Effects of aminoguanidine intervention on lens cell damage induced by D-galactose in rat eyes

AIM: To investigate the effects of aminoguanidine intervention on lens cell damage induced by D-galactose in rat eyes and its mechanism of action. METHODS: D-galactose (400 mg/kg) was injected into rats intraperitoneally for 14 weeks to induce the animal model of glycosylation and lens cell damage. Aminoguanidine (75 mg/kg, 150 mg/kg) were administered for 12 weeks by intragastric administration beginning at 3rd week. All animals were killed and blood samples were taken to measure the activity of aldose reductase, the level of fructosamine, the amounts of glycohaemoglobin and advanced glycation end-products. The lenses of eyes were taken to detect the activities of AR, GR, SOD and SDH. The amounts of AGEs, GSH, MDA or outleakage of LDH were measured, respectively. The ultrastructure and apoptosis of lens epithelial cells were examined by transmission electron microscope and flow cytometry, respectively. RESULTS: Animals were treated with D-galactose for 14 weeks, the serum level of fructosamine, the amounts of glycohaemoglobin and AGEs, and activity of AR were significantly increased. The amount of AGEs and activity of AR in lens were increased, the activity of antioxidase was decreased and oxidative product was increased. The apoptosis, the damages of mitochondria and cell nucleus in lens cells were observed. After treated with aminoguanidine for 12 weeks, the activity of AR and the level of fructosamine in serum, and the amounts of glycohaemoglobin and AGEs were significantly decreased (P<0.01). The outleakage of LDH and amount of MDA were also decreased (P<0.05, P<0.01), the activities of GR, SDH and SOD were increased (P<0.05, P<0.01). The apoptotic rate of lens cells was reduced (P<0.05, P<0.01). The morphology of mitochondria and cell nucleus were improved. CONCLUSION: D-galactose induces the damage of cell nucleus, the mitochondria and apoptosis in lens cells by glycosylation and oxidative stress. Aminoguanidine may supply the protective action through inhibiting the glycosylation and oxidative stress.