Bucolo C, Lin L R, Dang L, Giblin F J, Reddy V N
Eye Research Institute, Oakland University Rochester, MI 48309-4401.
Exp Eye Res. 1994 Jun;58(6):697-704. doi: 10.1006/exer.1994.1067.
Several recent reports have indicated that ganglioside treatment both in vivo and in vitro has a protective effect on the loss of membrane permeability resulting from inhibition of transport enzyme(s) in different experimental models. In this study we have investigated the effect of monosialoganglioside on oxidation-induced changes in organ-cultured rabbit lenses and in cultured dog lens epithelium and human retinal pigment epithelial cells. Exposure of organ-cultured lenses to 0.5 mM hydrogen peroxide for 1 hr increased the efflux of 86Rb from intact lenses and loss of myoinositol from the capsule epithelium. Pretreatment of the lenses with monosialoganglioside significantly reduced the efflux rate of 86Rb and loss of myoinositol. Monosialoganglioside also prevented morphological changes induced by 0.1 mM hydrogen peroxide in dog lens epithelium and loss of cell viability caused by docosahexaenoic acid in dog lens epithelium and in human retinal pigment epithelial cells. In contrast to the protective effect of monosialoganglioside on permeability and morphological changes in cultured cells, it had no effect against single-strand breaks of DNA in dog lens epithelium resulting from exposure to hydrogen peroxide, X-ray and UV-B radiation. Although the molecular mechanisms by which monosialoganglioside prevents permeability and morphological changes induced by hydrogen peroxide and docosahexaenoic acid are not known, it appears that this ganglioside serves as a membrane stabilizer rather than as a free-radical scavenger.
