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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism 879 (1986), S. 120-125 
    ISSN: 0005-2760
    Keywords: (Rat liver microsome) ; Ethane ; Lipid peroxidation ; Malondialdehyde ; n-Pentane
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1912
    Keywords: Catechols ; Pyrogallols ; Lipid peroxidation ; Liver microsomes ; Carbon tetrachloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Lipid peroxidation was induced in rat liver microsomes either by iron-ADP-complexes or by carbon tetrachloride in the presence of NADPH. Different compounds containing catechol or pyrogallol structures were examined for their activities to inhibit lipid peroxidation in both systems. In general, all compounds tested showed similar inhibitory activities on lipid peroxidation, if induced by ferrous ion-ADP-complexes or by carbon tetrachloride. This inhibition is explained by the suggestion that catechols and pyrogallos inhibit at the lipid site of the membrane, rather than at the enzymic site. Compounds not containing catechol or pyrogallol groups inhibited lipid peroxidation only weakly. O-Methylation resulted in a decrease of the inhibitory effect. Catecholor pyrogallol-derivatives which contained polar functional side chains, like carboxyl- or amino groups showed minor inhibitory effects compared to the esterified or N-alkylated compounds. Dihydroxychlorpromazine, 2-hydroxy-estradiol and 2-hydroxyethinylestradiol were the most effective inhbitors of microsomal lipid peroxidation (I50-values of 1×10−6 to 2×10−7 M). The inhibitory activity of α-tocopherol, glutathione and ascorbic acid, naturally occurring antioxidants, was about three orders of magnitude lower. Inhibition of lipid peroxidation induced by NADPH-cytochrome c reductase and iron-ADP-complexes in the presence of NADPH and liposomes was also observed with catechols. From our results we assume that the molecular structure of a catechol or pyrogallol functional group is a prequisite for an effective inhibition of lipid peroxidation by these chemicals. Furthermore, the results are discussed in relation to the requisite membrane affinity of catechols, pyrogallols and other antioxidants which might be used for inhibition studies on lipid peroxidation in vivo.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 298 (1977), S. 107-113 
    ISSN: 1432-1912
    Keywords: Ethanol ; Isolated hepatocytes ; Lipid peroxidation ; Liver damage ; Bromotrichloromethane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Isolated hepatocytes from rats consuming ethanol (8.5 g/kg) daily produce malondialdehyde in significantly higher amounts than liver cells from control animals. The release of LDH and the uptake of trypan blue in both types of hepatocytes do not differ during the incubation period of 2 h. GLDH, however, is only set free into the medium from liver cells of ethanol drinking rats, indicating that mitochondrial alterations are involved. Bomotrichloromethane (CBrCl3) promotes lipid peroxidation in hepatocytes from ethanol drinking rats in a much higher degree than in cells from control rats. The cell damage induced by CBrCl3 and indicated by a release of LDH and GLDH from the hepatocytes and their uptake of trypan blue is also much more pronounced in liver cells from ethanol drinking animals. The stronger action of CBrCl3 cannot be explained by an enhanced microsomal metabolism, because no increase of drug metabolizing enzymes could be observed. The relatively low ethanol consumption did not influence body growth and liver weight and did not evoke any triglyceride accumulation. The normal balance between processes favouring lipid peroxidations and reactions protecting the liver cells seems to be shifted to a state during alcohol intake which promotes formation of radicals.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Archives of toxicology 52 (1983), S. 135-147 
    ISSN: 1432-0738
    Keywords: Lipid peroxidation ; Ethane ; Pentane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The use of exhalation of ethane and n-pentane in experimental animals as parameters of lipid peroxidation led to an examination of pharmacokinetics of both compounds in rats. When rats were exposed, in a closed desiccator jar chamber, to a wide range of ethane concentrations, linear elimination pharmacokinetics were observed. n-Pentane, when concentrations higher than 100 ppm were applied, displayed saturation kinetics. These were formally explained by action of two competing metabolizing pathways or enzymes. Application of preexisting models could describe exhalation of both ethane and n-pentane by untreated control rats. Stimulation of lipid peroxidation by ferrous ions or by carbon tetrachloride resulted in dissimilar quantitative behaviours of ethane and n-pentane. Ethane production rates were enhanced after application of both compounds. Because of relatively slow metabolic eliminations this led to markedly elevated concentrations of ethane in the gas phase of the system. Pentane production rates were simultaneously enhanced. However, difficulties in interpretation arise because of rapid metabolic elimination of n-pentane. Compounds that diminish pentane metabolism are shown to evoke higher pentane concentrations in the system than compounds which only enhance the pentane production rate. Determinations of ethane exhalation should provide a more favourable parameter of lipid peroxidation than exhalation of pentane.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Archives of toxicology 60 (1987), S. 144-149 
    ISSN: 1432-0738
    Keywords: Redox cycling ; Oxygen radicals ; Lipid peroxidation ; DNA damage ; Protein alteration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The toxic effects of compounds which undergo redox cycling via enzymatic one-electron reduction are reviewed. First of all, the enzymatic reduction of these compounds leads to reactive intermediates, mainly radicals which react with oxygen, whereby superoxide anion radicals are formed. Further oxygen metabolites are hydrogen peroxide, singlet oxygen and hydroxyl radicals. The role of these oxygen metabolites in toxicity is discussed. The occurrence of lipid peroxidation during redox cycling of quinonoide compounds, e.g., adriamycin, and the possible relationship to their toxicity is critically evaluated. It is shown that iron ions play a crucial role in lipid peroxidation induced by redox cycling compounds. DNA damage by metal chelates, e.g., bleomycin, is discussed on the basis of findings that enzymatic redox cycling of a bleomycin-iron complex has been observed. The involvement of hydroxyl radicals in bleomycin-induced DNA damage occurring during redox cycling in cell nuclei is claimed. Redox cycling of other substances, e.g., aromatic amines, is discussed in relation to carcinogenesis. Other chemical groups, e.g., nitroaromatic compounds, hydroxylamines and azo compounds are included. Other targets for oxygen radical attack, e.g., proteins, are also dealt with. It is concluded that oxygen radical formation by redox cycling may be a critical event in toxic effects of several compounds if the protective mechanisms of cells are overwhelmed.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Archives of toxicology 49 (1982), S. 265-273 
    ISSN: 1432-0738
    Keywords: Isolated hepatocytes ; Carbon tetrachloride ; Ferrous ions ; Lipid peroxidation ; Ethane ; n-Pentane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Isolated rat hepatocytes (1×107 cells/ml) were aerobically incubated in Eagle's Minimum Essential Medium which contained 2.0% albumin. As potential parameters of lipid peroxidation ethane and n-pentane formed were measured in samples obtained from the gas phase above the incubation mixture. 15–30 nmol ethane or n-pentane were produced by 107 hepatocytes within 90 min. Carbon tetrachloride (CCl4) or ADP-complexed ferrous ions stimulated ethane and n-pentane formation considerably, depending on the concentrations of the compounds. With CCl4 107 cells formed max 180 nmol ethane and 140 nmol n-pentane within 90 min incubation, whereas with Fe(II) max 130 nmol ethane and 220 nmol n-pentane could be detected. When n-pentane was added to the gas phase above the incubation mixture containing either medium or medium plus hepatocytes its amount decreased by 30% within the first 5 min of incubation. However, afterwards only minor amounts of n-pentane disappeared, even in the presence of hepatocytes. This indicates that n-pentane equilibrates with the cell suspension under the conditions used. Cell viability, as determined by the release of lactate dehydrogenase into the medium and by the uptake of trypan blue by the cells, and the recovery of the cells decreased only in presence of relatively high concentrations of CCl4, or Fe(II) respectively. However, a maximal effect on ethane and n-pentane formation was reached already with lower concentration.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 281 (1989), S. 491-494 
    ISSN: 1432-069X
    Keywords: Epidermal keratinocytes ; Laser light ; Hematoporphyrin derivatives ; Lipid peroxidation ; Lysosomal enzymes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Human epidermal keratinocytes were grown in culture and the uptake of hematoporphyrin derivatives (HPDs) used in photodynamic therapy was estimated. Keratinocytes loaded with HPDs were irradiated with laser light of 632 nm generated by a helium-neon laser and cell toxicity was determined by the trypan blue exclusion test and the measurement of enzyme release. With increasing intracellular concentration of HPDs and with increasing intensity of the laser light, an increasing number of cells took up trypan blue and released the cytosolic enzyme lactate dehydrogenase and the lysosomal enzyme acid phosphatase after 1 h incubation of the irradiated cells at 37°C. Cytotoxicity was less pronounced when the irradiated cells were incubated at 0°C indicating the involvement of enzyme reactions in cell death. No lipid peroxidation as measured by malondialdehyde and ethane formation was detectable. Our results suggest that during photodynamic therapy with HPDs and laser light epidermal keratinocytes may be seriously damaged. The data indicate that not lipid peroxidation but rather the activation of lysosomal enzymes is responsible for the cytotoxicity observed.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 103 (1982), S. 135-143 
    ISSN: 1432-1335
    Keywords: Bleomycin ; Lipid peroxidation ; Lung toxicity ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Bleomycin was injected i.p. in rats, and the amount of expired ethane which indicateds lipid peroxidation was followed up for 78 h. Compared to controls neither 1x30 mg/kg and 2x30 mg/kg nor 1x70 mg/kg bleomycin led to increased ethane expiration, although body weight loss indicated toxicity. That pulmonary toxicity had been developed due to the acute bleomycin treatment could be demonstrated by histological examinations of lungs of the animals of the highest dosage group. The combined treatment of rats with bleomycin and ferrous ions neither resulted in an increase of ethane expired compared to that of the ferrous iontreated animals. Rather a decrease was observed. Our results indicate that acute bleomycin toxicity is not associated with increased lipid peroxidation. Furthermore, our data suggest that the bleomycin-ferrous-complex does not initiate lipid peroxidation in vivo.
    Type of Medium: Electronic Resource
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