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31.
A SXRF method for determining the relative concentration of trace elements in plasma protein affected by cisplatin 总被引:2,自引:0,他引:2
This article presents an analytical method for the determination of the relative concentrations of trace elements in plasma
protein by gel chromatography combined with SXRF (synchrotron radiation X-ray fluorescence). The fraction of plasma protein
of male Kunming mice (body weight 24.2±0.3 g), treated with a cisplatin ip injection at a dose of 10 mg/kg, was obtained by
the separation of a Sephadex G-50 column (buffered with ammonium acetate, pH 5.7). The SXRF experiments were performed at
the Beijing Electron Positron Collider synchrotron radiation facility. The elements (Pt, S, Ca, Fe, Ni, Cu, Zn, Se, Br, and
Sr) in the fraction of the plasma proteins (>22 kDa) were assayed using highly sensitive SXRF. The relative concentrations
of elements were calculated by a normalization of Compton scattering intensity around 22 keV, after the normalization for
the collection time of the X-ray spectrum and the counting of the ion chamber, and subtracting the contribution of the polycarbonate
film for the supporting sample. The determination could prove that the element Pt in plasma was bound with macromolecular
protein. Cu and S were present in the fraction of the protein in mice treated with cisplatin increase, and their ratios of
treated/control were 1.66±0.06 and 1.78±0.33, respectively; Zn decreased to a ratio of 0.78±0.09. Our results are in agreement
with others that cisplatin exposure leads to a marked loss of kidney copper and a moderate rise in kidney zinc. However, this
article primarily describes one of the analytical methods used; it does not emphasize the results of the effect of cisplatin
on trace elements in plasma protein. 相似文献
32.
Establishment and characterization of a cisplatin-resistant cell line (IGSK-1) from a poorly differentiated gastric adenocarcinoma 总被引:1,自引:0,他引:1
Ohi S Takahashi N Ninomiya K Nakajima M Hashimoto H Tachibana T Yanaga K Ishikawa H 《Human cell》2007,20(1):15-22
We successfully established a spontaneously cisplatin-resistant tumor cell line (designated as IGSK-1) derived from original gastric carcinoma. The patient was a 75-year-old Japanese woman. The histopathological diagnosis was gastric poorly differentiated adenocarcinoma accompanied with metastatic foci in lymph nodes, pT3, N2 M0, stage IIIB. The IGSK-1 cells grew as adhesive and monolayered cultures on the bottom of dishes. The susceptibility of the IGSK-1 cells to anti-cancer drugs was examined using oxygen electrode apparatus (Daikin, Tsukuba, JPN), and the results suggested TXL was effective, and CDDP, CPT-11 and 5-FU were not effective. Gastrin and somatostatin secretions were confirmed by immunohistochemical staining and also radioimmunoassay. Immunohistochemistry and radioimmunoassay for serotonin suggested the IGSK-1 cells might incorporate serotonin from the growth media. Spontaneously cisplatin-resistant gastric carcinoma cell line secreted gastrin and somatostatin is very important material for chemotherapy. 相似文献
33.
Co‐culture of bone marrow‐derived mesenchymal stem cells overexpressing lipocalin 2 with HK‐2 and HEK293 cells protects the kidney cells against cisplatin‐induced injury
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34.
目的:汉防己甲素和顺铂联合作用乳腺癌细胞,来提高癌细胞对顺铂的敏感性.方法:运用原子力显微镜对乳腺癌细胞表面的超微结构进行表征;MTr法和流式细胞术检测细胞的生长抑制率和细胞周期变化.结果:顺铂和汉防己甲素分别作用乳腺癌细胞48h IC50值为26.33μmoL/l和5.6μmok/l;联合用药组的IC50值为汉防己甲素2.5μmol/L和顺铂13.32μmol/l,在低浓度的联合用药作用乳腺癌细胞24h细胞膜表面结构被破坏,产生孔洞,作用48h被严重破坏使细胞周期在S比例增加为51.7%±0.30%.结论:提高了癌细胞对抗癌药物的敏感性,联合用药通过改变了细胞膜的结构对癌细胞进行有效杀伤,抑制肿瘤细胞生长. 相似文献
35.
Wild-type p53 has a major role in the response and execution of apoptosis after chemotherapy in many cancers. Although high levels of wild-type p53 and hardly any TP53 mutations are found in testicular cancer (TC), chemotherapy resistance is still observed in a significant subgroup of TC patients. In the present study, we demonstrate that p53 resides in a complex with MDM2 at higher cisplatin concentrations in cisplatin-resistant human TC cells compared with cisplatin-sensitive TC cells. Inhibition of the MDM2–p53 interaction using either Nutlin-3 or MDM2 RNA interference resulted in hyperactivation of the p53 pathway and a strong induction of apoptosis in cisplatin-sensitive and -resistant TC cells. Suppression of wild-type p53 induced resistance to Nutlin-3 in TC cells, demonstrating the key role of p53 for Nutlin-3 sensitivity. More specifically, our results indicate that p53-dependent induction of Fas membrane expression (∼threefold) and enhanced Fas/FasL interactions at the cell surface are important mechanisms of Nutlin-3-induced apoptosis in TC cells. Importantly, an analogous Fas-dependent mechanism of apoptosis upon Nutlin-3 treatment is executed in wild-type p53 expressing Hodgkin lymphoma and acute myeloid leukaemia cell lines. Finally, we demonstrate that Nutlin-3 strongly augmented cisplatin-induced apoptosis and cell kill via the Fas death receptor pathway. This effect is most pronounced in cisplatin-resistant TC cells. 相似文献
36.
Increased expression of DNA repair genes contributes to the extreme resistance shown by melanoma to conventional DNA-damaging chemotherapeutics. One such chemotherapeutic effective against a range of other cancers, but not melanoma, is cisplatin. The DNA repair protein, ERCC1, is needed to remove cisplatin-induced DNA damage. We have shown that ERCC1 is essential for melanoma growth and resistance to cisplatin in a mouse xenograft model. Untreated xenografts of our transformed Ercc1-proficient melanocyte cell line grew very rapidly as malignant melanoma. Cisplatin treatment caused initial shrinkage of xenografts, but cisplatin-resistant regrowth soon followed. Cells reisolated into culture had twofold elevated levels of ERCC1 compared to both input cells and cells reisolated from untreated xenografts. An isogenic Ercc1-deficient derivative grew equally well in vitro as the Ercc1-proficient melanocyte cell line. However, in xenografts, the Ercc1-deficient melanomas were much slower to establish and were completely cured by just two cisplatin treatments. 相似文献
37.
Protective agent, erdosteine, against cisplatin-induced hepatic oxidant injury in rats 总被引:5,自引:0,他引:5
Cisplatin, one of the most active cytotoxic agents against cancer, has several toxicities. Hepatotoxicity is one of them occurred
during high doses treatment. The aim of this study was to determine the effects of erdosteine against cisplatin-induced liver
injury through tissue oxidant/antioxidant parameters and light microscopic evaluation. The rats were randomly divided into
three groups: control (n=5), cisplatin (10 mg/kg, n=6) and cisplatin+erdosteine (50 mg/kg/day oral erdosteine, n=8) groups. The rats were sacrificed at the 5th day of cisplatin treatment. The liver tissues were examined with light microscopy
and oxidant/antioxidant biochemical parameters. The malondialdehyde (MDA) and nitric oxide (NO) levels were increased in the
cisplatin group in comparison with the control and cisplatin+erdosteine groups (p<0.05). There was no significant difference in MDA and NO levels between control and cisplatin+erdosteine groups. The activities
of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were higher in cisplatin+erdosteine group
than cisplatin group (p<0.05). However, the CAT and GSH-Px activities were significantly lower in cisplatin group than in control group (p<0.05). The light microscopic examination revealed that cytoplasmic changes especially around cells of central vein were observed
in cisplatin group. Hepatocellular vacuolization was seen in these cells. In the cisplatin plus erdosteine group, a decrease
in cytoplasmic changes with the hepatocytes and sinusoidal dilatations around cells of central vein were noticed in as compared
to cisplatin group. In the light of microscopic and biochemical results, it was concluded that cisplatin-induced liver damage
in high dose and erdosteine prevented this toxic side effect by the way of its antioxidant and radical scavenging effects.
(Mol Cell Biochem 278: 79–84, 2005) 相似文献
38.
Basma H El-Refaey H Sgagias MK Cowan KH Luo X Cheng PW 《Journal of biomedical science》2005,12(6):999-1011
Summary Chemotherapy has been used for treatment of breast cancer but with limited success. We characterized the effects of bcl-2
antisense and cisplatin combination therapy in two human isogenic breast carcinoma cells p53(+)MCF-7 and p53(−)MCF-7/E6. The
transferrin-facilitated lipofection strategy we have developed yielded same transfection efficiency in both cells. Bcl-2 antisense
delivered with this strategy significantly induced more cell death, apoptosis, and cytochrome c release in MCF-7/E6 than in MCF-7, but did not affect Fas level in both cells and activated caspase-8 equally. Cisplatin
exerted same effects on cell viability and apoptosis in both cells, but released smaller amounts of cytochrome c while activated more caspase-8 in MCF-7/E6. The combination treatment yielded greater effects on cell viability, apoptosis,
cytochrome c release, and caspase-8 activation than individual treatments in both cells although p53(−) cells were more sensitive. The
potentiated activation of caspase-8 in the combination treatment suggested that caspase-8-mediated (but cytochrome c-independent) apoptotic pathway is the major contributor of the enhanced cell killing. Thus, bcl-2 antisense delivered with
transferrin-facilitated lipofection can achieve the efficacy of killing breast cancer cells and sensitizing them to chemotherapy.
Bcl-2 antisense and cisplatin combination treatment is a potentially useful therapeutic strategy for breast cancer irrespective
of p53 status.
Hesham Basma and Hesham El-Refaey contributed equally 相似文献
39.
40.
Rafał Jakub Bułdak Renata Polaniak Łukasz Bułdak Krystyna Żwirska‐Korczala Magdalena Skonieczna Aleksandra Monsiol Michał Kukla Anna Duława‐Bułdak Ewa Birkner 《Bioelectromagnetics》2012,33(8):641-651
The aim of this study was to assess the influence of cisplatin and an extremely low frequency electromagnetic field (ELF‐EMF) on antioxidant enzyme activity and the lipid peroxidation ratio, as well as the level of DNA damage and reactive oxygen species (ROS) production in AT478 carcinoma cells. Cells were cultured for 24 and 72 h in culture medium with cisplatin. Additionally, the cells were irradiated with 50 Hz/1 mT ELF‐EMF for 16 min using a solenoid as a source of the ELF‐EMF. The amount of ROS, superoxide dismutase (SOD) isoenzyme activity, glutathione peroxidase (GSH‐Px) activity, DNA damage, and malondialdehyde (MDA) levels were assessed. Cells that were exposed to cisplatin exhibited a significant increase in ROS and antioxidant enzyme activity. The addition of ELF‐EMF exposure to cisplatin treatment resulted in decreased ROS levels and antioxidant enzyme activity. A significant reduction in MDA concentrations was observed in all of the study groups, with the greatest decrease associated with treatment by both cisplatin and ELF‐EMF. Cisplatin induced the most severe DNA damage; however, when cells were also irradiated with ELF‐EMF, less DNA damage occurred. Exposure to ELF‐EMF alone resulted in an increase in DNA damage compared to control cells. ELF‐EMF lessened the effects of oxidative stress and DNA damage that were induced by cisplatin; however, ELF‐EMF alone was a mild oxidative stressor and DNA damage inducer. We speculate that ELF‐EMF exerts differential effects depending on the exogenous conditions. This information may be of value for appraising the pathophysiologic consequences of exposure to ELF‐EMF. Bioelectromagnetics 33:641–651, 2012. © 2012 Wiley Periodicals, Inc. 相似文献