The UVR portion of sunlight has been shown to inactivate lens enzymes.
50 51 Direct UVR photolysis
50 51 and UVA-generated ROS by UVR-photolysis of lenticular sensitizers are among the major factors that may cause inactivation of enzymes.
14 15 50 Which part of UVR portion of light, UVB or UVA, is the most harmful to a human lens is still a matter of debate.
1 2 5 52 53 However, a recent report by Dillon et al.
52 has already established that due to the spectral characteristics of the cornea and aqueous humor of the human eye, the total UVB radiation that reaches the lens represents at most 2% of UVR. Only UVB wavelengths from 300 to 320 nm can reach the surface of the lens.
52 The energy of UVB photons in this range is not much different from the energy of UVA photons (e.g., E
300 = 95.3 kcal/mol vs. E
350 = 81.7 kcal/mol),
53 54 and, according to Sliney,
20 a total dose of only 50 to 200 nW/cm
2 of UVB light is absorbed by the human lens. According to Lofgren and Soderberg
21 all UVB irradiation that impinges on the rat lens is absorbed within the first 0.4 to 0.5 mm of the lens and does not reach the lens nucleus.
21 On the contrary, in primate lenses the total UVA light dose could range from 1.1 to 9.7 mW/cm
2,
16 all of which is absorbed by lenticular chromophores and can penetrate to the lens nucleus.
53 These data, combined with results from our laboratory that showed that aged lenses contain UVA responsive, ROS-producing sensitizers
14 15 (Table 2) , imply that the UVA portion of the sunlight may be involved in age-dependent lens protein modifications and particularly in the loss of the specific human lens enzymes. This hypothesis was studied on four lenticular enzymes—GR, G3PD, SOD, and GPx—the specific activity of which was shown to decrease with age and during cataractogenesis.
24 30 48 49 In addition, according to the literature, these four enzymes have already been shown to be inactivated, by direct UVA photolysis,
42 55 oxidation by ROS,
41 56 57 58 or both UVA photolysis and ROS oxidation.
42