Coloured filters are used to protect the lens, retina and other ocular tissues against the hazard of light damage and to improve the quality of vision mainly in cases of ocular media opacities. Four types of yellow, amber and orange filters have been designed as tinted glasses, shields and colour covering of spectacles. They were tested on 15 adult patients with partial cataract and on 80 children with congenital pathology (i.e. macular hypoplasia, albinism, aphakia after congenital cataract). The majority of the children had nystagmus. The filters with particular spectral characteristics provide reduction of light intensity in the light-damaging range by at least a factor of five. Optimal filters were selected by examination of visual acuity, contrast frequency sensitivity, glare sensitivity and subjective selection by the patients. The effects of filters were: 11-43% increase in corrected visual acuity, 27-34% increase in contrast sensitivity function (CSF) for all frequencies and a marked reduction in glare sensitivity. All patients reported subjective improvement including reduction of photophobia, eye-strain and eye discomfort. It is concluded that coloured filters are able to contribute substantially to rehabilitation of low-vision patients.
We have reproduced the model system containing A2-rhodopsin, NR-PE, A2-PE, and ATR-dimer-PE in order to study photosensitized damage of rhodopsin within photoreceptor membranes of rod outer segments. We have demonstrated that irradiation of such a system with visible light (400-700 nm) distorts the most important functional property of native visual pigment--its ability to regenerate after addition of 11-cis-retinal in the dark. We have also shown that all-trans-retinal bound to membrane phospholipids and rhodopsin has less photosensitizing activity that free all-trans-retinal.
Photoprotective activity of heteroaromatic compounds (derivatives of 3-hydroxypyridine, amino-6-hydroxybenzothiazole, and 5-hydroxybenzimidazole) was studied in the system of UV-induced cardiolipin peroxidation. Although all three compounds had the antioxidant effect during free radical oxidation of luminol, only derivatives of amino-6-hydroxybenzothiazole and 5-hydroxybenzimidazole inhibited the process of UV-induced lipid peroxidation. The 3-hydroxypyridine derivative did not inhibit UV-induced cardiolipin peroxidation, which was probably related to degradation of this compound under the influence of UV light and formation of degradation products that cannot inhibit free radical processes.
The functioning of visual rhodopsin as a photoelectric generator has been demonstrated with a direct method. Photoreceptor discs were incorporated into a phospholipid-impregnated collodion film. Illumination' of the resulting system with continuous light was found to induce formation of a n electric potential (the disc-free side positive) that was measured with two electrodes separated by the film. A photopotential exceeding 40 mV was shown. It dissipated before the light source was switched off. A 15 ns 530-nm laser flash induced the formation of a photopotential of up to 35 mV whose appearance was preceded with a small oppositely directed electrogenic phase. This 'negative' photoresponse took less than 200 ns. The 'positive' photoresponse was composed of at least two phases (tllz about 500 ps and several milliseconds). The latter was shown to correlated with formation of metarhodopsin 11.A 347-nm laser flash added after a 530-nm flash resulted in a photoelectric effect similar to that initiated by 530-nm flash but of opposite direction. The 347-nni rcsponse was completely abolished by hydroxylamine preventing the accumulation of metarhodopsin 11. The response at 530 nm proved to be hydroxylamine-resistant. Both the amplitude and the decay time of the flash-induced potential were maximal in the response to the first flash, each subsequent flash being less effective than the preceding one. Flashes were found to c a w acceleration of the photopotential decay. The latter effect proved to be due to a increase of membrane conductance that dcveloped faster than in 50 ms. Addition of 1 1-cis retinal after illumination improved the amplitude of the photoresponse but not the conductance. The light-induced increase in conductance was insensitive to hydroxylamine.It is suggested that a function of visual rhodopsin consists in generating a potential difference across the photoreceptor disc membrane which responds with a increase in membrane permeability to a rise of the membrane potential. A possible role of an electric breack-down of the membrane, induced by the rhodopsin-generated local or partially delocalized electric field has been discussed.Chronologically, the first idea about the biological function of bacteriorhodopsin was photoreception [ I , 21. Such an assumption seemed to be reasonable since it was known that phototaxis is inherent in Halobacteviu containing bacteriorhodopsin. However, the whole development of the bacteriorhodopsin study clearly showed that this pigment is a lightdependent H + pump. Recently in this group it was revcaled that the role of bacteriorhodopsin in the positive phototaxis is very indirect being confined to generation of ADH the level of which is monitored by an intracellular A&-measuring system producing a signal for taxis [3].As to animal (visual) rhodopsin, its direct involvement in photoreception in unquestionable. The problem is how rhodopsin fulfils the photoreceptor function. In this paper we would like to describe experiments indicating that visual rhodopsin, like its bacteria...
For the first time, it was found that the hormone melatonin exhibited antiglycation activity in vitro. It was shown that melatonin significantly slowed down the accumulation of fluorescent Schiff adducts formed as a result of BSA modification in the presence of high concentration of fructose. It was noted that, unlike the fructosylation reaction, melatonin did not affect the process of modification of BSA by methylglyoxal. We assume that melatonin is able to inhibit the development of the Maillard reaction but does not affect the process of BSA modification by reactive carbonyls.
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