title: Dose-response relationship for α-tocopherol prevention of ultraviolet radiation induced cataract in rat.
abstract: The purpose of this study is to establish the dose response relationship for α-tocopherol protection of ultraviolet radiation (UVR) induced cataract in the rat. Four groups of 20 six-week-old albino Sprague Dawley rats received 5, 25, 50, and 100 IU/day α-tocopherol, whilst another group of 20 rats without any α-tocopherol feeding was the control group. After 4 weeks of feeding, each rat was unilaterally exposed to 8 kJ/m(2) UVR-300 nm for 15 min. At 1 week after exposure, the rats were sacrificed and lens light scattering was measured quantitatively. Lens total reduced (GSH) and oxidized (GSSG) glutathione; glutathione reductase (GR) and peroxidase (GPx) were determined spectrophotometrically. The UVR-exposed lenses in the α-tocopherol fed groups developed superficial cataract, whereas lenses in the control group developed cortical and equatorial opacities. 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 and contralateral non-exposed lens decreased with increasing doses of α-tocopherol to an asymptote level. UVR-exposure 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 at any level of α-tocopherol supplementation. Orally administered α-tocopherol dose dependently protects against UVR-induced cataract. The protection is associated with an α-tocopherol dose-dependent GSH depletion secondary to UVR exposure. UVR-induced light scattering only occurs if the GSH depletion exceeds a threshold.
authors.affiliation: Dept. of Ophthalmology, Second Hospital, Shandong University, Jinan, China. jingw0313@yahoo.com
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Stefan
authors.initials: S
authors.lastname: Löfgren
authors.forename: Xiuqin
authors.initials: X
authors.lastname: Dong
authors.forename: Konstantin
authors.initials: K
authors.lastname: Galichanin
authors.forename: Per G
authors.initials: PG
authors.lastname: Söderberg
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D002386:Cataract / Q000378:metabolism / Q000517:prevention & control*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D007908:Lens, Crystalline / Q000378:metabolism / Q000528:radiation effects*; D011833:Radiation Injuries, Experimental / Q000378:metabolism / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012542:Scattering, Radiation; D014466:Ultraviolet Rays; D024502:alpha-Tocopherol / Q000008:administration & dosage*
chemical_list: D000975:Antioxidants; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005978:Glutathione; D024502:alpha-Tocopherol; D019803:Glutathione Disulfide