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  • 1
    Electronic Resource
    Electronic Resource
    Über Chrysiasis der Haut nach Goldbehandlung (1932)
    Springer
    Lung 79 (1932), S. 664-664 
    Details
    ISSN: 1432-1750
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02079283
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  • 2
    Electronic Resource
    Electronic Resource
    Reduced gluconeogenesis in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated rats (1990)
    Springer
    Archives of toxicology 64 (1990), S. 66-71 
    Details
    ISSN: 1432-0738
    Keywords: 2,3,7,8-Tetrachlorodibenzo-p-dioxin ; Hypoglycemia ; Gluconeogenesis ; Hypophysectomy ; Corticosterone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of a usually lethal dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 125 μg/kg) was studied on the conversion of14C-alanine into14C-glucose in male Sprague-Dawley rats by established procedures (determination of plasma alanine and blood glucose by enzymatic assays and isolation of14C-alanine and14C-glucose from whole blood by column chromatography). TCDD-treated rats converted significantly (p 〈 0.05) less14C-alanine into14C-glucose than did their pair-fed or ad libitum-fed counterparts, indicating reduced gluconeogenesis as a result of TCDD treatment. This finding suggests that reduced gluconeogenesis in TCDD-treated rats contributed to the progressively developing, severe hypoglycemia observed in these animals. Corticosterone, a key hormone in gluconeogenesis, provides partial protection from TCDD-induced toxicity in hypophysectomized rats. Therefore, the conversion of14C-alanine into14C-glucose was also determined in hypophysectomized rats dosed with TCDD (125 μg/kg) and given corticosterone (25 μg/ ml in drinking water). These rats also converted significantly (p 〈0.05) less14C-alanine into14C-glucose than did their pair-fed counterparts. However, in contrast to non-hypophysectomized TCDD-treated rats, these rats maintained marginal normoglycemia even at 64 days after dosing with TCDD, which suggests that the partial protective effect of corticosterone in hypophysectomized, TCDD-treated rats is unrelated to its effect on gluconeogenesis. The protection provided by corticosterone supplementation in TCDD toxicity is more likely due to reduced peripheral utilization of glucose enabling the animals to maintain marginal normoglycemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01973379
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  • 3
    Electronic Resource
    Electronic Resource
    Key enzymes of gluconeogenesis are dose-dependently reduced in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated rats (1991)
    Springer
    Archives of toxicology 65 (1991), S. 119-123 
    Details
    ISSN: 1432-0738
    Keywords: 2,3,7,8-Tetrachlorodibenzo-p-dioxin ; Dose-response ; Gluconeogenesis ; Phosphoenolpyruvate carboxykinase ; Pyruvate kinase ; Pyruvate carboxylase ; Glucose-6-phosphatase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Male Sprague-Dawley rats (240–245 g) were dosed ip with 5, 15, 25, or 125 μg/kg -,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in corn oil. Ad libitumfed and pair-fed controls received vehicle (4 ml/kg) alone. Two or 8 days after dosing five rats of each group were sacrificed, their livers removed and assayed for the activities of three gluconeogenic enzymes [phosphoenol-pyruvate carboxykinase (PEPCK; EC 4.1.1.32), pyruvate carboxylase (PC; EC 6.4.1.1.), and glucose-6-phosphatase (G-6-Pase, EC 3.1.3.9)], and one glycolytic enzyme [pyruvate kinase (PK; EC 2.7.1.40)] by established procedures. The activity of PK was not affected by TCDD at either time point. The activity of G-6-Pase tended to be decreased in TCDD-treated animals, as compared to pair-fed controls, but the decrease was variable without an apparent dose-response. The activity of PEPCK was significantly decreased 2 days after dosing, but a clear dose-response was apparent only at the 8-day time point. Maximum loss of activity at the highest dose was 56% below pair-fed control levels. PC activity was slightly decreased 2 days after TCDD treatment and displayed statistically significant, dose-dependent reduction by 8 days after dosing with a 49% loss of enzyme activity after the highest dose. It is concluded that inhibition of gluconeogenesis by TCDD previously demonstrated in vivo is probably due to decreased activities of PEPCK and PC. The data also support the prevailing view that PEPCK and PC are rate-determining enzymes in gluconeogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02034937
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  • 4
    Electronic Resource
    Electronic Resource
    Penetration, distribution and kinetics of 2,3,7,8-tetrachlorodibenzo-p-dioxin in human skin in vitro (1991)
    Springer
    Archives of toxicology 65 (1991), S. 421-428 
    Details
    ISSN: 1432-0738
    Keywords: Percutaneous absorption ; Distribution ; Human skin ; Stratum corneum ; Epidermis ; Dermis ; 2,3,7,8-Tetrachlorodibenzo-p-dioxin ; In vitro
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The in vitro penetration of3H-labeled 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) into human cadaver skin was studied at concentrations of 65 and 6.5 ng TCDD per cm2 of skin surface. Vehicles used were acetone to simulate exposure to TCDD as a dry material, and mineral oil to simulate exposure to TCDD in an oily medium. Penetration was performed for 30, 100, 300, and 1000 min in improved Franz cells. Skin was used either intact, or with stripped horny layer. Skin was sectioned along its natural layers and radioactivity determined in epidermis and dermis. TCDD did not readily penetrate into human skin in vitro. The vehicle of exposure to TCDD played an important role in dermal penetration. The rapidly evaporating acetone allowed TCDD to penetrate deeply into the loose surface lamellae of the horny layer, but then appeared to be poorly available for further penetration. Mineral oil as the vehicle, on the other hand, represented a lipophilic compartment which competed with lipophilic constituents of the stratum corneum for TCDD and hence slowed its penetration even more. The stratum corneum acted as a protective barrier, as its removal increased the amount of TCDD absorbed into layers of the skin. Hourly rates of absorption of TCDD per unit area of skin were calculated in two ways: a worst case scenario where TCDD absorbed into any layer of skin including the stratum corneum was used for regression analysis; and a physiological approach where only that amount of TCDD was considered absorbed which had penetrated beyond the epidermis into the region of dermal vascularization. Under worst case scenario conditions the stratum corneum appeared to mediate dermal absorption of TCDD, since calculated rates of absorption decreased when skin stripped of its stratum corneum was exposed to TCDD. This was, however, not the case with the physiological approach. There was a consistent relationship between concentration of TCDD applied and concentration of TCDD found in skin. Also, a clear-cut correlation was found between the amount of TCDD that penetrated and the time of exposure. The rate of penetration into intact skin of different concentrations of TCDD from acetone ranged from 100 to 800 pg TCDD per hour and cm2 of skin (worst case scenario), or 6 to 170 pg per hour and cm2 with the physiological approach. With mineral oil as the vehicle the rate of penetration into intact skin was lower, ranging from 20 to 220 pg and 1.4 to 18 pg, respectively, per hour and cm2 of skin. Our results on the distribution of TCDD in human skin also suggest that as yet unknown constituents of epidermis and upper dermis have a somewhat higher affinity towards TCDD than those of the lower dermis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02284267
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  • 5
    Electronic Resource
    Electronic Resource
    Tissue-specific alterations of de novo fatty acid synthesis in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated rats (1988)
    Springer
    Archives of toxicology 62 (1988), S. 146-151 
    Details
    ISSN: 1432-0738
    Keywords: 2,3,7,8-Tetrachlorodibenzo-p-dioxin ; TCDD ; De novo fatty acid synthesis ; Brown adipose tissue ; Thyroid hormones ; Thyroidectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract De novo fatty acid synthesis was determined by the3H2O method in numerous tissues and organs of TCDD-treated (125 μg/kg), pair-fed and free-fed male Sprague-Dawley rats to investigate if this important pathway of intermediary metabolism is altered by TCDD. Of the 12 tissues and organs examined, liver showed an increased, and interscapular brown adipose tissue (IBAT) a decreased de novo fatty acid synthesis when comparing TCDD-treated to pair-fed or free-fed control rats. De novo fatty acid synthesis was unaffected in other organs and tissues examined, with the exception that the concentration of3H-fatty acids in plasma reflected the increased rate of synthesis seen in the liver of TCDD-treated animals. Increased de novo fatty acid synthesis in liver coincided with increased plasma triiodothyronine (T3) concentrations, whereas decreased de novo fatty acid synthesis in IBAT parallelled decreased plasma thyroxine (T4) levels. Thyroidectomy decreased de novo fatty acid synthesis, as expected, in both liver and IBAT. However, TCDD elicited no response in either of these organs in thyroidectomized rats. This finding suggests that changes observed in non-thyroidectomized rats are probably secondary effects. Indeed, known tissue-specific effects of T3 on liver and T4 on IBAT provide a likely explanation for the altered de novo fatty acid synthesis of these organs. It is suggested that increased de novo fatty acid synthesis in the liver of TCDD-treated rats might be responsible for the additional wasting away observable in these animals as compared to pair-fed controls.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00570132
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  • 6
    Electronic Resource
    Electronic Resource
    Trenbolone growth promotant: covalent DNA binding in rat liver and inSalmonella typhimurium, and mutagenicity in the Ames test (1988)
    Springer
    Archives of toxicology 62 (1988), S. 103-109 
    Details
    ISSN: 1432-0738
    Keywords: Trenbolone ; Anabolic agent ; DNA binding ; Genotoxicity ; Ames test ; Salmonella typhimurium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract DNA binding in vivo: [6,7-3H]β-trenbolone (β-TBOH) was administered p.o. and i.p. to rats. After 8 or 16 h, DNA was isolated from the livers and purified to constant specific radioactivity. Enzymatic digestion to deoxyribonucleotides and separation by HPLC revealed about 90% of the DNA radioactivity eluting in the form of possible TBOH-nucleotide adducts. The extent of this genotoxicity, expressed in units of the Covalent Binding Index, CBI = (μmol TBOH bound per mol nucleotide)/(mmol TBOH administered per kg body weight) spanned from 8 to 17, i.e. was in the range found with weak genotoxic carcinogens.Ames test: low doses of β-TBOH increased the number of revertants inSalmonella strain TA100 reproducibly and in a dose-dependent manner. The mutagenic potency was 0.2 revertants per nmol after preincubation of the bacteria (20 min at 37° C) with doses between 30 and 60 μg per plate (47 and 94 μg/ml preincubation mixture). Above this dose, the number of revertants decreased to control values, accompanied by a reduction in survival. The addition of rat liver S9 inhibited the mutagenicity.DNA binding in vitro: calf thymus DNA was incubated with tritiated β-TBOH with and without rat liver S9. Highest DNA radioactivities were determined in theabsence of the “activation” system. Addition of inactive S9 (without cofactors) reduced the DNA binding by a factor of up to 20. Intermediate results were found with active S9.DNA binding in Salmonella: β-TBOH was irreversibly bound to DNA isolated fromS. typhimurium TA100 after incubation of bacteria with [3H]β-TBOH.Conclusions: Covalent DNA binding appears to be the mechanism of an activation-independent (“direct”) mutagenicity of TBOH which is not easily detected because of the bactericidal activity. The genotoxicity risk arising from exposure of humans to trenbolone residues in meat was estimated using the in vivo data and compared to that from the exposure to unavoidable genotoxins aflatoxin B1 and dimethylnitrosamine. It is concluded that trenbolone residues represent only a low genotoxic risk.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00570127
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  • 7
    Electronic Resource
    Electronic Resource
    Comparative toxicity of four chlorinated dibenzo-p-dioxins (CDDs) and their mixture (1992)
    Springer
    Archives of toxicology 66 (1992), S. 484-488 
    Details
    ISSN: 1432-0738
    Keywords: 2,3,7,8-Tetrachlorodibenzo-p-dioxin ; 1,2,3,7,8-Pentachlorodibenzo-p-dioxin ; 1,2,3,4,7,8-Hexachlorodibenzo-p-dioxin ; 1,2,3,4,6,7,8-Heptachlorodibenzo-p-dioxin ; Mixture ; Structure-activity relationship ; Acute toxicity ; Plasma tryptophan ; Ethoxyresorufin O-deethylase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Male Sprague-Dawley rats were treated with an LD20, an LD50, and an LD80 of 2,3,7,8-tetrachlorodibenzop-dioxin (tetra-CDD), 1,2,3,7,8-pentachlorodibenzo-p-dioxin (penta-CDD), 1,2,3,4,7,8-hexachlorodibenzo-p-dioxin (hexa-CDD), 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (hepta-CDD), respectively, and a mixture of the four homologues where each CDD was represented at one-fourth its previously established LD20, LD50, and LD80, respectively. Plasma tryptophan levels, liver ethoxyresorufin O-deethylase (EROD) activities, and liver weights were determined at 2 and 8 days after treatment. Plasma tryptophan levels were dose-dependently elevated, particularly at 8 days after treatment, by as much as 75% over control levels. EROD activity in CDD-treated animals was induced 27- to 28-fold, as compared with vehicle-treated controls, but did not show any dose-response. Liver weights were also significantly increased by the CDD treatments, but the increase was not dose related. There was no correlation between plasma tryptophan levels, a biomarker of acute toxicity of CDDs, and EROD activity, a biomarker of arylhydrocarbon (Ah) receptor-mediated enzyme induction. It is concluded that the acute toxicity of CDDs, which correlates and shows perfect structure-activity relationship with reduced activities of key enzymes of intermediary metabolism, and the induction of enzymes by much lower doses of CDDs in the liver, have different mechanisms of action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01970673
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  • 8
    Electronic Resource
    Electronic Resource
    Comparative toxicity of four chlorinated dibenzo-p-dioxins (CDDs) and their mixture (1992)
    Springer
    Archives of toxicology 66 (1992), S. 478-483 
    Details
    ISSN: 1432-0738
    Keywords: 2,3,7,8-Tetrachlorodibenzo-p-dioxin ; 1,2,3,7,8-Pentachlorodibenzo-p-dioxin ; 1,2,3,4,7,8-Hexachlorodibenzo-p-dioxin ; 1,2,3,4,6,7,8-Heptachlorodibenzo-p-dioxin ; Mixture ; Structure-activity relationship ; Acute toxicity ; Phosphoenolpyruvate carboxykinase ; Pyruvate carboxylase ; γ-Glutamyl transpeptidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Male Sprague-Dawley rats were treated with an LD20, LD50 and LD80 respectively, of tetra-, penta-, hexa-,hepta-CDD and a mixture of the four CDDs, all carrying chlorine substituents in the biologically crucial 2, 3, 7, and 8 positions. Specific activities of two key enzymes of gluconeogenesis, viz, phosphoenolpyruvate carboxykinase (PEPCK) and pyruvate carboxylase (PC), as well as the activity of the preneoplastic marker enzyme γ-glutamyl transpeptidase (γ-GT), were determined in livers of CDD-treated and ad libitum-fed control animals. PEPCK activity showed evidence for dose-related inhibition on the second day after dosing; PC activity was slightly reduced, whereas γ-GT activity was dose-dependently inhibited. By 8 days after dosing PEPCK activities were dose-dependently decreased after administration of all four CDDs and their mixture. PC activities were significantly reduced, but no dose-response was evident. The activity of γ-GT was dosedependently inhibited, but only to a value of 25% below control activities. It is concluded that CDDs share a common mechanism of acute toxicity, viz, inhibition of glucocorticoid-dependent enzymes which results in a derailment of intermediary metabolism not compatible with survival of the animals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01970672
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  • 9
    Electronic Resource
    Electronic Resource
    Über eine bisher nicht beschriebene Dermatose: Haemorrhagisches, papulo-bullöses und ulzeröses Exanthem, verursacht durch hämatogene Infektion mit gramnegativen Bazillen (1915)
    Springer
    Archives of dermatological research 121 (1915), S. 613-629 
    Details
    ISSN: 1432-069X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01961100
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  • 10
    Electronic Resource
    Electronic Resource
    Ein Fall einer bisher nicht beschriebenen Hauterkrankung (Epidermodysplasia verruciformis) (1922)
    Springer
    Archives of dermatological research 141 (1922), S. 193-203 
    Details
    ISSN: 1432-069X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01938833
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