AIM:To study the effect of zinc on galactose-induced cell apoptosis in human lens epithelial cells(HLEC).

METHODS:HLEC cell line SRA01/04 cells were cultured in DMEM medium and divided into six groups: control group, galactose treatment group, zinc supplement group, zinc supplementation combined with galactose treatment group, zinc deficiency group, zinc deficiency combined with galactose treatment group. The cell viabilities were assayed by MTT, cell morphology and apoptosis were detected by fluorescence microscope and flow cytometry, respectively.

RESULTS:The cell viabilities induced by galactose(0, 25, 50, 75, 100, 125mmol/L)were(100.0±5.4)%,(97.5±3.2)%,(91.3±5.3)%,(93.4±0.6)%,(86.6±1.4)% and(83.5±0.4)%, respectively. When the concentration of galactose was 100 and 125mmol/L, cell viability was significantly decreased, compared with the untreated cells(P<0.05). Fluorescence microscopy results showed that the cell nucleus remained uniformly stained in control group and zinc supplement group. Nuclear shrinkage, a typical apoptotic morphology, was visible in some cells in the galactose treatment group, zinc supplementation combined with galactose treatment group, zinc deficiency group and zinc deficiency combined with galactose treatment group. The cell apoptosis in the six groups were(1.5±0.1)%,(7.1±0.2)%,(1.4±0.1)%,(4.4±0.2)%,(5.5±0.2)% and(15.8±0.3)%, respectively. The cell apoptosis were significant increased in galactose treatment group, zinc supplementation combined with galactose treatment group, zinc deficiency group and zinc deficiency combined with galactose treatment group, compared with the control group(P<0.05), and those of zinc supplementation combined with galactose treatment group were significant decreased, and zinc deficiency combined with galactose treatment group were increased(P<0.05), compared with the galactose treatment group.

CONCLUSION:Zinc supplementation protects human lens epithelial cells against apoptosis induced by galactose and may have an inhibition effect on cataract formation.