Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.3.5.1 (succinate dehydrogenase)
8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of selenium on 7,12-dimethylbenzanthracene-induced mammary tumorigenesis were examined in C57BL X DBA/2f F1 mice fed a semipurified diet. Mice fed 0.2 ppm selenium developed 56% mammary tumors; in contrast, mice fed 2.0 ppm selenium developed only 16% mammary tumors at 11 months of age. Mice fed the 2.0-ppm selenium diet grew as well as did their counterparts fed the 0.2-ppm selenium diet. In a separate experiment, the level of selenium-dependent glutathione peroxidase was measured in the mammary glands of control and 7,12-dimethylbenzanthracene-treated BALB/c mice fed basal and selenium-supplemented diets. 7,12-Dimethylbenzanthracene treatment resulted in decreased glutathione peroxidase activity n mice fed both low (0.03 ppm)- and high (1.50 ppm)-selenium diets. Thus, the chemopreventive effects of selenium could not be attributed to maintaining high levels of glutathione peroxidase. In a second series of experiments, the effects of selenium were further examined on the growth of mammary cell line YN-4 in monolayer cell culture. The mitochondrial inclusions seen in cells exposed to 5 X 10(-6) M selenium could not be correlated with changes in the activity of the mitochondrial enzymes, cytochrome c oxidase and succinate dehydrogenase, thus implying that there was no demonstratable impairment of mitochondria. The examination of selenium-treated cells with flow cytofluorometry indicated that cells were blocked in S-G2 phases of the cell cycle. This latter result illustrates one feasible approach towards identifying specific mechanisms for the chemopreventive effects of selenium.
Cancer Res 1983 May
PMID:Selenium and mouse mammary tumorigenesis: an investigation of possible mechanisms. 640 37

Experiments were carried out to determine if the difference in rates of cell proliferation between normal and neoplastic cells may be related to altered levels of oxidative enzymes. Assays were performed using homogenates from hepatocellular carcinoma HC-252, a rapidly growing and moderately well-differentiated tumor; from normal liver; and from the liver of the tumor-bearing ACI rat. Results of the mitochondrial enzymes indicated that the activities of cytochrome oxidase and succinate dehydrogenase were 3-fold lower in tumor homogenates than in liver homogenates. Monoamine oxidase activity could not be detected in HC-252; mixing experiments indicated no inhibitor was present in HC-252. Activities of th peroxisomal enzymes, urate oxidase, D-amino acid oxidase, and L-alpha-hydroxy acid oxidase were either undetected in the tumor or were 12-fold lower than in liver homogenates. The activity of xanthine oxidase, a cytoplasmic enzyme, was 5- to 6-fold lower in the tumor. Catalase activity in the tumor was also lower than in liver; this may be indicative of a lower oxidative environment at the cellular level. These enzyme activities of the liver of tumor-bearing rats were in the same range as those of normal rat liver, except that D-amino acid oxidase activity was slightly lower, and catalase activity was markedly lower and varied in a wide range. These results show an inverse correlation between the activities of oxygen-utilizing enzymes and rates of proliferation of one tumor line and its control. The possible implications of these results in neoplasia, cell proliferation, and cellular aging are discussed.
Cancer Res 1980 Dec
PMID:Oxidoreductase activities in normal rat liver, tumor-bearing rat liver, and hepatoma HC-252. 689 80

Sequential alterations in enzyme histochemical profiles and reaction of hepatocytes to rapid iron overload were examined in male BALB/c mice during chronic, safrole exposure. At 24 weeks after initiation of safrole treatment, foci of enzyme-altered hepatocytes were noted. These foci were composed of cells showing a decrease in reactivity for glucose-6-phosphatase (Glc-6-Pase) and succinate dehydrogenase (SDH) and an increase for gamma-glutamyl transpeptidase (gamma-Glu-T). In control, iron-loaded mice, the livers were intensely siderotic. In safrole-exposed, iron-loaded mice, foci of iron-negative hepatocytes, varying from a few cells to a lobule in diameter, were initially noted at 24 weeks. Both enzyme-altered and iron-negative foci occurred in the livers of exposed mice at all time periods after 24 weeks. After 36, 52, and 75 weeks of safrole treatment, hepatocellular adenomas were noted with altered enzyme histochemical profiles. Hepatocytes from adenomas were characterized by a decreased staining for Glc-6-pase and SDH and increased staining for gamma-Glu-T and glucose-6-phosphate dehydrogenase (Glc-6-PD). In addition, a few nodules showed a decrease in staining for 5'nucleotidase. In iron-loaded mice, hepatocytes of adenomas showed a decreased to negative reaction for iron when the surrounding parenchyma was siderotic. Hepatocellular carcinomas (HPC) occurred in livers of mice exposed to safrole for 52-75 weeks. The cells of HPC displayed similar enzyme histochemical reactions as cells of adenomas. They were decreased for Glc-6-Pase and SDH activity and increased for gamma-Glu-T and Glc-6-PD. In iron-loaded mice, the HPC cells were negative for stainable iron. Foci, adenomas, and HPC displayed some variability in enzyme histochemical reactions. Variability existed between lesions as well as between cells of the same lesion.
J Natl Cancer Inst 1981 Aug
PMID:Biology of hepatocellular neoplasia in the mouse. II. Sequential enzyme histochemical analysis of BALB/c mouse liver during safrole-induced carcinogenesis. 694 76

A test system using dehydrogenase activity for predicting the response to chemotherapeutic agents against cancer cells was introduced. Agar plate assay, INK which test, and SDI test commonly employed in the clinical study were also reviewed. Agar plate assay resembles antibiotic disc sensitivity test. The cancer uniformly suspended in the agar medium was exposed to drugs on paper discs for few hours. After removal of the disc, methylene blue or 2, 6-dichlorophenol indophenol was applied as a dehydrogenase indicator. INK test was introduced by Nishioka et al. in 1957. Several fragments of fresh cancer tissue were incubated with chemotherapeutic agents in roller test tubes. Twenty-four hours later, 2, 6-dichlorophenol indophenol was applied as a dehydrogenase indicator. To develop a simple, rapid, and comparable test, SDI test was introduced by us in 1964. A fresh cancer tissue was minced and made into the cell suspension. After cancer cells were exposed to chemotherapeutic agents, the activities of succinic dehydrogenase of the treated cells were measured by the reduction of 2, 3, 5-triphenyl tetrazolium chloride. Some points to be improved were investigated and discussed.
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PMID:[In vitro tumor sensitivity tests to chemotherapeutic agents by the suppression of dehydrogenase activity]. 718 14

Integrating microdensitometry has been used to quantitate changes in 4 cytoplasmic enzymes (NADH dehydrogenase, succinate dehydrogenase, acid phosphatase and alpha-naphthyl butyrate esterase), DNA, RNA and glycogen in developing macrophages from 17 patients with non-Hodgkin's lymphoma and 19 normal subjects. Cytochemical measurements were made at intervals over 6 days of suspension culture; over 16 000 individual cells were examined in total and the results subjected to analysis of variance. While the levels of enzymes and RNA of both groups showed increases over the period of culture, the levels of alpha-naphthyl butyrate esterase in the patients' cells were consistently lower than the corresponding values for the normal cells and glycogen levels were higher, these differences satisfying the pre-determined requirements for statistical significance. It is concluded that (a) maturational changes take place in cytochemical constituents of developing macrophages of non-Hodgkin's lymphoma (b) there are disturbances affecting the amounts of the specific enzyme alpha-naphthyl butyrate esterase and glycogen (c) these abnormalities may be part of a compromise of host defense mechanisms by the disease, although a pre-existing defect in esterase increasing the susceptibility to malignancy is another possibility, and (d) the methods used may be of value in future investigations of the cause of the disturbances and their correction.
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PMID:Abnormalities of esterase and glycogen in developing macrophages in non-Hodgkin's lymphoma: a quantitative cytochemical study. 757 45

We studied the tumor host response to excessive doses of an anabolic steroid (nandrolone propionate, 2.5 mg 20 g intraperitoneally every second day for 11 days) with respect to body composition and tumor cell kinetics in MCG 101 sarcoma-bearing mice (C57BL/6J) with progressive cachexia. Although survival and food intake were not affected, a significant weight gain was observed that was essentially attributed to water retention. Net protein content was increased only to a minor extent (15%), of which only the liver accounted for a significant part of the body compartments. Hepatic protein accumulation was obviously caused by decreased protein degradation, since hepatic RNA content was unchanged. After anabolic steroid administration, reduced histochemical staining of succinate dehydrogenase was observed in skeletal muscles rich in oxidative type 1 fibers, but it was not different from that of tumor-bearing control animals, which was also confirmed by measurements of citrate synthase and cytochrome c oxidase activities in skeletal muscle and liver tissue. The anabolic steroid had no significant effect on tumor growth in terms of weight progression, energy state, polyamine synthesis rate, cell division rate, and cell cycle cytocompartments. We conclude that anabolic steroid supplementation is not therapeutically beneficial in counteracting progressive weight loss in experimental cancer.
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PMID:Effects of nandrolone propionate on experimental tumor growth and cancer cachexia. 772 66

In order to study the mechanism of the effects of M phi on tumor cells, enzyme cytochemistry and morphometry were used to investigate the activities of cytochrome oxidase (CO), succinate dehydrogenase (SD), lactate dehydrogenase (LDH) and acid phosphatase (ACP) in A549 pulmonary alveolar cell carcinoma cells which had been interacted with normal and CP-activated macrophages respectively. It was found that when E/T = 10:1, the enzyme activity of the cancer cell mitochondria, CO, SD, LDH were decreased, and when E/T = 20:1, the activity of the lysosomal enzyme ACP was increased. These results indicate that when the E/T ratio was appropriate, activated M phi may injure the mitochondria and lysosomes and affect the aerobic respiration and oxidative phosphorylation of cancer cells. This may be one of the cytostatic and cytotoxic mechanisms of activated M phi on tumor cells.
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PMID:[Enzyme cytochemistry and morphometric study of the effects of macrophages on A549 pulmonary alveolar cell carcinoma cell line]. 780 50

Class pi-glutathione S-transferase (GSTP-1) is one of several factors proposed to affect drug sensitivity to cisdiamminedichloroplatinum (II) (CDDP). It has also been investigated as a potential marker for the serodiagnosis of various types of cancers. In this study, attempts were made to quantify mRNA levels of the enzyme in healthy and cancerous gastric mucosa specimens, and to evaluate their significance in inherent drug resistance to CDDP. Thirty gastric cancer specimens were analysed by northern blotting with radiolabelled GSTP1 cDNA. Of these, the chemosensitivities of 22 specimens were evaluated by the succinic dehydrogenase inhibition (SDI) test. GSTP-1 mRNA was detected in all the specimens, with slightly increased, but non-significant expression in the neoplasms. Comparison of these drug sensitivities with results of northern blotting analysis showed no inverse correlation, as was expected from the widely investigated role of the enzyme in drug resistance.
Eur J Cancer 1994
PMID:Expression of pi-glutathione S-transferase gene (GSTP1) in gastric cancer: lack of correlation with resistance against cis-diamminedichloroplatinum (II). 785 16

Lactobacillus casei, which shows antitumoral activity mediated by the stimulation of cellular defence mechanisms, and its peptidoglycan were tested for their ability to inhibit in vitro the viability of various murine (Yac-1, P815, Ehrlich ascites tumor, mammary carcinoma) and human (K562, KB) tumor cell lines through primary cytotoxic activity. Treatment of these tumor line with L. casei or its peptidoglycan at different doses and for different times demonstrated a decrease in viability by 25-30%. This cytotoxic activity was revealed by 51Cr release, succinate dehydrogenase (SDH) activity, ATP assays and morphological alterations in the treated tumor cells. Immunoenzymatic assays (ELISA) showed a precise ratio of binding between Ehrlich ascites or YAC-1 cell membranes and peptidoglycan. This binding is discussed with regard to the structure of the peptidoglycan molecule. The results suggest that L. casei and its derivative peptidoglycan have both a stimulating activity in normal cells and an inhibiting activity in tumor cells, as has been found for other immunomodulatory complexes.
Cancer Lett 1994 Sep 30
PMID:Non-immunologically-mediated cytotoxicity of Lactobacillus casei and its derivative peptidoglycan against tumor cell lines. 792 9

For antitumor drug sensitivity testing we have been performing the succinic dehydrogenase inhibition test using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). A new tetrazolium salt 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenyl-amino) carbonyl]-2H-tetrazolium hydroxide (XTT) has been synthesized recently, and we have been conducting basic studies using it. We were able to obtain a high degree of sensitivity by adding phenazine methosulfate as a promoter in this assay. In these assays, there was a positive correlation between absorbance and cell count and XTT assay was more sensitive than MTT assay. In XTT assay, the production of formazan increases with reaction time over a protracted period of time, we assessed the possibility of performing assays with fewer cells than MTT was used. The results using cancer cell lines showed that when reacted for a longer time (6 h), it was possible to perform adequate assays using this method with 5,000 cells per well, and it will be useful when the amount of biopsy specimen is limited. We also evaluated the inhibition index of each of the drugs, comparing it with the MTT assay.
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PMID:High-sensitivity antitumor drug sensitivity testing. 797 Apr 99


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