Method  Five groups of 20 six-week-old albino Sprague Dawley rats were used in this study. One group without any α- tocopherol feeding was the control group, whilst the other 4 groups were received 5, 25, 50, and 100 IU/day of α- tocopherol. After 4 weeks of feeding, each rat was unilaterally exposed to 8 kJ/m² UVR-300 nm for 15 min. At 1 week after exposure to UVR, the rats were sacrificed, the lenses were extracted, and forward light scattering was measured. Lens total reduced (GSH) and oxidized (GSSG) glutathione; glutathione reductase (GR) and peroxidase (GPx) were determined spectrophotometrically.

Results  The UVR-exposed lenses in the α-tocopherol fed groups developed superficial and slight equatorial cataract, whereas lenses in the control group developed cortical and dense equatorial opacities. Forward light scattering in lenses from the α-tocopherol-supplemented rats was lower than in lenses from the control group. The difference of light scattering between the exposed lens and its contralateral non-exposed lens decreased with increasing doses of α-tocopherol supplementation with a rate constant of 4.8 IU/day to an asymptote level. The exposure to UVR caused a significant depletion of lens GSH in rats without or at low α-tocopherol supplementation. The depletion of GSH became less with higher α-tocopherol supplementation. There was no detectable difference in lens GSSG, GR or GPx activity at any level of α-tocopherol supplementation.

Conclusions  Orally administered α-tocopherol dose dependently protects against UVR-induced cataract. The protection of UVR-induced light scattering is associated with an α-tocopherol dose-dependent GSH depletion secondary to UVR exposure without any effects on total lens GSSG, GR or GPx activity. UVR-induced light scattering only occurs if the GSH depletion exceeds a threshold.