Vaishaali Gunalan, Research fellow, M Optom

Vision Research Foundation, Sankara Nethralaya, Chennai, India

Ultraviolet radiation (UVR) – A component of solar radiation:

Over the past 2 decades, there has been documented depletion of the ozone layer that drew the interests of many researchers and epidemiologists. The year 1997-2000 showed about 6% & 4% loss in the thickness in the mid-latitudes of the southern and northern region respectively⁽¹⁾⁽²⁾. Every 1% reduction in the ozone causes 0.2% – 2% increase in the shorter wavelengths of UVR (Figure 1(A)) reaching the earth’s surface⁽²⁾. Due to the availability of artificial sources in recent years, the UVR exposure increases significantly in addition to the emission from the sun (Figure 1 (B)).

Figure 1: (A) Diagrammatic representation of a classification of UVR and its amount reaching the earth’s surface. (B) Illustration of the amount of UVR being absorbed and transmitted in the human eye.

What happens inside the eye after absorption and transmission?

There is a plethora of studies since the early 90’s reporting on various hazards of UVR on ocular tissues. Though there are well- established information and awareness on these hazards (Table 1), the question “how it is caused” still is not yet completely answered as there are multiple mechanisms involved. However, there are five common mechanisms are discussed in many kinds of literatures. They are direct DNA damage (Figure 2), dysfunction of enzymes, ion pump inhibition, p53 mutation, membrane damage and apoptosis (Figure 3).

Table 1: UVR related ocular conditions on various structures.

Direct DNA damage:

Figure 2: Illustration and process of direct DNA damage due to UVR. Figure courtesy for Skin layers: https://www.dreamstime.com/royalty-free-stock-photo-skin-cross-section-image9845525

The sunburn (SC) arises due to DNA damage is a “protective factor”, since it helps in the formation of tumour suppression gene (TSG) (P53 gene). The increase in the severity of UVR induced DNA damage resulted SC’s, increases the activation of the p53 gene and helps in reducing the risk of skin malignancies. On the other side, mutation of the TSG in the epithelial cell (Keratinocytes), leads to the tumour promoting effects of UVR⁽³⁾.

Apoptosis: “Programmed cell death”:

Figure 3: Illustration and process of apoptosis mechanism due to UVR. Figure courtesy for corneal image: https://nkcf.org/about-keratoconus/how-the-human-eye-works/

The “Apoptosis” mechanism takes place in the “Retina”, due to excitation of retinal cells and pigments with UVR exposure. Though, it is well protected by cornea and lens; in case of absence of the filtering capacity of the lens, retina would almost certainly sustain the UVR damage, leading to the formation of free radicals and causing apoptosis⁽²⁾.

Dysfunction of enzymes & Ion pump inhibition:

In few hours of UVR exposure, the cortical enzyme (Lactate dehydrogenase) of the lens is deactivated. Following day (Figure 4) due to apoptosis and in the loss of the metabolic component of the cells, water and ion homeostasis of the anterior layer is disturbed, also influences the deep cortical layer. These results in the extracellular accumulation of calcium show up as “flake-like opacities” in both central and equatorial portions of the epithelium. On 7<^th day, flake-like opacities become a well-grooved opacity⁽⁶⁾. In the cortex, the vacuolar and extracellular spaces were noted as equatorial opacities and osmotic swelling. Interestingly, the superficial fibres are not damaged as deep fibres (10^th or 40^th layer). On 56^th day, the opacities substantially reduced on both epithelium and cortex. However, there was some fine opacity that was observed in the deeper lens cortex’s equatorial region in the shape of “shell”. In a long time UVR exposure, these subtle opacities may accumulate and can strengthen the possibility of “cortical cataract”^(6).

Figure 4: Illustration of lenticular changes in epithelium following UVR exposure; top view- Equatorial view and bottom- magnified view of the anterior surface: (A) Nonexposed lens, (B) 1 day, (C) 7 days, and (D) 56 days. The images in all the three rows (top, bottom and middle) are the same through A to D. At 1 day of exposure: (B) Flaky opacities are diffused over the anterior surface. (C) At day 7 and (D) after 56 days of exposure, a very slight ring-shaped opacity (arrows) was seen in both equatorial and anterior view. p: denotes posterior, a denotes anterior and eq denotes equatorial. Figure courtesy: Michael R, Vrensen GFJM, Marle J Van, Lo S. Repair in the Rat Lens after Threshold Ultraviolet Radiation Injury. 2000;41(1):204–12.

References:

1. McKenzie RL, Björn LO, Bais A, Ilyasd M. Changes in biologically active ultraviolet radiation reaching the Earth’s surface. Photochem Photobiol Sci. 2003;2(1):5–15.
2. Oliva MS, Taylor H. Ultraviolet radiation and the eye. Int Ophthalmol Clin. 2005;45(1):1–17.
3. Kulms D, Schwarz T. Molecular mechanisms of UV-induced apoptosis. 2000;(7):195–201.
4. Ren H, Wilson G. The effect of ultraviolet-B irradiation on the cell shedding rate of the corneal epithelium. 1994;72:447–52.
5. Podskochy A, Gan L, Fagerholm P, Ph D. Apoptosis in UV-exposed Rabbit Corneas. 2000;19(1):99–103.
6. Michael R, Vrensen GFJM, Marle J Van, Lo S. Repair in the Rat Lens after Threshold Ultraviolet Radiation Injury. 2000;41(1):204–12.