Divergent effects of lycopene on pancreatic alpha and beta cells / 生理学报

Lycopene is an antioxidant which has potential anti-diabetic activity, but the cellular mechanisms have not been clarified. In this study, different concentrations of lycopene were used to treat pancreatic alpha and beta cell lines, and the changes of cell growth, cell apoptosis, cell cycle, reactive oxygen species (ROS), ATP levels and expression of related cytokines were determined. The results exhibited that lycopene did not affect cell growth, cell apoptosis, cell cycle, ROS and ATP levels of alpha cells, while it promoted the growth of beta cells, increased the ratio of S phase, reduced the ROS levels and increased the ATP levels of beta cells. At the same time, lycopene treatment elevated the mRNA expression levels of tnfα, tgfβ and hif1α in beta cells. These findings suggest that lycopene plays cell-specific role and activates pancreatic beta cells, supporting its application in diabetes therapy.

Overexpression of eIF-5A2 in mice causes accelerated organismal aging by increasing chromosome instability.

BACKGROUND: Amplification of 3q26 is one of the most frequent genetic alterations in many human malignancies. Recently, we isolated a novel oncogene eIF-5A2 within the 3q26 region. Functional study has demonstrated the oncogenic role of eIF-5A2 in the initiation and progression of human cancers. In the present study, we aim to investigate the physiological and pathological effect of eIF-5A2 in an eIF-5A2 transgenic mouse model. METHODS: An eIF-5A2 transgenic mouse model was generated using human eIF-5A2 cDNA. The eIF-5A2 transgenic mice were characterized by histological and immunohistochemistry analyses. The aging phenotypes were further characterized by wound healing, bone X-ray imaging and calcification analysis. Mouse embryo fibroblasts (MEF) were isolated to further investigate molecular mechanism of eIF-5A2 in aging. RESULTS: Instead of resulting in spontaneous tumor formation, overexpression of eIF-5A2 accelerated the aging process in adult transgenic mice. This included decreased growth rate and body weight, shortened life span, kyphosis, osteoporosis, delay of wound healing and ossification. Investigation of the correlation between cellular senescence and aging showed that cellular senescence is not required for the aging phenotypes in eIF-5A2 mice. Interestingly, we found that activation of eIF-5A2 repressed p19 level and therefore destabilized p53 in transgenic mouse embryo fibroblast (MEF) cells. This subsequently allowed for the accumulation of chromosomal instability, such as errors in cell dividing during metaphase and anaphase. Additionally, a significantly increase in number of aneuploidy cells (p < 0.05) resulted from an increase in the incidences of misaligned and lagging chromosomal materials, anaphase bridges, and micronuclei in the transgenic mice. CONCLUSION: These observations suggest that eIF-5A2 mouse models could accelerate organismal aging by increasing chromosome instability.

[Effect of vitamin C antioxidative protection on human red blood cells].

In order to investigate the effect of antioxidants on human blood, vitamin C was selected and added into plastic blood storage bags with CPD, and stored at 25 degrees C. During 6 days of storage, some indexes as ATP, SOD, MDA, K(+) concentration and superoxide radicals were detected and were compared with control group, The results showed that ATP and SOD activity in whole blood with vitamin C during 6 days of storage was higher then that in control group (P < 0.05, P < 0.01), the MDA and plasma K(+) concentrations in stored whole blood with vitamin C during 6 days of storage were lower than that in control group (P < 0.05, P < 0.01), the superoxide radical concentrations in stored whole blood with vitamin C decreased lower than that in control group (30%). The conclusion was made that vitamin C increases activities of ATP and SOD, decreases concentrations of MDA, plasma K(+) and superoxide radicals during blood preservation.