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General and specific diseases

1: Anticancer Res 1997 Mar-Apr;17(2A):1163-6

Effect of ascorbate oxidase on radical intensity and cytotoxic activity of ascorbate.

Sakagami H, Satoh K.

Department of Biochemistry, School of Medicine, Showa University, Tokyo, Japan.

In order to test whether ascorbyl radical can directly induce apoptotic cell death, it was produced by the reaction of sodium L-ascorbate with L-ascorbate oxidase. Sodium L-ascorbate induced cytotoxicity against both human glioblastoma and promyelocytic leukemic cell lines. The addition of ascorbate oxidase significantly enhanced both degradation and radical generation of ascorbate, but completely eliminated its cytotoxic activity against both of these cells. These data demonstrate that the ascorbyl radical is not the sole determinant of apoptosis induction.

PMID: 9137465 [PubMed - indexed for MEDLINE]

1: Pathol Oncol Res 1999;5(3):223-8

Antiproliferative properties of the lazaroids U-83836E and U-74389G on glioma cells in vitro.

Durmaz R, Deliorman S, Isiksoy S, Uyar R, Erol K, Tel E.

Medical Faculty of Osmangazi University, Department of Neurosurgery, Eskisehir, 90-26480, Turkey. This email address is being protected from spambots. You need JavaScript enabled to view it.

The 21-aminosteroids (lazaroids) are a new family of steroid compounds that inhibit lipid peroxidation reactions. They are novel antioxidant agents, which have been shown to have antiproliferative properties on cancer cells and also are thought to prevent free radical-mediated blood-brain barrier damage. In order to understand the effect of lazaroids on glioma, we tested U-83836E and U-74389G at doses ranging between 0.1 100 m mM on primary cultures of glioblastoma multiforme from three patients, rat C6 glioma cell line, and 5 th subculture established from one of the patients. The effects of both compounds on cell proliferation were determined using 3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) colorimetric assay. U-83836E in the primary cultures was found to have 50% inhibitory concentrations (IC50 ) of 6.30, 6.75 and 6.50 m mM, respectively. The IC50 value of U-74389G was calculated as 91 m mM in only one of the patients. On C6 glioma cells, while the IC50 of U-83836E was 45 m mM, U-74389G showed no cytotoxic effect. On the 5 th subculture, U-83836E had an IC50 of 37.5 m mM, but the cytotoxic effects of U-74389G was less than in that of the primary culture. In conclusion, these compounds were found to be more cytotoxic in primary culture than the cell lines and there were also differences between their members in the inhibition of cell survival.

PMID: 10491022 [PubMed - indexed for MEDLINE]

1: Nat Immun 1998;16(1):27-33

Biotherapy with the pineal immunomodulating hormone melatonin versus melatonin plus aloe vera in untreatable advanced solid neoplasms.

Lissoni P, Giani L, Zerbini S, Trabattoni P, Rovelli F.

Division of Radiation Oncology, San Gerardo Hospital, Monza, Milan, Italy.

The possibility of natural cancer therapy has been recently suggested by advances in the knowledge of tumor immunobiology. Either cytokines such as IL-2, or neurohormones, such as the pineal indole melatonin (MLT), may activate anticancer immunity. In addition, immunomodulating substances have also been isolated from plants, particularly from Aloe vera. Preliminary clinical studies had already shown that MLT may induce some benefits in untreatable metastatic solid tumor patients, whereas, for the time being, no clinical trial has been performed with aloe products. We have carried out a clinical study to evaluate whether the concomitant administration of aloe may enhance the therapeutic results of MLT in patients with advanced solid tumors for whom no effective standard anticancer therapies are available. The study included 50 patients suffering from lung cancer, gastrointestinal tract tumors, breast cancer or brain glioblastoma, who were treated with MLT alone (20 mg/day orally in the dark period) or MLT plus A. vera tincture (1 ml twice/day). A partial response (PR) was achieved in 2/24 patients treated with MLT plus aloe and in none of the patients treated with MLT alone. Stable disease (SD) was achieved in 12/24 and in 7/26 patients treated with MLT plus aloe or MLT alone, respectively. Therefore, the percentage of nonprogressing patients (PR + SD) was significantly higher in the group treated with MLT plus aloe than in the MLT gorup (14/24 vs. 7/26, p < 0.05). The percent 1-year survival was significantly higher in patients treated with MLT plus aloe (9/24 vs. 4/26, p < 0.05). Both treatments were well tolerated. This preliminary study would suggest that natural cancer therapy with MLT plus A. vera extracts may produce some therapeutic benefits, at least in terms of stabilization of disease and survival, in patients with advanced solid tumors, for whom no other standard effective therapy is available.

Publication Types: Clinical Trial Controlled Clinical Trial

PMID: 9789122 [PubMed - indexed for MEDLINE]

1: Anticancer Res 1999 Jul-Aug;19(4B):3125-32

Induction of cell death by ascorbic acid derivatives in human renal carcinoma and glioblastoma cell lines.

Makino Y, Sakagami H, Takeda M.

First Department of Biochemistry, School of Medicine, Showa University, Tokyo, Japan.

Sodium-L-ascorbate, L-ascorbic acid, D-isoascorbic acid, sodium 5,6-benzylidene-L-ascorbate and sodium-6-beta-O-galactosyl-L-ascorbate, which produce ascorbyl radicals during the oxidative degradation, also induced cytotoxicity against cultured human renal carcinoma (TC-1) and glioblastoma multiform tumor (T98G) cell lines. On the other hand, L-ascorbic acid 2-phosphate magnesium and L-ascorbic acid 2-sulfate dipotassium salt, which do not produce the ascorbyl radical, were inactive. This suggests the possible role of the ascorbyl radical for cell death induction. T98G cells were more resistant to ascorbate analogs than TC-1 and HL-60 cells, possibly due to higher intracellular glutathione concentrations. Ascorbate treatment induced rapid elevation of both intracellular concentration of cAMP and Ca2+ in HL-60 cells, but not in TC-1 and T98G cells. However, the elevation of cAMP by theophyline and N,2-dibutyryl adenosine 3,5 cyclic monophosphate (dibutyryl cAMP) resulted in a decrease in the viable cell number. This suggests the possible role of cAMP for ascorbate-induced cell death.

PMID: 10652601 [PubMed - indexed for MEDLINE]

1: Nutr Cancer 2000;38(1):40-9

Oxidant stress and glioblastoma multiforme risk: serum antioxidants, gamma-glutamyl transpeptidase, and ferritin.

Schwartzbaum JA, Cornwell DG.

Division of Epidemiology and Biometrics, College of Medicine and Public Health, Ohio State University, and Comprehensive Cancer Center, Columbus, OH 43210, USA.

Case-control studies of serum antioxidants are difficult to interpret, because antioxidants may be altered by the disease under study. However, because glioblastoma multiforme (GBM) is a relatively rare disease, a cohort study would require a large sample observed for many years. In the present case-control pilot study (34 cases and 35 controls), we evaluated the association between serum levels of ascorbic acid (AA) and alpha- and gamma-tocopherol (alpha-T and gamma-T) measured before diagnostic surgery. To control for influence of GBM on serum AA, alpha-T, and gamma-T, we adjusted for oxidant stress indexes (gamma-glutamyl transpeptidase and uric acid) and an acute-phase response index (serum ferritin). When adjusted, AA is inversely related to GBM (p for trend = 0.007). In addition, AA interacts with alpha-T to further reduce GBM risk (test for interaction, p = 0.04). gamma-T is not associated with GBM (p = 0.71). However, gamma-glutamyl transpeptidase (p = 0.004), coenzyme Q (p = 0.01), and ferritin (p = 0.009) are positively and uric acid (p = 0.000) is negatively related to GBM. We conclude that 1) AA and alpha-T are jointly related to GBM after adjustment for GBM-produced oxidant stress and 2) there is a strong association between the presence of GBM and oxidant stress.

PMID: 11341043 [PubMed - indexed for MEDLINE]

1: J Neurooncol 2001 Aug;54(1):15-22

Antiproliferative and apoptotic effect of ascorbyl stearate in human glioblastoma multiforme cells: modulation of insulin-like growth factor-I receptor (IGF-IR) expression.

Naidu KA, Tang JL, Naidu KA, Prockop LD, Nicosia SV, Coppola D.

Department of Neurology, H. Lee Moffitt Cancer Center and Research Institute, College of Medicine, University of South Florida, Tampa, USA. This email address is being protected from spambots. You need JavaScript enabled to view it.

Human glioblastomas (gliomas) are characterized as highly invasive and rapidly growing brain tumors. In this study, we present data on in vitro effect of ascorbyl stearate (Asc-S), a liphophilic derivative of ascorbic acid on cell proliferation, transformation, apoptosis and modulation of expression of insulin-like growth factor-I receptor (IGF-IR) in human glioblastoma multiforme (T98G) cells. Asc-S showed significant inhibition of fetal bovine serum and human recombinant insulin-like growth factor-I (IGF-I) dependent cell proliferation in a dose dependent manner. Treatment of T98G cells with 0, 50, 100 and 150 microM Asc-S for 24h slowed down the cell multiplication cycle with significant accumulation of cells at late S/G2-M phase of cycle. Asc-S treatment (100 microM) reversed the transformed phenotype as determined by clonogenecity in soft agar and also induced apoptosis of T98G. These changes were found to be associated with significant decrease in IGF-IR expression in dose and time dependent manner compared to untreated controls. The data clearly demonstrate that Asc-S has antiproliferative and apoptotic effect on T98G cells probably through modulation of IGF-IR expression and consequent facilitation of programmed cell death.

PMID: 11763418 [PubMed - indexed for MEDLINE]

1: Anticancer Res 1997 Mar-Apr;17(2A):1125-9

Effect of metal ions on radical intensity and cytotoxic activity of ascorbate.

Satoh K, Sakagami H.

Analysis Center, School of Pharmaceutical Sciences, Showa University, Tokyo, Japan.

Various metal ions were investigated for their ability to modify the radical intensity and cytotoxic activity of sodium ascorbate or ascorbic acid. The addition of metal ions, such as Cu+, Cu2+, Fe2+, Zn2+, Mn2+ and Fe3+, dose-dependently enhanced the ascorbyl radical intensity whereas Na+, K+, Ca2+ and Mg2+ were totally inactive. The enhancement of ascorbyl radical intensity by metal ions was tightly coupled with the accelerated degradation of ascorbate. Addition of either serum or albumin significantly reduced the stimulation effect of Cu2+, and almost completely eliminated that of Fe3+ and Zn2+. The noncytotoxic concentration of Cu2+ significantly enhanced the cytotoxicity of ascorbate against cultured human glioblastoma T98G cell line. The present data suggest the possible role of metal ions in the regulation of the biological activity of ascorbate.

PMID: 9137459 [PubMed - indexed for MEDLINE]

1: Free Radic Biol Med 1997;23(2):260-70

Effect on an iron-chelator on ascorbate-induced cytotoxicity.

Sakagami H, Satoh K, Fukuchi K, Gomi K, Takeda M.

Department of Biochemistry, School of Medicine, Showa University, Tokyo, Japan.

We investigated the effect of deferoxamine mesylate (DFO), an iron chelator, to test whether ascorbate-induced cytotoxicity is due to iron-catalyzed oxidation. Exposing human promyelocytic leukemic HL-60 cells to either sodium ascorbate or ascorbic acid for 1 h resulted in the progressive production of apoptotic cells characterized by cell shrinkage, as well as nuclear and internucleosomal DNA fragmentation. The addition of micromolar to millimolar concentrations of DFO during the 1-h exposure did not inhibit, but rather enhanced the ascorbate-induced apoptosis in both regular and serum-free RPMI1640 medium. However, a higher concentration of serum significantly inhibited the ascorbate-induced cytotoxicity. In contrast, the cytotoxic activity of ascorbate against T98G human glioblastoma cells was enhanced or reduced by micromolar and millimolar concentrations of DFO, respectively. Ascorbate significantly increased the oxidation potential in the culture medium, and the pro-oxidant action of ascorbate was further augmented by the presence of the cells. DFO did not significantly affect the ascorbyl radical intensity and only slightly reduced the ascorbate-elevated oxidation potential. These data demonstrated that ascorbate can induce cytotoxicity even in iron-deficient medium.

PMID: 9199888 [PubMed - indexed for MEDLINE]

1: Anticancer Res 1996 Sep-Oct;16(5A):2629-34

Ca2+ mobilization during cell death induction by sodium 5, 6-benzylidene-L-ascorbate.

Takahashi H, Sakagami H, Ohata H, Iida M, Momose K, Yamamura M, Takeda M.

First Department of Biochemistry, School of Medicine, Showa University, Tokyo, Japan.

The cytotoxic activity of sodium 5,6-benzylidene-L-ascorbate (SBA) against human KG-1-C glioma and T98G glioblastoma cell lines was augmented by pretreatment of the cells with L-buthionine-[S, R]-sulfoximine (BSO), which reduced the intracellular glutathione concentrations. SBA produced shrunken cells and large DNA fragments, without the induction of nuclear and internucleosomal DNA fragmentation. The rapid elevation of intracellular free Ca2+ concentration observed after SBA treatment was further augmented by BSO pretreatment. A confocal experiment with Fluo-3 fluorescence revealed that SBA markedly elevated the free Ca2+ concentration in the nuclear region, but did not significantly affect that in the cytoplasmic region. The present study suggests that the nuclear accumulation of Ca2+ is an important initial step for cell death induction by SBA.

PMID: 8917362 [PubMed - indexed for MEDLINE]

1: Oncology 1996 Jan-Feb;53(1):43-6

Increased survival time in brain glioblastomas by a radioneuroendocrine strategy with radiotherapy plus melatonin compared to radiotherapy alone.

Lissoni P, Meregalli S, Nosetto L, Barni S, Tancini G, Fossati V, Maestroni G.

Division of Oncological Radiotherapy, San Gerardo Hospital, Monza, Italy.

The prognosis of brain glioblastoma is still very poor and the median survival time is generally less than 6 months. At present, no chemotherapy has appeared to influence its prognosis. On the other hand, recent advances in brain tumor biology have suggested that brain tumor growth is at least in part under a neuroendocrine control, mainly realized by opioid peptides and pineal substances. On this basis, we evaluated the influence of a concomitant administration of the pineal hormone melatonin (MLT) in patients with glioblastoma treated with radical or adjuvant radiotherapy (RT). The study included 30 patients with glioblastoma, who were randomized to receive RT alone (60 Gy) or RT plus MLT (20 mg/daily orally) until disease progression. Both the survival curve and the percent of survival at 1 year were significantly higher in patients treated with RT plus MLT than in those receiving RT alone (6/14 vs. 1/16). Moreover, RT or steroid therapy-related toxicities were lower in patients concomitantly treated with MLT. This preliminary study suggests that a radioneuroendocrine approach with RT plus the pineal hormone MLT may prolong the survival time and improve the quality of life of patients affected by glioblastoma.

Publication Types: Clinical Trial Randomized Controlled Trial

PMID: 8570130 [PubMed - indexed for MEDLINE]

1: Anticancer Res 1995 Jul-Aug;15(4):1241-6

The inhibitory effect of conjugated dienoic derivatives (CLA) of linoleic acid on the growth of human tumor cell lines is in part due to increased lipid peroxidation.

Schonberg S, Krokan HE.

UNIGEN Center for Molecular Biology, University of Trondheim, Norway.

We have examined the effects of linoleic acid, LA (18:2 n-6) and its naturally occurring conjugated derivatives (CLA) on the growth of three different lung adenocarcinoma cell lines (A-427, SK-LU-1, A549) and one human glioblastoma cell line (A-172). CLA exerted a dose dependent reduction in proliferation of the lung adenocarcinoma cell lines with A-427 being the most sensitive one, but had virtually no effect on A-172. In contrast, LA had no inhibitory effect on either cell line. A significant increase in lipid peroxidation (measured as formation of malondialdehyde, MDA) was observed after exposure of the lung adenocarcinoma cell lines to 40 microM CLA. This level was approximately 2-fold higher than after exposure to 40 microM LA. The formation of MDA was completely abolished by 30 microM vitamin E, but the growth rates were only partially restored, indicating that cytotoxic lipid peroxidation products are only in part responsible for the growth inhibitory effects of CLA.

PMID: 7654003 [PubMed - indexed for MEDLINE]

1: Biol Trace Elem Res 1995 Jul;49(1):1-7

Effect of selenium on malignant tumor cells of brain.

Zhu Z, Kimura M, Itokawa Y, Nakatsu S, Oda Y, Kikuchi H.

Department of Hygiene, Faculty of Medicine, Kyoto University, Japan.

Some reports have demonstrated that selenium can inhibit tumorigenesis in some tissues of animal. However, little is known about the inhibitory effect on malignant tumor cells of brain. The purpose of our study was to determine the biological effect of selenium on growth of rat glioma and human glioblastoma cell lines. Cell lines C6 and A172 were obtained from Japanese Cancer Research Resources Bank, Tokyo, Japan (JCRB). Cells were cultured in Dulbecco's Modified Eagle's Medium (DMEM) supplemented with 10% fetal calf serum at 37 degrees C in a humidified atmosphere of air and 5% CO2. Antiproliferative effects of selenium were evaluated using growth rate assay quantifying cell number by MTT assay. An antiproliferative effect of selenium was found in two cell lines, which was more effective on human A172 glioblastoma and less effective on rat C6 glioma.

PMID: 7577318 [PubMed - indexed for MEDLINE]

1: J Immunol 1994 Sep 15;153(6):2681-90

Activation of NF-kappa B and induction of vascular cell adhesion molecule-1 and intracellular adhesion molecule-1 expression in human glial cells by IL-1. Modulation by antioxidants.

Moynagh PN, Williams DC, O'Neill LA.

Department of Biochemistry and Biotechnology Institute, Trinity College, University of Dublin, Ireland.

The infiltration of leukocytes into the central nervous system is associated with many pathologic conditions of the brain. The mechanisms by which these immune cells can penetrate the blood-brain barrier and remain within the brain are not understood. However, elevated brain levels of the pro-inflammatory cytokine IL-1 appear to accompany pathogenesis. The present study provides the first evidence that IL-1 can induce the expression of adhesion molecules for leukocytes on glial cells and suggests a role for the transcription factor NF-kappa B in the induction process. Human rIL-1 alpha was found to induce the expression of the cell adhesion molecules, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) but not E-selectin in human 1321N1 astrocytoma. Both VCAM-1 and ICAM-1 were detectable from 3 h and remained sustained for up to 72 h. Induction was inhibited by the IL-1 receptor antagonist. IL-1 alpha was also shown to induce the expression of VCAM-1 and ICAM-1 in a receptor-dependent fashion in human A172 glioblastoma. Activation of the transcription factor NF-kappa B was also observed in 1321N1 astrocytoma in response to IL-1 alpha treatment and was similarly abolished by pretreatment of cells with antagonist. Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma. However, both of these antioxidants demonstrated complex modulatory effects on the induction of cell adhesion molecule expression by IL-1. The induction of VCAM-1 but not of ICAM-1 proved susceptible to inhibition by both PDTC and NAC. The expression of adhesion molecules for leukocytes on glial cells in response to IL-1 may represent an important mechanism for retention of immune cells in the central nervous system that may be a prologue to inflammatory conditions in the brain.

PMID: 7521369 [PubMed - indexed for MEDLINE]

1: J Neurooncol 1994;21(2):127-33

Levels of water-soluble antioxidants in astrocytoma and in adjacent tumor-free tissue.

Landolt H, Langemann H, Probst A, Gratzl O.

Department of Neurosurgery, Cantonal Hospital, Basel, Switzerland.

The aim of the present study was to investigate the oxidative status in astrocytoma. Samples of brain tissue from the centre to the periphery of the tumor were obtained from 11 astrocytoma patients undergoing computer tomography-guided stereotaxic operation, who had been previously treated with the corticosteroid dexamethasone. Part of the sample was investigated histologically for clarification of tumor type, and the presence of neoplastic and non-neoplastic tissue and necrosis. The rest was used for the quantification of the antioxidants ascorbic acid, uric acid, glutathione and cysteine by high performance liquid chromatography, and for quantification of DNA. Levels of antioxidants were calculated as micrograms/g fresh tissue and mumol/g DNA, a parameter related to cell content. There was significantly more DNA in neoplastic samples than in non-neoplastic ones, indicating increased cell density. Uric acid (micrograms/g fresh tissue) was significantly increased in neoplastic compared with non-neoplastic tissue, and levels were even higher in necrotic tissue. There were no significant differences between neoplastic and non-neoplastic tissue levels of ascorbic acid, glutathione or cysteine, expressed as micrograms/g fresh tissue. However, when levels of these three compounds were expressed as mumol/g DNA, i.e. taking into account the higher cell density, ascorbic acid, glutathione and cysteine were significantly reduced in neoplastic samples compared with non-neoplastic ones. Results thus show that there are differences between the antioxidant levels in astrocytoma and non-neoplastic tissue, providing additional support for the hypothesis that free radicals play a role in tumor growth.

PMID: 7861188 [PubMed - indexed for MEDLINE]

1: Anticancer Res 1991 Jul-Aug;11(4):1533-8

Induction of tumor degeneration by sodium benzylideneascorbate.

Sakagami H, Asano K, Fukuchi K, Gomi K, Ota H, Kazama K, Tanuma S, Kochi M.

First Department of Biochemistry, School of Medicine, Showa University, Tokyo, Japan.

Intravenous administration of sodium benzylideneascorbate (SBA) rapidly necrotized inoperable human lung cancer, and induced degeneration of 3'-methyl-4-dimethylaminoazobenzene-induced rat hepatocellular carcinoma (vacuolar, eosinophilic degeneration, nuclear debris) without affecting the serum glutamic oxaloacetic transaminase, gamma-glutamyl transpeptidase and total protein levels. Cultured normal human lung and skin fibroblasts, and human glioma and glioblastoma cell lines were relatively resistant to SBA, when compared to human myelogenous leukemic cell lines. SBA had no apparent host immunopotentiation activity such as stimulation of cytokine action or production; activation of monocyte or polymorphonuclear cells; or modulation of poly (ADP-ribose) glycohydrolase activity. The data suggest that the antitumor activity of SBA might be produced by direct action of authentic SBA or its metabolized form(s), rather than by immunopotentiation of the hosts.

PMID: 1746910 [PubMed - indexed for MEDLINE]

1: Neurosurgery 1990 Oct;27(4):523-31

Ultrastructural evidence for differentiation in a human glioblastoma cell line treated with inhibitors of eicosanoid metabolism.

Wilson DE, Anderson KM, Seed TM.

Department of Neurosurgery (DEW), Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois.

Human glioblastoma cells incubated in the presence of inhibitors of eicosanoid biosynthesis show decreased cellular proliferation without cytotoxicity. We studied the ultrastructural morphology of a human glioblastoma cell line cultured with nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, or 5,8,11,14-eicosatetraynoic acid, a cyclooxygenase and lipoxygenase inhibitor. When glioblastoma cells were treated for 3 days with antiproliferative concentrations of either agent, they shared many morphological characteristics, including evidence for increased astrocytic differentiation with only limited signs of toxicity. The inhibited glioma cells demonstrated an increase in the number and length of astrocytic processes containing greater numbers of glial filaments, and the NDGA-treated cells also demonstrated extensive lateral pseudopod formation along the processes. The glioblastoma cell shape also became more elongated, losing the usual nuclear lobularity and nuclear inclusions, especially in NDGA-treated cells. Many cytoplasmic organelles packed the cytosol of the inhibited glioma cells, including prominent Golgi apparatus, dilated smooth endoplasmic reticulum evolving into dilated vesicles, cytoplasmic vacuoles, and numerous concentric laminations. There was limited evidence for toxicity, however, as the mitochondria were more pleomorphic with some mitochondrial distention and disruption of the cristae along with an increase in cytoplasmic vacuolization. We conclude that the inhibitors of eicosanoid biosynthesis, NDGA and 5,8,11,14-eicosatetraynoic acid, not only suppress glioblastoma cell proliferation, but also induce increased astrocytic differentiation.

PMID: 2234352 [PubMed - indexed for MEDLINE]

1: Cancer Lett 1982 Feb;15(2):173-8

Regulation of cell division in a human glioma cell clone by arachidonic acid and alpha-tocopherolquinone.

Liepkalns VA, Icard-Liepkalns C, Cornwell DG.

A human glioma cell clone (12-18 CV), derived from a previously characterized glioblastoma multiforme cell line, was established in culture. Lipid peroxidation (thiobarbituric acid test) occurred when either 8,11,14-eicosatrienoic acid or 5,8,11-eicosatetraenoic acid (arachidonic acid) was added to the cells in culture. The extent of lipid peroxidation was similar in fetal brain cells (CH II) treated with these polyunsaturated fatty acids. The antioxidant, alpha-tocopherolquinone, inhibited lipid peroxidation in both the glioma cell clone and fetal brain cells. Arachidonic acid significantly reduced cell division in both the glioma cell clone and fetal brain cells. alpha-Tocopherolquinone restored cell division to control levels in both cultures. These data show that cells from a tumor clone retain the capacity for lipid peroxidation. Furthermore, cell division in a tumor clone is correlated with lipid peroxidation in the same way that cell division in other cell lines is correlated with lipid peroxidation.

PMID: 6284351 [PubMed - indexed for MEDLINE]

1: Beitr Pathol 1974 Mar;151(3):281-96

[Neutron activation analysis of the trace elements cobalt, iron, rubidium, selenium, zinc, chromium, silver, cesium, antimony and scandium in surgical specimens of human brain tumors. 1]

[Article in German]

Schicha H, Muller W, Kasperek K, Schroder R.

PMID: 4365800 [PubMed - indexed for MEDLINE]

1: Nervenarzt 1973 Jun;44(6):325-6

[Scintigraphy with Se-75 Na selente in brain tumors and cardiovascular attacks]

[Article in German]

Rau H, Meienberg O, Langlotz M, Piroth D, Imhof H.

PMID: 4353220 [PubMed - indexed for MEDLINE]

1: Arkh Patol 1969;31(1):48-52

[Histochemical characteristics of ascorbic acid in nervous system tumors]

[Article in Russian]

Kasab'ian SS, Belikov ES.

PMID: 4313175 [PubMed - indexed for MEDLINE]