Abstract:AIM:To investigate the effect of high glucose on the redox system of the cultured rat lenses in vitro, and evaluate the effect of thioltransferase(TTase)against oxidative stress in diabetic cataract.
METHODS: Lenses were incubated with different concentrations of glucose: control group(5.5mmol/L), high glucose groups(35.5, 65.5, 95.5mmol/L)and mannitol control group for 7d. Following incubation, the lenses were evaluated daily using a dissecting microscope. After 7d of incubation, lenses were homogenized in lysis buffer and processed for measurement the activity of TTase, catalase(CAT), superoxide dismutase(SOD)and the specific value of GSSG/T-GSH.
RESULTS: The lenses treated with high glucose exhibited mistlike opacity in the early stages, while the lenses of control group remained relatively transparent. With the rise of the concentration of high glucose, the activity of TTase increased and the maximum appeared in 35.5mmol/L group(1.743±0.20mU/mg protein, P<0.01). No changes were observed in the mannitol control group(P>0.05). The specific value of GSSG/T-GSH of lenses with high glucose groups increased compared with the control groups, there were 2.89, 2.57 and 2.42 times to the normal control group(P<0.05). There was no significant difference between each group treated with high glucose, and the difference was also no significant between the mannitol group and the control group. Compared with the control group, the activities of CAT and SOD decreased in the high glucose treatment groups, the activities of SOD were 0.71, 0.52 and 0.49 times to the normal control group(P<0.05), and the activities of CAT were 0.47,0.56 and 0.50 times to the normal control group(P<0.05). There was no significantly different between each group treated with high glucose.
CONCLUSION: The antioxidant system of the lens was activated by the high glucose following the increased activity of TTase, the specific value of GSSG/T-GSH, and the decreased activities of CAT and SOD. The gradually decreased oxidation resistance in the lens may contribute to the development of diabetic cataract.