Toxicity of Ultraviolet Radiation Exposure to the Lens Expressed by Maximum Tolerable Dose

Söderberg, Per G.; Löfgren, Stefan; Ayala, Marcelo; Dong, Xiaofang; Kakar, M.; Mody, V.

doi:10.1159/000060811

Cited by 40 publications

(49 citation statements)

References 13 publications

(14 reference statements)

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“…Maximum sensitivity of the rat lens to UVR-B is around 300 nm. The dose 1 kJ/m 2 was chosen to be below the threshold dose 15 . The exposure time of 15 min was selected to induce maximum damage to the lens 21 .…”

Section: Discussionmentioning

confidence: 99%

Characterization of Molecular Mechanisms of <em>In vivo</em> UVR Induced Cataract

Galichanin

Talebizadeh

Söderberg

2012

JoVE

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Cataract is the leading cause of blindness in the world 1 . The World Health Organization defines cataract as a clouding of the lens of the eye which impedes the transfer of light. Cataract is a multi-factorial disease associated with diabetes, smoking, ultraviolet radiation (UVR), alcohol, ionizing radiation, steroids and hypertension. There is strong experimental 2-4 and epidemiological evidence 5,6 that UVR causes cataract. We developed an animal model for UVR B induced cataract in both anesthetized 7 and non-anesthetized animals 8 .The only cure for cataract is surgery but this treatment is not accessible to all. It has been estimated that a delay of onset of cataract for 10 years could reduce the need for cataract surgery by 50% 9. To delay the incidence of cataract, it is needed to understand the mechanisms of cataract formation and find effective prevention strategies. Among the mechanisms for cataract development, apoptosis plays a crucial role in initiation of cataract in humans and animals 10. Our focus has recently been apoptosis in the lens as the mechanism for cataract development 8,11,12 . It is anticipated that a better understanding of the effect of UVR on the apoptosis pathway will provide possibilities for discovery of new pharmaceuticals to prevent cataract.In this article, we describe how cataract can be experimentally induced by in vivo exposure to UVR-B. Further RT-PCR and immunohistochemistry are presented as tools to study molecular mechanisms of UVR-B induced cataract. Video LinkThe video component of this article can be found at http://www.jove.com/video/4016/ Protocol 1. Exposure to Ultraviolet Radiation 1. 15 min before the exposure, anesthetize a female Sprague-Dawley rat with a mixture of 90 mg/kg Ketalar (ketamine) and 10 mg/kg Rompun (xylazine) by intraperitoneal injection. 2. Place the animal in a rat restrainer and tighten the belts until immobilization of the rat without causing a trunk squeeze 13 . 3. Instill Mydriacyl (tropicamide), 10 mg/ml, in both eyes of the rat to induce mydriasis. 4. Place the animal so that one eye is positioned against a narrow beam of UVR at 300 nm 14 with 10 nm full width at half maximum and shield the contralateral eye with black tape. 5. Expose the rat unilaterally to sub-threshold dose 1 kJ/m 2 UVR-B at 300 nm for 15 min 15 . Dissection1. After pre-determined post exposure interval (1, 5, 24 and 120 hr), sacrifice the six week old rat (weight < 200 g) by carbon dioxide asphyxiation and dislocation of the cervical vertebrae. 2. Enucleate eyes. Thereafter, put the eye cornea down, posterior side up. Then, punch a minimal hole by applying a 27 gauge cannula and push tangentially to the sclera to avoid damaging the lens that is very close to the sclera. Then use a pair of ophthalmic surgery scissors to cut circumferentially just behind the limbus until the posterior portion of the sclera can be lifted off. Then, lift the lens with a blunt curved forceps. 3. Remove remnants of the ciliary body from the lens equator under a microscope, keep...

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Section: Discussionmentioning

confidence: 99%

Characterization of Molecular Mechanisms of <em>In vivo</em> UVR Induced Cataract

Galichanin

Talebizadeh

Söderberg

2012

JoVE

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“…12 In order to estimate threshold dose despite the fact that there is no absolute threshold for in vivo UVR-induced cataract, it was suggested to use the maximum tolerable dose, (MTD 2.3:16 ), as a meaningful estimate of toxic dose. 13 It was demonstrated that reciprocity largely holds for in vivo UVR-300 nm exposures in the exposure time interval 7.5-120 min, but there is a slightly higher sensitivity with exposure times of around 15 min (Figure 6). 14 The slightly higher sensitivity for exposures around 15 min was attributed to the depletion of preexisting anti-oxidation defense.…”

Section: Experimental Evidencementioning

confidence: 95%

Does infrared or ultraviolet light damage the lens?

Söderberg

Talebizadeh

et al. 2016

Eye

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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 dosedependent 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.

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“…UVA makes up most of the UVR reaching the earth. UVB makes up merely 5% of the UVR reaching the earth, and UVC does not reach the earth at all [3, 4, 5, 6, 7, 8, 9, 10, 11]. The UVR with a wavelength of less than 295 nm are all absorbed by the cornea.…”

Section: Introductionmentioning

confidence: 99%

“…The UVR with a wavelength of less than 295 nm are all absorbed by the cornea. As far as the wavelengths between 295 and 400 nm (UVB and UVA) are concerned, these reach and are then absorbed by the lens [3, 4, 5, 6, 7, 8, 9, 10, 11]. The most important pathological effect induced by UVR on the lens is cataract formation, which occurs either directly or indirectly on the grounds of the lens being exposed to UVR for long years.…”

Section: Introductionmentioning

confidence: 99%

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The Effect of N-Acetyl Serotonin on Ultraviolet-Radiation-Induced Cataracts in Rats

et al. 2003

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Aims: To investigate the effects of ultraviolet radiation (UVR) on cataract development in rat lenses and whether or not N-acetyl serotonin has an effect on changes in these lenses. Material and Methods: The study was performed using 5 groups of Sprague-Dawley albino rats, with each group consisting of 15 rats. The 5th group being the control group did not receive any applications, whilst the other 4 groups received a daily dose of 0.2 J/cm²/day UVR (305 nm wavelength) for 60 days. A dose of 4 mg/kg/0.1 ml N-acetyl serotonin was injected intraperitoneally to group 1 and group 2 every day and on alternate days, respectively. Group 3 received an intraperitoneal injection of 0.1 ml phosphate buffer solution every day, whilst group 4 received no injection. On the 60th day, an intracardiac withdrawal of blood was performed, after the rats had been anesthetized with ether. Following the withdrawal of blood, the rats were killed using a high dose of ether and their eyes were enucleated. The lens fresh weights, plasma malondialdehyde (P-MDA), erythrocyte glutathione peroxidase (E-GSHPx), erythrocyte glutathione reductase, blood reduced glutathione (B-RGSH), erythrocyte catalase (E-CAT), lenticular malondialdehyde, lenticular superoxide dismutase (L-SOD), lenticular glutathione peroxidase (L-GSHPx) and lenticular glutathione (L-GSH) levels were all assessed. Results: The lens fresh weights were determined to be lower in group 1 and in the control group in comparison with the other groups (p < 0.01). Whilst the P-MDA level was found to be lower (p < 0.001), the E-GSHPx level was higher (p < 0.01) in the control group than in the other groups. The E-GSHPx level was higher in groups 1 and 2 than in groups 3 and 4 (p < 0.01). The B-RGSH level was higher in the control group than in the other groups (p < 0.001). The E-CAT level was higher in both the control group and group 1 than in groups 2, 3 and 4 (p < 0.01), whilst it was higher in group 2 when compared to groups 3 and 4 (p < 0.01). The L-SOD levels were found to be higher in the control group and group 1 than in groups 2, 3 and 4 (p < 0.001). Whilst the L-GSHPx levels were determined to be higher only in the control group (p < 0.001), the L-GSH levels were higher in the control group and group 1 than in the other groups (p < 0.001). Conclusions: In recent years, the depletion of the atmospheric ozone layer has resulted in the penetration of more UVR to the earth, which causes various effects on different tissues of organisms. N-acetyl serotonin, a melatonin precursor, may well be effective in the prevention of the negative effects induced by the UVR upon the lens tissue, in which case the capability of melatonin to capture free radicals as well as its antioxidative properties should be taken into consideration.

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Toxicity of Ultraviolet Radiation Exposure to the Lens Expressed by Maximum Tolerable Dose

Cited by 40 publications

References 13 publications

Characterization of Molecular Mechanisms of <em>In vivo</em> UVR Induced Cataract

Characterization of Molecular Mechanisms of <em>In vivo</em> UVR Induced Cataract

Does infrared or ultraviolet light damage the lens?

The Effect of N-Acetyl Serotonin on Ultraviolet-Radiation-Induced Cataracts in Rats

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