Does infrared or ultraviolet light damage the lens?

In daylight, the human eye is exposed to long wavelength ultraviolet radiation (UVR), visible radiation and short wavelength infrared radiation (IRR). Almost all the UVR and a fraction of the IRR waveband, respectively, left over after attenuation in the cornea, is absorbed in the lens. The time delay between exposure and onset of biological response in the lens varies from immediate-to-short-to-late. After exposure to sunlight or artificial sources, generating irradiances of the same order of magnitude or slightly higher, biological damage may occur photochemically or thermally. Epidemiological studies suggest a dose-dependent association between short wavelength UVR and cortical cataract. Experimental data infer that repeated daily in vivo exposures to short wavelength UVR generate photochemically induced damage in the lens, and that short delay onset cataract after UVR exposure is photochemically induced. Epidemiology suggests that daily high-intensity short wavelength IRR exposure of workers, is associated with a higher prevalence of age-related cataract. It cannot be excluded that this effect is owing to a thermally induced higher denaturation rate. Recent experimental data rule out a photochemical effect of 1090 nm in the lens but other wavelengths in the near IRR should be investigated.

Toxicity of ultraviolet radiation exposure to the lens expressed by maximum tolerable dose.

The maximum tolerable dose (MTD2.3:16) for avoidance of cataract on exposure to ultraviolet radiation (UVR)-300 nm in the rat was here estimated at 3.65 kJ/m2. Sprague-Dawley rats were unilaterally exposed to UVR in the 300 nm wavelength region. One week after the exposure, the intensity of forward light scattering was measured. Toxicity for continuous response events can be estimated with MTD. Current safety standards for avoidance of cataract after exposure to UVR are based on a binary response event. It has, however, recently been shown that UVR-induced cataract is a continuous dose-dependent event. MTD provides a statistically well-defined criterion of toxicity for continuous response events.

Lens lactate dehydrogenase inactivation after UV-B irradiation: an in vivo measure of UVR-B penetration.

PURPOSE: To elucidate the spatial distribution of inactivation of lactate dehydrogenase (LDH) in ultraviolet-B radiation (UVR-B)-exposed eyes. To determine the in vivo penetration depth of UVR-B in the lens. METHODS: LDH activity in cornea and lens was investigated with an enzyme histochemical technique. Thirty rats were exposed in vivo to UVR-B of approximately 300 nm, and the eyes were enucleated and frozen at 0, 2, and 6 hours after exposure. LDH activity in frozen sections was determined quantitatively in the corneal epithelium and four different regions in the lens. UVR-B penetration depth was estimated by using a calculated Lambertian absorption coefficient. RESULTS: The LDH activity was decreased in the cornea and the outer anterior lens cortex at all three time points. The average decrease in enzyme activity in the time range was 35% in the cornea and 20% in the outer anterior lens cortex. UVR-B inhibition of LDH was immediate and not dependent on an inflammatory reaction within the eye. Penetration depth, corresponding to 1/e(2) ( approximately 14%) residual UVR-B intensity, was 0.45 mm. CONCLUSIONS: UVR-B does not exhibit any significant effect on LDH activity in the major part of the lens, and this is attributed to the shallow penetration (0.45 mm) of UVR-B into the anterior parts of the lens.

Influence of exposure time for UV radiation-induced cataract.

PURPOSE: It is believed that for a certain ultraviolet radiation (UVR) exposure, the biologic effect depends on the product of irradiance and exposure time (the reciprocity Bunsen-Roscoe law). The purpose of this study was to investigate the validity of the reciprocity law for UVR-induced cataract. METHODS: Two experiments were conducted. In the first one, 100 Sprague-Dawley rats were exposed to UVR divided into five groups according to exposure time: 7.5, 15, 30, 60, and 120 minutes. In the second experiment, 80 Sprague-Dawley rats were exposed to UVR divided into four groups according to exposure time: 5, 7.5, 11, and 15 minutes. All the animals were unilaterally exposed to the same dose of UVR (8 kJ/m(2)) in the 300-nm wavelength region. One week after exposure both lenses were removed to measure the intensity of forward light scattering and for microphotography. Groups were compared by evaluating the difference between exposed and nonexposed eyes. RESULTS: The group exposed to UVR for 5 minutes had the lowest intensity of forward light scattering. The highest intensity of forward light scattering was found in the group that was exposed for 15 minutes. With longer exposure intervals, the intensity of forward light scattering decreased as the exposure time increased. No difference in intensity of forward light scattering was found between the groups exposed for 60 and 120 minutes. CONCLUSIONS; Exposure time strongly influenced cataract formation after low-dose UVR. In this model of UVR-induced cataract, the photochemical reciprocity law was modulated by a biologic response.

In vivo cataract after repeated exposure to ultraviolet radiation.

The purpose of this study was to investigate the effects of repeated close-to-threshold ultraviolet radiation (UVR) doses in the rat lens. Sprague Dawley rats received two UVR exposures (lambda(max) = 300 nm, lambda0.5 = 10 nm) separated by different time intervals. The animals were unilaterally irradiated with 4 kJ m(2-1) UVR in each exposure. The intervals between both exposures were: 6 hr, 1 day, 3 days, 9 days and 30 days. At 1 week after the last exposure both lenses were removed, microphotographs were taken and intensity of forward light scattering was measured. Evaluating the difference between exposed and non-exposed eyes, the forward light scattering in the 6 hr and 1 day interval group was not significantly different. The most intense forward light scattering was found in the group that was allowed 3 days interval between exposures. Thereafter, the intensity of scattering decreased as the time interval between exposures increased. The lowest intensity of forward light scattering was detected in the 30 days interval group. Three days after a UVR exposure, the lens showed the highest sensitivity for a second UVR exposure. One month after the first exposure lenses undergo physiological repair and interactions between exposures seem to decrease.

3 year simvastatin treatment and lens nuclear back scattering.

AIM: To determine if 3 year treatment of hypercholesterolaemia with simvastatin causes an increase of lens nuclear back scattering. METHODS: 160 patients with hypercholesterolaemia in the Scandinavian Simvastatin Survival Study (4S) were followed for 3 years. Half (80) of the patients took simvastatin and half (80) received placebo. The lens was photographed with a Topcon SL-45 slit lamp camera at the beginning and at 1 year intervals. A common lens nuclear area was used for measuring lens nuclear back scattering. RESULTS: Nuclear back scattering increased with age and there was more pronounced scattering in women than in men. Lens nuclear back scattering did not differ significantly between the simvastatin and placebo groups, but the power was low (0.2). Lens nuclear back scattering increased during the study period independently of baseline back scattering, age, and sex for both groups. CONCLUSION: Although no significant difference was found between the simvastatin and placebo groups, the currently available data are insufficient for exclusion of the possibility that taking simvastatin during a 3 year period increases nuclear back scattering. However, a possible minor increase of nuclear back scattering is clinically irrelevant considering known beneficial effects of simvastatin on coronary heart disease.

Repair in the rat lens after threshold ultraviolet radiation injury.

PURPOSE: To investigate the development and recovery of lens damage after in vivo close-to-threshold exposure to ultraviolet B radiation. METHODS: One eye of young, female Sprague-Dawley rats was exposed to 5 kJ/m2 narrowband ultraviolet radiation (UVR) (lambda(max) = 302 nm) for 15 minutes. Groups of rats were killed 1, 7, and 56 days after exposure. The structure of the exposed and nonexposed lenses was examined with light microscopy, scanning electron microscopy, transmission electron microscopy, freeze-fracture, fluorescent membrane staining, and Fourier transform analysis. RESULTS: One day after UVR exposure the lens surface had flakelike opacities. Seven days after exposure, the lens surface appeared opaque and corrugated, and the equatorial cortex had small opacities. At 56 days postexposure, the surface and equator appeared clear, but the cortex had a subtle shell-shaped opacity. At 1 day postexposure, apoptotic cell death occurred in the lens epithelium, but the cortical fibers were normal. At 7 days postexposure, the epithelium and the fibers between the 10th and 40th growth shell below the capsule contained extracellular spaces of different sizes. After 56 days, the epithelial layer appeared normal, and the extracellular spaces had disappeared; but abnormal fibers were found between the 60th and 100th growth shell below the capsule. Fibers above and below the damaged growth shells appeared fully normal. CONCLUSIONS: A close-to-threshold dose of UVR causes cataract, which is largely reversible. The UVR exposure leads to apoptosis in the lens epithelium, and after a latency period of several days, lens fibers are abnormal. Extracellular spaces develop in the epithelium and fibers. Within several weeks after exposure, the epithelium fully recovers and new fibers develop normally. The originally affected fibers are repaired. However, this repair is incomplete, leaving a small zone of enhanced light scattering in the equatorial cortex.

Failure of ascorbate to protect against broadband blue light-induced retinal damage in rat.

BACKGROUND: Excessive generation of free radicals due to light absorption is proposed as the most likely mechanism for photochemical retinal damage. The observed reduction of green light-induced retinal injury after ascorbate treatment is believed to be an antioxidative effect. The aim of the present study was to evaluate the possible protection of ascorbate against blue light-induced photoreceptor damage. METHODS: Cyclic light-reared albino rats were injected intraperitoneally with either ascorbate (1 mg/g body weight) or, as placebo, physiological saline 24 h before and just prior to exposure to blue light. After 20-22 h of dark adaptation, two groups of the rats were exposed in pairs to the blue light (400-480 nm) for 6 h at an average irradiance of 0.7 W/m(2) in the cage. Six days after light exposure, all rats were killed and retinal samples were analyzed. RESULTS: Diffuse blue light irradiation resulted in an uneven distribution of damage in the retina. As judged from the pathological changes in the retina irradiated, no microscopic difference was observed between the two groups. The preserved thickness of the outer nuclear layer was on average 61.3% in the ascorbate-treated and 66.4% in the placebo-treated group. The photoreceptor loss was not significantly different between the two groups. CONCLUSION: The ascorbate did not protect the retina from blue-light induced damage. This favors the assumption that the mechanisms for blue light-induced retinal damage might differ from that for green light.

Lens opacities after repeated exposure to ultraviolet radiation.

PURPOSE: To investigate the effect of the interval between two, near-threshold exposures to ultraviolet radiation (UVR) on cataract development. METHODS: One eye of Sprague-Dawley rats was exposed twice to 4 kJ/m2 narrow band UVR (lambdaMAX=300 nm) for 15 min each. The interval between exposures was 0, 6, 24 or 48 h. One week after the first exposure both lenses were removed for photography and measurement of the intensity of forward light scattering to quantify lens opacities. RESULTS: All exposed lenses developed cataract. Forward light scattering was the same after double exposure with no interval or a 6 h interval. Forward light scattering after a 24 or 48 h interval was nearly twofold greater than that following no interval or a 6 h interval. The exposed lenses in all groups had mild anterior surface opacities and intense equatorial opacities as judged with a stereomicroscope. CONCLUSION: Two, near-threshold UVR exposures at 0 or a 6 h interval produce the same degree of lens opacification. When the second exposure follows 24 or 48 h after the first, lenticular damage increases. Repair processes between 24 and 48 h after exposure appear to be sensitive to UVR, and an additional exposure during this time may aggravate cataract development.

Apoptosis in the rat lens after in vivo threshold dose ultraviolet irradiation.

PURPOSE: To investigate DNA damage in the rat lens after in vivo close-to-threshold exposure to ultraviolet radiation (UVR). METHODS: Sprague-Dawley rats received 5 kJ/m2 UVR (lambdaMAX = 300 nm, lambda0.5 = 10 nm) unilaterally for 15 minutes. Animals were killed at 1, 6, and 24 hours and at 1 week after exposure. DNA-strand breaks were investigated in sagittal paraffin sections using the TdT-dUTP terminal nick-end labeling (TUNEL) technique and propidium iodide for counterstaining. Other lenses were prepared for transmission electron microscopy (TEM). RESULTS: TUNEL-positive nuclei were found at only 24 hours after UVR exposure. About one tenth of the epithelial cell nuclei were TUNEL positive, and affected cells were scattered over the entire epithelium. No TUNEL-positive cells were found at 1 or 6 hours or at 1 week after UVR exposure or in the nonexposed lenses. TEM verified the occurrence of programmed cell death and showed the breakdown of the apoptotic cells by adjacent cells. No signs of necrosis were found. CONCLUSIONS: Threshold-dose UVR induces programmed cell death that peaks 24 hours after exposure and involves the entire epithelium. Dead cells are removed from the epithelium by phagocytosis.

Histochemical determination of lactate dehydrogenase activity in rat lens; influence of different parameters.

PURPOSE: 1. To optimize a histochemical technique for the determination of lactate dehydrogenase activity in rat lens. 2. To determine the distribution of lactate dehydrogenase activity within the lens. 3. To analyse different components of variation in the method. METHODS: A total of 24 six-week-old Sprague-Dawley rats were used. Cryosections of whole eyes were incubated with different media. The influence of incubation time, pH, the concentration of dye, lactate, nicotinamide dinucleotide, phenazine methosulfate, sodium azide, hydrazine and polyvinyl alcohol on the enzyme histochemical reaction was investigated. The staining reactant was nitrobluetetrazolium and the staining density was measured with a microscope-based photometer. RESULTS: The lactate dehydrogenase activity was highest in the epithelium, followed by the nucleus, the anterior cortex, and the posterior cortex. The three largest components of variation in the analyses were rats, sections (including variation in section thickness) and density measurements (including variation within the different regions). CONCLUSION: The composition of the final incubation medium for the detection of lactate dehydrogenase activity in rat lens are similar to that shown for other tissues. Lactate dehydrogenase activity varies in different regions of the lens.

Dose-response function for lens forward light scattering after in vivo exposure to ultraviolet radiation.

BACKGROUND: It is known that different types of radiation, as well as aging and metabolic disorders, can cause cataract. Several epidemiological investigations show a correlation between cataract development and the dose of ultraviolet radiation (UVR) received. It is well established experimentally that exposure of animal eyes to UVR induces cataract. The purpose of the present study was to determine the dose-response function for UVR-induced opacities in the rat lens after in vivo exposure. METHODS: Sprague-Dawley rats received 0.1, 0.4, 1.3, 3, 5, 8 or 14 kJ/m2 UVR (lambda MAX = 300 nm, lambda 0.5 = 10 nm) unilaterally for 15 min. At 1 week after exposure both lenses were removed, photographs were taken and the intensity of forward-scattered light was measured. RESULTS: One week after UVR exposure, opacities occurred on the lens surface, as observed with a microscope. With increased UVR dose the opacities became more intense and occurred also in the equatorial area of the lens, but not in the nucleus. The intensity of forward light scattering increased with increased UVR dose between 3 and 14 kJ/m2. No significant change in intensity of forward light scattering was observed for lower UVR doses. CONCLUSION: The intensity of forward light scattering in the rat lens increase exponentially with increased UVR dose between 0.1 and 14 kJ/m2.

Ablation rate of PMMA and human cornea with a frequency-quintupled Nd:YAG laser (213 nm).

BACKGROUND AND OBJECTIVE: As an alternative to the standard excimer laser used for PRK, we investigated the ablation rate at 213 nm of PMMA, and human corneas under controlled hydration. STUDY DESIGN/MATERIALS AND METHODS: The output of a frequency-quintupled Nd:YAG laser (213 nm) was transformed into a quasi-Gaussian beam. PMMA and corneal lenticules maintained under controlled hydration were ablated until perforation was detected. RESULTS: The ablation rate of PMMA and cornea at 213 nm were similar to that at 193 nm when radiant exposure was below 200 mJ/cm2 and increased gradually between one and two times faster than that at 193 nm when radiant exposure was > 200 mJ/ cm2. CONCLUSIONS: PMMA and cornea ablation at 213 nm are similar to that at 193 nm and are different from that at 248 nm. The difference between PMMA and cornea ablation rates should be considered when using PMMA to test ablated diopter and smoothness for photorefractive surgery.

Long-term development of lens opacities after exposure to ultraviolet radiation at 300 nm.

The long-term development of lens opacities after short-term exposure to ultraviolet radiation (UVR) was determined. Altogether, 200 Sprague-Dawley rats received unilaterally 5 or 20 kJ/m2 UVR (lambda MAX = 300 nm, lambda 0.5 = 10 nm) in vivo, during 15 min. At 1, 4, 8, 16 and 32 weeks after exposure subgroups of 20 rats from each dose group were sacrificed. Both lenses were removed for measurement of intensity of forward scattered light. It was found that exposed lenses scatter light more than their contralaterals and that a higher dose induces more light scattering. After exposure to 5 kJ/m2, the mean difference in scattering remained unchanged between 1 and 32 weeks' latency, but the distribution of the individual differences in scattering became skew. For several animals, lens opacities induced by 5 kJ/m2 seemed to decrease during the observation period. Earlier observations in complement to current findings implicate that it is optimal to detect close-to-threshold UVR-induced cataract at 1 week after exposure.

Rat lens glycolysis after in vivo exposure to narrow band UV or blue light radiation.

UV radiation and short wavelength visible light are known to damage various tissues in the eye. This paper investigates the effect on rat lens glycolysis after in vivo exposure with 90 kJ m-2 narrow band UV radiation (UVB, 300 nm) and 90 kJ m-2 blue light (435 nm) radiation. After exposure, all lenses were incubated in Medium 199. Samples of culture medium were withdrawn after 2, 4, 6 h and 5, 10, 20 h in two UVB studies and after 5, 10 and 20 h in a blue light study. Lactate is the major end product of lens glycolysis. Lactate was determined with a modified enzymatic-photometric method. Intralenticular lactate was determined in one UVB experiment. In the UVB experiments we found a lower lactate production in the exposed lenses 2-6 h after exposure. There was an accumulation of lactate inside UVB-exposed lenses after 6 h incubation compared with their contralateral lenses. No significant effect on lactate production was observed in the blue light experiment. CONCLUSIONS. UVB induced a reversible inhibition of glycolysis. UVB also induced an accumulation of lactate inside the lens. Blue light tended to increase glycolysis.

Receptor and neural visual readaptation after exposure to colored flash.

The time needed to recover optokinetic nystagmus or electroretinography complexes after a glare inducing flash was measured to study the receptor and neural visual readaptation. Electroretinographs and optokinetic nystagmus were evoked with low intensity stimuli. The light from a flash tube was filtered with an interference filter (Tmax = 536 or 622 nm) and evenly distributed into a Goldmann hemisphere observed by the subject. The Recovery of the amplitude of the a-wave of the electroretinography is quicker than the recovery of optokinetic nystagmus after a low intensity glare inducing flash. The recovery time was shorter for a red than for a green flash of equivalent dose for both recovery modalities. The time difference between electroretinography a-wave and optokinetic nystagmus recovery was the same and independent of glare inducing flash wavelength. The recovery of the amplitude of the a-wave of the electroretinography was quicker than the recovery of optokinetic nystagmus after a low intensity glare inducing flash. This time difference between the recovery modalities may in part be due to the difference between the physiological stimuli used, but it is believed that most of the time difference is because the recovery of optokinetic nystagmus monitors more of the afferent visual pathway with complex post receptor neural mechanisms than the recovery of the a-wave.

The significance of ultraviolet radiation for eye diseases. A review with comments on the efficacy of UV-blocking contact lenses.

Acute and cumulative ultraviolet radiation (UVR) exposure has been proposed as an important causative factor in the development of a whole spectrum of eye diseases. The present review examines the scientific evidence for and against such an association, with special emphasis on recent additions to the literature. The sun is the main UVR source on earth, and it is beyond scientific doubt that the cornea can be harmed by both acute and cumulative ambient exposures. There is also powerful epidemiological support for an association between chronic UVR exposure and the formation of cataracts and pterygia. The evidence in support of UVR linkage to pinguecula, ocular neoplasms and retinal changes is weaker--in part because there are fewer studies reported in the literature. It is concluded that UVR-blocking hydrogel contact lenses and spectacles are two equally effective preventive measures in minimizing unnecessary suffering and health costs, especially for people who spend a significant time outdoors and for those who live in more UV intense environments. UVR-blocking contact lenses and spectacles must not, however, be substitutes in situations that require UVR-blocking safety goggles.

Filter goggles imitating dark adaptation for measurement of visual readaptation after flash exposure.

The effect of red pass goggles (cut off wavelength = 650 nm) imitating dark adaptation on measurement of visual readaptation after flash exposure was investigated in humans. The results showed that there is no statistically significant difference between visual readaptation time measured with ordinary dark adaptation and that with goggles for adaptation. No statistically significant difference was found between females and males. It is suggested that red pass goggles can be practicably used to simulate dark adaptation in measuring visual readaptation time. Visual readaptation time was measured as the interval between the triggering of a green flash and the reappearance of optokinetic nystagmus. Optokinetic nystagmus was induced by a moving vertical grating and recorded by DC EOG.

Measurement of visual readaptation time after flash exposure using optokinetic nystagmus.

It is concluded that measurement of visual readaptation time (RAT) using optokinetic nystagmus (OKN) is a repeatable measure of visual recovery after flash exposure. The semi-automatic method for measurement of RAT used here requires further development, but it is anticipated that the improved method will provide an efficient tool for increased understanding of the physiology of flash blindness. In this study on humans, it was found that if RAT is recorded twice on the same occasion, the second RAT is shorter. However, there was no systematic difference between RAT recordings on consecutive occasions. The newly developed semi-automatic method was found to provide RATs comparable to those obtained by manual measurement on a paper print out of EOG recordings. In RAT estimation, the variability between subjects shadows other sources of random variability. The least number of subjects needed in each group to detect a 20% alteration of RAT due to an experimental factor (alpha = 0.05, beta = 0.05) was estimated to 13 with independent groups design. For paired design < 10 are needed. OKN was elicited with a horizontally moving vertical grating. The eye movement was recorded by DC EOG. A sudden flash of green light temporarily abolished the OKN. The internal between the flash and the reappearance of OKN was measured as the RAT.

Influence of target direction, luminance and velocity on monocular horizontal optokinetic nystagmus.

The present investigation demonstrates that the slow phase of human monocular horizontal optokinetic nystagmus (OKN) stimulated during scotopic vision does not depend on target direction but does depend on target luminance and velocity. OKN was elicited by a horizontally moving vertical grating projected inside a modified Goldman's perimeter hemisphere. Each of six target velocities (20, 40, 60, 80, 100 and 120 deg/s) were tested on each subject with step-wise increased target luminance. Eye movement was recorded by DC EOG. Both right and left target directions were tested. It was found that there is no directional preference in OKN gain (slow phase velocity/stimulus velocity). For the target velocities 20-80 deg/s, OKN gain increases with increasing target luminance with an exponential decline. The exponential luminance constant increases as target velocity increases. The maximum OKN gain decreases as target velocity increases. The threshold luminance needed to initiate OKN increases with increasing target velocity. A linear relationship was found between OKN gain and target luminance for the target velocities 100 deg/s and 120 deg/s.