov retinalamina v eksperimental'noi modeli fotokhimicheskogo povrezhdeniya setchatki krolika.

Purpose - to investigate functional and morphological effects of peptide bioregulator (Retinalamin) in modeling of photochemical damage to rabbit retina. MATERIAL AND METHODS: The study was conducted on 36 rabbits (72 eyes) randomized into 4 equal groups: two experimental groups received parabulbar injections of Retinalamin («Geropharm¼, Russia) in each eye in dosages of 0.25 mg/kg in a course of 10 days starting from day 1 and day 10 of the experiment, respectively, and two control groups that received injections of normal solution with the same regimen. To simulate photochemical damage to the retina, exposure to light with a wavelength of 405 nm, a power density of 5 mW/cm2 and daily exposure time of 4 h was performed for 20 days. Multifocal and flicker 30 Hz electroretinogram (mfERG and fERG) were recorded, and histological studies of retina samples with quantitative assessment of retinal cells apoptosis by the TUNEL method were conducted before, as well as 10, 20 and 30 days after the start of light exposure. RESULTS: Ophthalmoscopic signs of light-induced retinal degeneration were revealed 6-10 days after start of exposure in all groups. When registering mfERG and fERG in all groups, there was a significant decrease in the amplitude of N1 and P1 peaks, retinal density of the bioelectric response of the P1 component, as well as the amplitude of fERG on days 10 and 20 after the beginning of light exposure (p<0.001 in comparison with the background values), and a slight increase in the indicators on day 30. Histological examination revealed a significant decrease in the number of cells in the outer nuclear layer and an increase in the proportion of apoptotic cells in the outer and inner nuclear layers on days 10 and 20 of the experiment, with a decrease on day 30 (after cessation of light exposure). Comparison of the groups receiving Retinalamin injections from days 1 or 10 of light exposure between themselves and the control groups revealed no significant differences in any of the studied parameters (p>0.05). CONCLUSION: No significant functional and morphological evidence of neuroprotective effects of Retinalamin were found in the model of photochemical damage to rabbit retinas.

Application of Focal Photoinduced Thrombosis for Modeling Spinal Cord Ischemia.

Typical ischemic damage to neurons were detected in the focus of experimental photothrombosis and in the transition zone. They were associated with symptoms of impaired motor functions and dysfunction of pelvic organs. The applied method of focal photothrombosis can be used for simulation of spinal cord ischemia for the development of methods for pharmacological correction and restoration of impaired sensorimotor functions.

The Protective Effects of Blue Light-Blocking Films With Different Shielding Rates: A Rat Model Study.

PURPOSE: To examine light emitting diode (LED)-induced retinal photochemical damage and assess the protective performance of blue light-shielding films with different shielding rates in Sprague-Dawley rats (SD rats). METHODS: SD rats were randomly divided into five groups: blank control (group I), white LED illumination (group II), and white LED illumination combined with shielding of blue light of wavelength 440 nm at 40%, 60%, and 80% (groups III, IV, and V). The illumination was 200 lux. All animals underwent electroretinography (ERG), hematoxylin-eosin (H&E) staining, immunohistochemical (IHC) staining, and transmission electron microscopy (TEM) observation after 14 days of dark-adaptation before illumination, after 14 days of cyclic illumination, and after 14 days of darkness for recovery following illumination. RESULTS: ERG showed retinal functional loss after LED light exposure. However, retinal cell function was partly recovered after a further 2 weeks of dark adaptation. H&E staining and TEM revealed increases in photoreceptor cell death after illumination. IHC staining demonstrated that oxidative stress was associated with retinal injury. Although retinal light injury was discovered in the LED light-exposure groups, shielding 60% of blue light of wavelength 440 nm (bandwidth 20 nm) protected retinas. CONCLUSIONS: Cyclic illumination of low light intensity (200 lux) for 14 days produced retinal degeneration; shielding 60% of blue light may protect retinas from light damage. TRANSLATIONAL RELEVANCE: This study found the effective shielding rate that could protect retinas from light damage when shielding specific narrow-band harmful blue light; thus providing a more normative method for protecting eyes from blue light hazard.

Protect effect of Delphinidin on light induced oxidative damage of retina / 国际眼科杂志(Guoji Yanke Zazhi)

@#AIM: To investigate the mechanism of Delphinidin(Dp)in protecting retinal against light induced oxidative damage.<p>METHODS: All 661W photosensitive cells were treated with 2 000Lx light(48h)and/or different concentrations of Dp(5, 10, 20μmol/L, 24h). Cell activity, intracellular LDH activity, TBARS content and antioxidant enzymes(SOD, GSH-Px, GST)activity were determined respectively. After the healthy SD rats were treated with 3 000 Lx light(24h)and/or Dp \〖100mg/(kg·d)for 4wk\〗, then changes in retinal tissue structure were observed and fluctuations in oxidative stress index(SOD, GSH-Px, GST)were determined.<p>RESULTS: The results of <i>in vitro</i> experiments showed that the cell activity was significantly decreased after irradiation, the LDH activity and TBARS content were increased, and the activity of antioxidant enzyme system were decreased. However, Dp treatment could increase cell viability, decrease LDH activity and TBARS content, and increase the activity of antioxidant enzyme system. <i>In vivo</i> experiments showed that Dp can protect the structural integrity of retina, reduce the content of TBARS in retinal tissue, and increase the activity of SOD, GSH-Px and GST.<p>CONCLUSION: Dp may protect retinal against Photochemical factors -induced oxidative damage by regulating the oxidation-antioxidant system.

Light-induced disulfide dimerization of recoverin under ex vivo and in vivo conditions.

Despite vast knowledge of the molecular mechanisms underlying photochemical damage of photoreceptors, linked to progression of age-related macular degeneration, information on specific protein targets of the light-induced oxidative stress is scarce. Here, we demonstrate that prolonged intense illumination (halogen bulb, 1500 lx, 1-5 h) of mammalian eyes under ex vivo (cow) or in vivo (rabbit) conditions induces disulfide dimerization of recoverin, a Ca(2+)-dependent inhibitor of rhodopsin kinase. Western blotting and mass spectrometry analysis of retinal extracts reveals illumination time-dependent accumulation of disulfide homodimers of recoverin and its higher order disulfide cross-linked species, including a minor fraction of mixed disulfides with intracellular proteins (tubulins, etc.). Meanwhile, monomeric bovine recoverin remains mostly reduced. These effects are accompanied by accumulation of disulfide homodimers of visual arrestin. Histological studies demonstrate that the light-induced oxidation of recoverin and arrestin occurs in intact retina (illumination for 2 h), while illumination for 5 h is associated with damage of the photoreceptor layer. A comparison of ex vivo levels of disulfide homodimers of bovine recoverin with redox dependence of its in vitro thiol-disulfide equilibrium (glutathione redox pair) gives the lowest estimate of redox potential in rod outer segments under illumination from -160 to -155 mV. Chemical crosslinking and dynamic light scattering data demonstrate an increased propensity of disulfide dimer of bovine recoverin to multimerization/aggregation. Overall, the oxidative stress caused by the prolonged intense illumination of retina might affect rhodopsin desensitization via concerted disulfide dimerization of recoverin and arrestin. The developed herein models of eye illumination are useful for studies of the light-induced thiol oxidation of visual proteins.

Black rice anthocyanidins prevent retinal photochemical damage via involvement of the AP-1/NF-κB/Caspase-1 pathway in Sprague-Dawley rats.

The effects of black rice anthocyanidins (BRACs) on retinal damage induced by photochemical stress are not well known. In the present study, Sprague-Dawley rats were fed AIN-93M for 1 week, after which 80 rats were randomly divided into two groups and treated with (n = 40) or without BRACs (n = 40) for 15 days, respectively. After treatment, both groups were exposed to fluorescent light (3,000 ± 200 lux; 25°C), and the protective effect of dietary BRACs were evaluated afterwards. Our results showed that dietary BRACs effectively prevented retinal photochemical damage and inhibited the retinal cells apoptosis induced by fluorescent light (p < 0.05). Moreover, dietary BRACs inhibited expression of AP-1 (c-fos/c-jun subunits), up-regulated NF-κB (p65) expression and phosphorylation of IκB-α, and decreased Caspase-1 expression (p < 0.05). These results suggest that BRACs improve retinal damage produced by photochemical stress in rats via AP-1/NF-κB/Caspase-1 apoptotic mechanisms.

Black rice anthocyanidins prevent retinal photochemical damage via involvement of the AP-1/NF-kappaB/Caspase-1 pathway in Sprague-Dawley Rats

The effects of black rice anthocyanidins (BRACs) on retinal damage induced by photochemical stress are not well known. In the present study, Sprague-Dawley rats were fed AIN-93M for 1 week, after which 80 rats were randomly divided into two groups and treated with (n = 40) or without BRACs (n = 40) for 15 days, respectively. After treatment, both groups were exposed to fluorescent light (3,000 +/- 200 lux; 25degrees C), and the protective effect of dietary BRACs were evaluated afterwards. Our results showed that dietary BRACs effectively prevented retinal photochemical damage and inhibited the retinal cells apoptosis induced by fluorescent light (p < 0.05). Moreover, dietary BRACs inhibited expression of AP-1 (c-fos/c-jun subunits), up-regulated NF-kappaB (p65) expression and phosphorylation of IkappaB-alpha, and decreased Caspase-1 expression (p < 0.05). These results suggest that BRACs improve retinal damage produced by photochemical stress in rats via AP-1/NF-kappaB/Caspase-1 apoptotic mechanisms.

Protective Effect of Yiqimingmu Oral Solution on Rats' Retina with Photochemical Damage / 中国药房

OBJECTIVE:To observe the protective effect of the traditional Chinese medicine Yiqimingmu oral solution on photochemical damage of retina in rats. METHODS:SD rats were divided into four groups randomly:negative control group, model group, low dose Yiqimingmu oral solution group and high dose Yiqimingmu oral solution group. All the groups except the control one were continually exposed to Lux (1 900?106.9) green fluorescent light for 24 hours to establish retinal photochemical damage model. The low dose and high dose groups were administered intragastrically with Yiqimingmu oral solution (15mL?kg-1?d-1 and 30mL?kg-1?d-1) 7 days before light expose. Normal saline solution was administered intragastrically in control and model group. At 6 hours and 6, 14 days after light expose, the content of malandialdehyde (MDA) and activity of SOD in rats' retina were measured. The histopathologic changes were observed by transmission electron microscopy and light microscopy. RESULTS:At 6 and 14 days after light expose, the activity of SOD in Yiqimingmu solution high dose group were higher than in the model control group(P

Protective effects of taurine on retina photochemical damage in rats / 第三军医大学学报

Objective To establish the animal model of photochemical damage and investigate the protective effects and mechanism of taurine on the retina photochemical damage in rats. Methods Fifty rats were randomly divided into normal control group, light damage group and 4% taurine supplementation group. After 15 day cyclic light and 24-hour dark adaptation, the last two groups were exposed to (3000?200) lx transmitted by six cold white lights. After 24-hour exposure, the rats were stayed in darkness. The retinal morphology was detected through light and electron microscope and the retinal function was detected by Scot-ERG. The concentration of MDA and the activity level of SOD/GSH-px were measured. Results In light damage group, the a and b amplitude (Aa/Ab) were significantly decreased, but in taurine group, except the decreased Aa, others were of no significant changes. The retina inner and outer segments were swollen and in disorder after exposure, the outer nuclear layer got thinner than that of control. The mitochondria in light damage group was swollen, but in taurine group changes were less significant. After exposure, the concentration of MDA in retina was markedly increased in light damage group and the activity level of SOD/GSH-px were decreased, but in taurine group MDA slightly increased and SOD/GSH-px was up-regulated but of no significance. Conclusion Dietary supplementation with 4% taurine partially protected photoreceptor from degeneration, which might correlate with the antioxidation and inhibition of free radical character of taurine.