Ultraviolet radiation effects on rat lens lactate dehydrogenase. An estimation of UVR penetration depth into the eye.

Stefan Löfgren, MD (a, b), Per G. Söderberg, MD, PhD (a), Ralph Michael, MMedSci, Dipl. Ing. (a)

(a) St. Erik´s Eye Hospital, Research Department, S-112 82 Stockholm, Sweden

(b) Department of Medical Biochemistry and Biophysics, Biophysics Section,

Karolinska Institutet, Stockholm, Sweden

E-mail: stefanl@mango.mef.ki.se

(Poster presented at the 1st Internet Conference on Photochemistry and Photobiology, 1997)

Introduction

Since a long time it has been known that experimental exposure to ultraviolet radiation (UVR) damages the lens and induces cataract. Epidemiological studies show a correlation between exposure to solar UVR-B (280-315 nm) and increased incidence of cataract (reviewed by Bergmanson & Söderberg 1995). One hypothesis for the experimental UVR-induced cataractogenesis is that shortage of energy inhibits the ion-pumps (Söderberg 1990). UVR decreases the lens glycolytic activity in vivo (Löfgren & Söderberg 1995) and decreases lactate dehydrogenase (LDH) activity in vitro (Chen et al. 1989). To further elucidate if the UVR inhibition of glycolysis in the lens in vivo (Löfgren & Söderberg 1995) could be caused by LDH inhibition, an optimised histochemical procedure for the determination of LDH in lens sections was employed (Löfgren & Söderberg, 1997).

The histochemical technique was also applied to obtain information on the penetration of UVR-300 nm into the lens. Transmittance studies on different species have shown that only a minor part of UVR-300 nm falling on the cornea reaches the anterior surface of the lens and of that, in practice all radiation is attenuated within the lens (Bachem 1956, Barker 1979, Boettner & Wolter 1962, Gorgels et al. 1992, Maher 1978).