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  • 1
    Electronic Resource
    Electronic Resource
    Positive correlation between decreased cellular uptake, NADPH-glutathione reductase activity and adriamycin resistance in Ehrlich ascites tumor lines (1987)
    Springer
    Archives of toxicology 60 (1987), S. 154-157 
    Details
    ISSN: 1432-0738
    Keywords: Adriamycin ; Ehrlich ascites tumor ; Resistance ; NADPH-glutathione reductase ; Cellular uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract From a wild type strain of Ehrlich ascites tumor (EATWT) sublines resistant to daunorubicin (EATDNM), etoposide (EATETO), and cisplatinum (EATCIS) have been developed in vivo. Increase in survival and cure rate caused by adriamycin (doxorubicin) have been determined in female NMRI mice which were inoculated i. p. with EAT cells. Adriamycin concentrations causing 50% inhibition of 3H-thymidine (ICT) and 3H-uridine incorporation (ICU) and intracellular adriamycin steady-state concentrations (SSC) were measured in vitro. Adriamycin resistance increased and SSC decreased in the following sequence: EATWT — EATCIS — EATDNM — EATETO. When ICT and ICU were corrected for intracellular adriamycin concentrations in consideration of the different SSC (ICTC, ICUC), ICTC and ICUC still varied up to the 3.2 fold in EATCIS, EATDAM and EATETO in comparison to EATWT. Thus, in addition to different SSC other factors must be responsible for adriamycin resistance. Therefore, enzymes which may play a role in the cytotoxicity related to adriamycin metabolism (NADPH-cytochrome P-450 reductase, NADPH-glutathione reductase, NADP-glucose-6-phosphate dehydrogenase, NADP-isocitrate dehydrogenase) were measured. In contrast to the other parameters determined, NADPH-glutathione reductase was significantly (p〈0.01) increased up to the 3.2 fold parallel to adriamycin resistance as determined by increase in life span, cure rate, ICTC, and ICUC, respectively. It is concluded that high activities of NADPH-glutathione reductase may contribute to an increase in adriamycin resistance of malignant tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296970
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  • 2
    Electronic Resource
    Electronic Resource
    Toxikologie der synthetischen Antioxidantien BHA und BHT im Vergleich mit dem natürlichen Antioxidans Vitamin E (1993)
    Springer
    European food research and technology 196 (1993), S. 329-338 
    Details
    ISSN: 1438-2385
    Source: Springer Online Journal Archives 1860-2000
    Topics: Process Engineering, Biotechnology, Nutrition Technology
    Description / Table of Contents: Zusammenfassung Die Toxikologie der Lebensmittelzusatzstoffe Butylhydroxyanisol (BHA) und Butylhydroxytoluol (BHT) sowie des natürlich vorkommenden Vitamin E (α-Tocopherol) wird beschrieben. Alle drei Verbindungen verursachen im Tierversuch bei hoher Dosierung Störungen der Blutgerinnung, die mit einem Vitamin-K-Antagonismus erklärbar sind. Spezifische toxische Effekte auf die Lunge sind nur mit BHT beobachtet worden. Die sonst beschriebenen toxischen Wirkungen von BHA und BHT sind wenig charakteristisch und treten zum Teil erst bei sehr hoher Dosierung und bei Langzeitbehandlung auf. BHA induziert jedoch bei Tieren dosisabhängig Tumoren des Vormagens, während BHT im Langzeitversuch Lebertumoren erzeugt. Da es keinen Hinweis auf eine Gentoxizität von BHA und BHT gibt, sprechen alle bisherigen Befunde dafür, daß BHA und BHT Tumorpromotoren sind. Im Gegensatz zu BHA und BHT ist Vitamin E nicht cancerogen. Andererseits besitzen alle drei Antioxidantien auch anticancerogene Eigenschaften. Die Aufnahme hoher Dosen, wie sie für diese Effekte notwendig sind, verbietet sich jedoch bei BHA und BHT wegen ihrer cancerogenen Wirkungen. Die vorliegende Übersicht kommt zu dem Schluß, daß die in Lebensmitteln, Arzneimitteln und Cosmetica zur Zeit verwendeten Konzentrationen von BHA und BHT wahrscheinlich unbedenklich sind. Vitamin E kann darüber hinaus auch in höheren Dosen eingenommen werden, ohne daß unerwünschte Wirkungen auftreten.
    Notes: Abstract The toxicology of the food preservatives butylhydroxyanisole (BHA) and butylhydroxytoluene (BHT) as well as the naturally occurring vitamin E (α-tocopherol) is described. In high dosages all three compounds induce in animals impairment of blood clotting, which can be explained by an antagonism with vitamin K. Specific toxic effects to the lung have only been observed with BHT. The other described toxic effects of BHA and BHT are less characteristic and often occur only after high dosage and long-term treatment. However, BHA induces in animals tumours of the forestomach, which are dose dependent, whereas BHT induces liver tumours in long-term experiments. Because there is no indication of genotoxicity of BHA and BHT, all published findings agree with the fact that BHA and BHT are tumour promoters. In contrast to BHA and BHT, vitamin E is not carcinogenic. On the other hand, all three antioxidants have also anticarcinogenic properties. The intake of the necessary high doses as for these effects are, however, contraindicated with BHA and BHT because of their carcinogenic effects. The present overview concludes that the concentrations of BHA and BHT nowadays used in food, drugs and cosmetics are probably harmless. In addition, vitamin E can also be used in higher doses without the occurrence of adverse effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01197931
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  • 3
    Electronic Resource
    Electronic Resource
    Changes in the classification of carcinogenic chemicals in the work area (1998)
    Springer
    International archives of occupational and environmental health 71 (1998), S. 566-574 
    Details
    ISSN: 1432-1246
    Keywords: Key words Chemical carcinogens ; List of MAK and BAT Values ; Cancer risk
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Carcinogenic chemicals in the work area are currently classified into three categories in section III of the German List of MAK and BAT Values (list of values on maximum workplace concentrations and biological tolerance for occupational exposures). This classification is based on qualitative criteria and reflects essentially the weight of evidence available for judging the carcinogenic potential of the chemicals. It is proposed that these categories – IIIA1, IIIA2, IIIB – be retained as Categories 1, 2, and 3, to correspond with European Union regulations. On the basis of our advancing knowledge of reaction mechanisms and the potency of carcinogens, these three categories are supplemented with two additional categories. The essential feature of substances classified in the new categories is that exposure to these chemicals does not contribute significantly to risk of cancer to man, provided that an appropriate exposure limit (MAK value) is observed. Chemicals known to act typically by nongenotoxic mechanisms and for which information is available that allows evaluation of the effects of low-dose exposures, are classified in Category 4. Genotoxic chemicals for which low carcinogenic potency can be expected on the basis of dose-response relationships and toxicokinetics, and for which risk at low doses can be assessed are classified in Category 5. The basis for a better differentiation of carcinogens is discussed, the new categories are defined, and possible criteria for classification are described. Examples for Category 4 (1,4-dioxane) and Category 5 (styrene) are presented.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004200050325
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  • 4
    Electronic Resource
    Electronic Resource
    Lack of in vivo lipid peroxidation in experimental paraquat poisoning (1980)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 310 (1980), S. 241-243 
    Details
    ISSN: 1432-1912
    Keywords: Paraquat ; lipid peroxidation ; ethane ; oxygen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ethane evolution was measured in rats breathing pure oxygen. Animals injected i.p. with a lethal dose of paraquat (50 mg/kg) developed signs of pulmonary insufficiency within 3 hours and died within 24 hours. Ethane evolution, a parameter of lipid peroxidation in vivo, was increased over control levels only by 26% after 4 hours. It is concluded that this increase is too small to support the theory that lipid peroxidation is the biochemical mechanism of paraquat toxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00499917
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  • 5
    Electronic Resource
    Electronic Resource
    Toxic drug effects associated with oxygen metabolism: Redox cycling and lipid peroxidation (1981)
    Springer
    Cellular and molecular life sciences 37 (1981), S. 1233-1241 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Various endogenous and exogenous compounds exert cytotoxic effects via oxygen reduction. In general, these are reduced by intracellular enzymes (reductases of various kinds) in one-electron transfer reactions, before they in turn reduce O2 to $$O_2^{\underset{\raise0.3em\hbox{$\smash{\scriptscriptstyle\cdot}$}}{ - } } $$ , the superoxide anion radical. Thus, a cycle is formed of O2 uptake at the expense of cellular reducing equivalents, notably NADPH, generating further active oxygen species (figs 1,2). Structures capable of ‘redox cycling’ include catechols and other quinone compounds, iron chelates, and aromatic nitro compounds. Several anticancer agents, and also some mutagens, operate on this principle, and their toxic effects may be explained by redox cycling. The particular importance of hypoxic conditions for deleterious O2 effects is given by the concomitant flux through reductive as well as oxidative pathways. Toxic effects include membrane damage resulting from peroxidative reactions of polyunsaturated fatty acids (lipid peroxidation), as well as the attack of reactive oxygen species on proteins (enzymes) and nucleic acids; thus O2 metabolism is linked to carcinogenicity and mutagenicity. Lipid peroxidation is also induced by various halogenated compounds such as carbon tetrachloride. Again, hypoxic conditions are particularly critical because, on the one hand, metabolic activation leading to the free radical is enhanced and, on the other hand, oxygen required for the maintenance of lipid peroxidation is still available. — Powerful antioxidant systems of the cell maintain low steady state concentrations of oxygen metabolites, and toxic effects may, in part, also be expleined by the constant drain of reducing equivalents resulting from redox cycling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01948335
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