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Objective To evaluate the internal irradiation biological effects of 125I-UdR chitosan nanoparticles in hepatoma cells.Methods The accumulation and distribution of 125I-UdR-CS-DLN in hepatoma cells HepG2 and human liver tissue cells HL-7702 were observed with a confocal microscopy.The internal irradiation biological effects were evaluated by MTT assay,flow cytometry and single cell gel electrophoresis.The apoptosis of in situ rabbit liver tumor treated with 125I-UdR-CS-DLN was assayed by TUNEL staining technique.Results After 30 min of nano-particle treatment,its accumulation in the cytoplasm of HepG2 cells was significantly greater than that in HL-7702 cells.When the concentrations of 125I-UdR-CS-DLN was higher than 37 kBq/ml,the cell viability of HepG2 was significantly lower than that of lL-7702 at 24 and 48 h post-treatment(t =-4.46-6.31,P＜0.05),and the HepG2 cells were arrested at G1 phase and significantly impaired at G2/M phase.In addition,the degrees of DNA doublestrand break of both cell lines irradiated by 125I-UdR-CS-DLN were significantly higher than those treated with 125I-UdR,and the DNA repair capacity of HepG2 cells was significantly lower than that of HL-7702 cells(OTM:t =2.94,P ＜0.05;TDNA％:t =10.64,P ＜0.01).TUNEL staining showed that cell apoptosis could be induced in the rabbit liver carcinoma by 125I-UdR-CS-DLN but not by 125I-UdR.Conclusions The amount of 125I-UdR-CS-DLN absorbed by hepatoma cells is significantly higher than that of 125I-UdR,which suggests that 125 I-UdR-CS-DLN induces more stronger internal radiation biological effects of apoptosis and DNA damage on hepatoma cells.
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Objective To compare the incorporation method of 3H-TdR and 125Ⅰ-UdR on determining the proliferation effect of lymphocytes. Methods The proliferation effects of lymphocyte and Daudi lymphoma cells were estimated by 3H-TdR and 125Ⅰ-UdR incorporation. Results The incorporating fraction of 3H-TdR and 125Ⅰ-UdR into lymphocyte was 20.95% ± 1.06% and 1.00% ±0.04%,respectively, and the incorporating fraction for the lymphoma cells was 29. 94% ± 4. 10% and 6. 02% ±0. 73% ,respectively. The incorporation fractions of 3H-TdR into lymphocyte and lymphoma cells were much higher than those of 125Ⅰ-UdR, but the incorporating fractions of 3H-TdR or 125Ⅰ-UdR into the lymphoma cells were much higher than those of lymphocytes. Conclusions For lymphocytes, 125Ⅰ-UdR cannot substitute 3H-TdR as a tracer agent. But for lymphoma cells, whether 125Ⅰ-UdR could be replace 3H-TdR or not needs further research.
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Objective To evaluate the killing effect and the uptake of 125I-UdR on human lymphoma Raji and Daudi cell lines. Methods The amount of 125I-UdR in the cells and cell nuclei were determined after incubation of different time in RPMI 1640 culturing medium containing different concentrations of 125I-UdR. The killing effects of 125I-UdR on Raji and Daudi cell lines were estimated through MTT assay and cell cycle was analyzed by propidium iodide (PI) staining. Results The amounts of 125I-UdR in Raji and Dandi cells and cell nuclei were much higher than that of Na125I(P < 0.05). The amounts of 125l-UdR in Raji and Daudi cells were 14414±95 and (6916± 53.69) Bq/106 cell when the concentration was 100 kBq/ml. The amounts of Na125I were 68± 3.8 and (324±32.8) Bq/106 cell. The uptake of 125I-UdR in Raji and Daudi cells and cell nuclei increased with the 125I-UdR concentration and incubated time. The cell surviving fractions of 125I-UdR groups was much lower than that of Na125I groups (P < 0.05). When the concentration was 500 kBq/ml and incubated time was 48 hours, the Raji and Dandi cell surviving fractions of125I-UdR groups were (19.78 ± 1.39)% and (43.17 ± 2.69) % ;those of Na125I groups were (79.10 ± 1.79) % and (80.36 ± 6.12) %. The surviving fractions of 125I-UdR groups reduced with the 125I-UdR concentration. Conclusions 125I-UdR can be specially ingested by Raji and Daudi cells and incorporated into DNA, then the cells will be killed. The uptake of 125I-UdR is dose and time dependent.
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The reduced level of high density lipoprotein (HDL) in plasma is a strong predictor of atherosclerotic vascular disease risk. However, like low density lipoprotein (LDL), HDL is readily oxidized by a variety of oxidants in vitro . This review briefly discussed about the susceptibility of HDL to oxidation, the site and physiologic oxidants of HDL oxidation in vivo ,structural change in oxidized HDL, as well as the influence of different changes in structure of oxidized HDL on the protective function of HDL against atherosclerosis.