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  • 1
    Electronic Resource
    Electronic Resource
    The role of conjugation reactions in detoxication (1987)
    Springer
    Archives of toxicology 60 (1987), S. 22-29 
    Details
    ISSN: 1432-0738
    Keywords: UDP-glucuronosyltransferase ; Glutathione transferases ; Methylcholanthrene ; Benzopyrenes ; Liver neoplasms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract (1) The role of conjugating enzymes is best understood by looking at the interaction between phase I (mostly cytochromes P-450) and phase II (conjugation) enzymes of drug metabolism. A balance between phase I and II enzymes of detoxication largely determines the disposition to drug toxicity. Reactive electrophilic metabolites, generated by phase I enzymes, are often controlled by GSH-tansferases, whereas nucleophilic metabolites such as phenols are controlled by UDP-glucuronosyltransferases (GT) and sulfotransferases. It is more and more recognized that the control of the more stable and more abundant nucleophiles is as important as the control of electrophiles, since the former can be readily converted to electrophiles. For example, phenols and quinols can undergo quinone/quinol redox-cycles with the generation of reactive oxygen species. In the case of benzo(a)pyrene-3,6-quinol toxicity can be prevented by glucuronidation. (2) Conjugating enzymes consist of families of isoenzymes with distinct but overlapping substrate specificity. Rather than dealing with individual isoenzymes, adaptive programs are emphasized by which gene expression of a battery of phase I and II enzymes is turned on by certain types of inducing agents. Mechanistically best known is the program turned on by 3-methylcholanthrene-type inducers which includes enhanced synthesis of certain isoenzymes of cytochrom P-450, GT and probably GSH-transferase. The program may adapt the organism to efficiently detoxify and eliminate aromatic compounds such as benzo(a)pyrene. Evidence is presented that this program exists in both rodents and humans. (3) The balance between phase I and II enzymes is permanently altered after initiation of hepatocarcinogenesis. Cytochromes P-450 are decreased both in liver foci of altered hepatocytes and nodules, whereas GTs and GSH-transferases are increased. The altered enzyme pattern is consistent with increased toxin resistance of initiated hepatocytes. This toxin-resistance phenotype leads to selective growth of initiated hepatocytes during continuous exposure to carcinogens and may thus facilitate the evolution of cancer cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296941
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Decrease in glucokinase and glucose-6-phosphatase and increase in hexokinase in putative preneoplastic lesions of rat liver (1987)
    Springer
    Journal of cancer research and clinical oncology 113 (1987), S. 430-436 
    Details
    ISSN: 1432-1335
    Keywords: 2-Acetylaminofluorene ; Liver carcinogenesis ; Preneoplasias ; Enzyme histochemistry ; Immunohistochemistry ; Microdissection ; Micro-analysis ; Glucose-6-phosphatase ; Glucokinase ; Hexokinase ; Pyruvate kinase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Preneoplastic liver lesions were produced in female Wistar rats by oral administration of 2-acetyl-aminofluorene for 165 days succeeded by a carcinogen-free standard diet up to 420 days. During the treatment numerous altered hepatic foci (AHF) and hyperplastic nodules (HN) were detected histochemically by a focal decrease or lack of adenosine-5-triphosphatase and glucose-6-phosphatase (G-6-Pase) activities. In addition, the immunohistochemically demosntrable amount of L-type pyruvate kinase was clearly reduced. The histochemically demonstrated decrease of G-6-Pase was substantiated by microbiochemical determination of the enzyme activity in microdissected material. Moreover, during the experimental period a continuous decrease in glucokinase and an increase in hexokinase was detected microbiochemically within AHF and HN. These alterations indicate, a shift in the carbohydrate metabolism from gluconeogenesis to glucose utilization and pentose-phosphate-pathway for biosynthesis of nucleic acids. Beside other oncofetal markers, HK may be used as indicator of the early stages of liver carcinogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00390036
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Intermediate filament typing of the human embryonic and fetal notochord (1995)
    Springer
    Cell & tissue research 280 (1995), S. 455-462 
    Details
    ISSN: 1432-0878
    Keywords: Intermediate filaments ; Notochord ; Cytokeratins ; Cadherins ; Human, embryo
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract In order to characterize human notochordal tissue we investigated notochords from 32 human embryos and fetuses ranging between the 5th and 13th gestational week, using immunohistochemistry to detect intermediate filament proteins cytokeratin, vimentin and desmin, the cytokeratin subtypes 7, 8, 18, 19 and 20, epithelial membrane antigen (EMA), and adhesion molecules pan-cadherin and E-cadherin. Strong immunoreactions could be demonstrated for pan-cytokeratin, but not for desmin or EMA. Staining for pan-cadherin and weak staining for E-cadherin was found on cell membranes of notochordal cells. Also it was demonstrated that notochordal cells of all developmental stages contain the cytokeratins 8, 18 and19, but not 7 or 20. Some cells in the embryonic notochord also contained some vimentin. Vimentin reactivity increased between the 8th and 13th gestational week parallel to morphological changes leading from an epithelial phenotype to the chorda reticulum which represents a mesenchymal tissue within the intervertebral disc anlagen. This coexpression reflects the epithelial-mesenchymal transformation of the notochord, which also loses E-cadherin expression during later stages. Our findings cannot elucidate a histogenetic germ layer origin of the human notochord but demonstrate its epithelial character. Thus, morphogenetic inductive processes between the human notochord and its surrounding vertebral column anlagen can be classified as epithelial-mesenchymal interactions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00307819
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Intermediate filament typing of the human embryonic and fetal notochord (1995)
    Springer
    Cell & tissue research 280 (1995), S. 455-462 
    Details
    ISSN: 1432-0878
    Keywords: Key words: Intermediate filaments ; Notochord ; Cytokeratins ; Cadherins ; Human ; embryo
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. In order to characterize human notochordal tissue we investigated notochords from 32 human embryos and fetuses ranging between the 5th and 13th gestational week, using immunohistochemistry to detect intermediate filament proteins cytokeratin, vimentin and desmin, the cytokeratin subtypes 7, 8, 18, 19 and 20, epithelial membrane antigen (EMA), and adhesion molecules pan-cadherin and E-cadherin. Strong immunoreactions could be demonstrated for pan-cytokeratin, but not for desmin or EMA. Staining for pan-cadherin and weak staining for E-cadherin was found on cell membranes of notochordal cells. Also it was demonstrated that notochordal cells of all developmental stages contain the cytokeratins 8, 18 and 19, but not 7 or 20. Some cells in the embryonic notochord also contained some vimentin. Vimentin reactivity increased between the 8th and 13th gestational week parallel to morphological changes leading from an epithelial phenotype to the chorda reticulum which represents a mesenchymal tissue within the intervertebral disc anlagen. This coexpression reflects the epithelial-mesenchymal transformation of the notochord, which also loses E-cadherin expression during later stages. Our findings cannot elucidate a histogenetic germ layer origin of the human notochord but demonstrate its epithelial character. Thus, morphogenetic inductive processes between the human notochord and its surrounding vertebral column anlagen can be classified as epithelial-mesenchymal interactions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00307819
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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