[Studies on cold resistance of hazel determined and analyzed by atomic absorption spectrometry].

Using annual branch of hazel as the experimental materials, the K(+)-leakage and relative electric conductivity of three hazel species (six hazel clones) which had been treated with different low temperature were determined by electro-conductivity gauge and atomic absorption spectrometry. Regression models were established for low temperature to the K(+)-leakage or the relative electric conductivity of six hazel clones. The results showed that there was the same result of cold resistance for all clones using the two methods of comprehensive evaluation, and the indicator of K(+)-leakage rate determined by atomic absorption spectrometry can be used as a means of early identification of cold resistance of hazel clones. There were obvious differences among the clones in the ability of cold resistance. The order of the ability of cold resistance for the six hazel clones was C7R7 > Z-9-40 > C6R1 > CS2R1 > Z-9-22 > Z-9-30, and the order of the ability of cold resistance for the three hazel species was C. heterophylla > C. heterophyllax X (C. heterophylla X C. avellana) > C. heterophylla X C. avellana. The median lethal temperature of tissue for all clones is -26(-)-40 degrees "C.

[Role of nuclear factor of kB in tumor necrosis factor alpha-mediated INS-1 cell apoptosis].

OBJECTIVE: To investigate the effect of cytokine tumor necrosis factor alpha(TNFalpha) on pancreatic beta cells apoptosis and the effect of transcription factor nuclear factor of kappa B (NF-kB) on TNFalpha-mediated apoptosis. METHODS: INS-1 cells, a pancreatic beta cell line, were cultured,and recombinant DNA technique, transfection and reinfection technology were used to obtain INS-1/IkBDeltaN cells expressing inhibitor of kB (IkB)alphaDeltaN, mutant IkBalpha (inhibitor of NF-kB). DNA fragmentation assay and fluorescence analysis using a kB-luc reporter gene were applied to observe the NF-kB activity and beta cell apoptosis. RESULTS: NF-kB activity induced by IL-Ibeta was detectable in INS-1 cells but not in INS-1/IkBDeltaN cells. After incubation of the cells with IL-1beta (10 micro g/L), TNFalpha (100 micro g/L) and interferon (IFN)gamma (100 000 U/L) for 48 hours, the combination of TNFalpha and IFNgamma induced apoptosis in INS-1 cells but not in INS-1/IkBDeltaN cells. No apoptosis was observed after incubation of INS-1 cells with IL-1beta or IFNgamma or IL-1beta plus IFNgamma. CONCLUSION: Apoptosis is one of the TNFalpha-induced beta-cell death forms. NF-kB may play an important role in the TNFalpha-mediated beta-cell apoptosis. Inhibition of NF-kB activation protects beta-cells from TNFalpha-induced apoptosis.

[The effect of peroxisome proliferator-activated receptor alpha and gamma ligands on free fatty acid-induced INS-1 cell impairment].

OBJECTIVE: To investigate the effect of peroxisome proliferator-activated receptor alpha and gamma (PPARalpha and PPARgamma) ligands on free fatty acid (FFA)-induced pancreatic beta-cell impairment. METHODS: Insulinoma cell line beta-cell (INS-1 cells) were treated with PPARalpha ligand (clofibrate) and PPARgamma ligands (troglitazone and thiazolidinedione). C, N diphenyl-N'-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) viability assay and DNA fragmentation analysis were used to evaluate the effect of PPARalpha and PPARgamma ligands on FFA-induced INS-1 cell impairment. RESULTS: The viability of INS-1 cells decreased after incubation of the cells with FFA (0.25 - 1 mmol/L) for 24 hours. FFA (1 mmol/L) was also found to induce INS-1 cell apoptosis. Comparison of the cells treated with or without clofibrate (100 micro mol/L), troglitazone (10 micro mol/L) and thiazolidinedione (100 micro mol/L), we found that these PPARalpha and PPARgamma ligands could protect INS-1 cells from the cytotoxicity of FFA, including lipoapoptosis. CONCLUSION: FFA mediates significant lipotoxicity and lipoapoptosis in beta-cells and application of PPARalpha and PPARgamma ligands might be of value in protection of beta-cells from FFA cytotoxicity.