A CPD photolyase gene PnPHR1 from Antarctic moss Pohlia nutans is involved in the resistance to UV-B radiation and salinity stress.

In Antarctic continent, the organisms are exposed to high ultraviolet (UV) radiation because of damaged stratospheric ozone. UV causes DNA lesions due to the accumulation of photoproducts. Photolyase can repair UV-damaged DNA in a light-dependent process by electron transfer mechanism. Here, we isolated a CPD photolyase gene PnPHR1 from Antarctic moss Pohlia nutans, which encodes a protein of theoretical molecular weight of 69.1 KDa. The expression level of PnPHR1 was increased by UV-B irradiation. Enzyme activity assay in vitro showed that PnPHR1 exhibited photoreactivation activity, which can repair CPD photoproducts in a light-dependent manner. The complementation assay of repair-deficient E. coli strain SY2 demonstrated that PnPHR1 gene enhanced the survival rate of SY2 strain after UV-B radiation. Additionally, overexpression of PnPHR1 enhanced the Arabidopsis resistance to UV-B radiation and salinity stress, which also conferred plant tolerance to oxidative stress by decreasing ROS production and increasing ROS clearance. Our work shows that PnPHR1 encodes an active CPD photolyase, which may participate in the adaptation of P. nutans to polar environments.

Inhibition Mechanism of Novel Pyrazolo[1,5-a]pyrazin-4(5H)-one Derivatives Against Proliferation of A549 and H322 Cancer Cells.

OBJECTIVE: To explore the inhibition mechanism and safety of pyrazolo[1,5-a]pyrazin-4(5H)-one derivatives against proliferation of human lung cancer A549 cells, H322 cells, and human umbilical vein endothelial cell (HUVEC). METHODS: Cells were treated with 40 Μmol/L of the ppo3a, ppo3b, ppo3i, and 0.1% DMSO (control) for 48 hours, respectively. Apoptosis was determined by Hoechst 33258 staining assay in H322 and A549 cells. Cell cycle distribution was determined by flow cytometry analysis in A549 cell. LC3-II, p53, and heat shock protein (HSP) 70 protein levels were detected by Western blotting in A549 cells treated with ppo3b for 48 hours. The morphology and viability of HUVEC were observed by inverted microscope and sulforhodamine B (SRB) assay. RESULTS: Ppo3a, ppo3b, and ppo3i significantly induced apoptosis in H322 and A549 cells. A strong G1-phase arrest was concomitant with the growth inhibitory effect on A549 cells. Ppo3b effectively elevated the p53 protein level, but significantly reduced the HSP70 protein level. There were no significantly inhibitory effect on the morphology and viability of HUVEC when treated with ppo3a, ppo3b, and ppo3i. CONCLUSIONS: ppo3a, ppo3b, and ppo3i could inhibit H322 proliferation through apoptosis and inhibit A549 through apoptosis and G1-phase arrest. The protein p53 and HSP70 might involve in the inhibition effects. These derivatives might be a clue to find effective and safe drug for lung cancers.

Selective killing effect of oxytetracycline, propafenone and metamizole on A549 or Hela cells.

OBJECTIVE: To determine the selective killing effect of oxytetracycline, propafenone and metamizole on A549 or Hela cells. METHODS: Proliferation assay, lactate dehydrogenase (LDH) assay, apoptosis detecting, flow cytometry and western blot were performed. RESULTS: It was found that treatment with propafenone at the concentration of 0.014 g/L or higher for 48 h could induce apoptosis in Hela cells greatly, while it was not observed in oxytetracycline and metamizole at the concentration of 0.20 g/L for 48 h. Oxytetracycline, propafenone and metamizole all displayed evident inhibitory effects on the proliferation of A549 cells. The results of LDH assay demonstrated that the drugs at the test range of concentration did not cause necrosis in the cells. Propafenone could elevate the protein level of P53 effectively (P<0.01). CONCLUSIONS: Oxytetracycline, propafenone and metamizol (dipyrone) all displayed evident inhibitory effects on the proliferation of A549 cells. Propafenone also displayed evident inhibitory effects on the proliferation of Hela cells.

[Study on the relations between overweight, obesity, blood pressures, serum lipids and glucose in schoolchildren of Shijiazhunag].

OBJECTIVE: To explore the clustering character of overweight and obesity with multiple cardiovascular disease risk factors such as blood pressure, serum lipids and glucose, and to provide evidence for intervention in childhood. METHODS: A cross-sectional study was conducted on 913 children aged 7-13 years in urban area of Shijiazhuang. Measurements included height, weight, systolic blood pressure (SBP), diastolic blood pressure (DBP) and fasting serum total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and serum glucose (GLU). RESULTS: Overall prevalence rate of overweight and obesity was 29.24% (boys: 34.98% vs. girls: 24.23%). When compared with normal children, children with overweight or obesity had significantly higher levels of SBP, DBP, TC, TG but low HDL-C. The prevalence rates of high SBP, DBP, TC, TG, GLU and low HDL-C in overweight and obese children were higher than in normal children. After adjusted for gender and age, the odds ratios of overweight and obese children for high SBP, DBP, TC, TG, GLU and low HDL-C were 6.77, 3.22, 2.55, 6.42, 3.85 and 2.94 (95% CI: 4.15-11.04, 1.38-7.49, 1.59-4.11, 3.46-11.92, 1.69-8.78 and 1.83-4.73), respectively. Odds ratios of overweight and obese children holding any one, two or three of the selected six risk factors appeared to be 2.74, 13.15 and 15.33 (95% CI : 1.92-3.92, 6.69-25.87 and 4.17-56.39), respectively. CONCLUSION: Childhood overweight and obesity increased the clustering of children's risk factors on cardiovascular diseases, as well as increasing the risk of children acquiring multiple cardiovascular disease risk factors. Controlling overweight and obesity would help early prevention on children from getting cardiovascular diseases.