Protective effect of vitamin E on age-related alterations of Kupffer cell energy metabolism.

Aim: To investigate the mechanism of age-related reduction of Kupffer cell (KC) phagocytic capacity and the protective management.
Methods: Using rhodamine 123 fluorescence density and rate of glucose utilization as parameters, we measured the mitochondrial energy metabolism status in vitro and the glucose utilization capacity of isolated rat liver Kupffer cells (KCs) from rats of various ages (6 mo, 12 mo, 18 mo and 24 mo) and the effect of vitamin E (VE) pretreatment (500 mg/kg/wk × 13 wk).
Results: The rate of KC glucose utilization and the rhodamine fluorescence density of KC mitochondria of 18 mo-old untreated rats (NVEG) were significantly lower than that of 6 mo-old NVEG by 19.3% (4.0 nmol·h ± 0.4 nmol·h(-1) 10.6 cells(-1) vs 5.7 nmol·h ± 0.6 nmol·h(-1) 10(6) cells(-1), P < 0.05) and 19.5% (80.5 ± 6.3 vs 100.0 ± 4.7, P < 0.01) respectively; Rate of KC glucose utilization and the rhodamine fluorescence density of KC mitochondria of 6 mo-old rats were also lower than the 24 mo-old NVEG by 35.1% (3.7 nmol·h ± 0.6 nmol·h(-1)10(6) cells(-1) vs 5.7 nmol·h ± 0.6 nmol·h(-1) 10(6) cells(-1), P < 0.01) and 32.1% (67.9 ± 7.4 vs 100.0 ± 4.7, P < 0.01) respectively. The two parameters of 18 mo-old VE pretreated rats (VEG) were significantly higher than those of 18 mo-old NVEG, and statistically comparable to those of 6 mo-old VEG. The two parameters of the 24 mo-old VEG were significantly higher in comparison with those of 24 mo-old NVEG, but still significantly lower than those of 6 mo-old VEG.
Conclusion: Aging has a significantly negative effect on KC energy metabolism, which can be alleviated by VE pretreatment.