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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1981-04-17
    Description: In alcoholic liver injury, necrosis is involved in the progression from benign fatty liver to alcoholic hepatitis and cirrhosis. However, there is no practical model of alcohol-dependent liver cell necrosis. The calcium-dependent killing of cultured rat hepatocytes by two different membrane-active hepatotoxins, galactosamine and phalloidin, is potentiated by ethyl alcohol. This indicates that some general physical effect of alcohol on cellular membranes renders cells susceptible to otherwise nonlethal injuries. The in vitro model described in this report may thus be used to search for a general mechanism underlying alcohol-related tissue injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schanne, F A -- Zucker, A H -- Farber, J L -- Rubin, E -- AA 03442/AA/NIAAA NIH HHS/ -- AM 19154/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1981 Apr 17;212(4492):338-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209533" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/pharmacology ; Cell Membrane/drug effects ; Cells, Cultured ; Drug Synergism ; Ethanol/pharmacology ; Female ; Galactosamine/pharmacology ; In Vitro Techniques ; Liver/drug effects ; Liver Diseases, Alcoholic/*pathology ; Necrosis ; Phalloidine/pharmacology ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1979-11-09
    Description: Primary cultures of adult rat hepatocytes were treated in the presence or absence of extracellular calcium with ten different membrane-active toxins. In all cases more than half the cells were killed in 1 to 6 hours in the presence but not in the absence of extracellular calcium. An effect of calcium on the primary mechanism of membrane injury by any of the agents cannot be implicated. Viability, as determined by trypan blue exclusion correlated well with other indices of viability such as plating efficiency and the hydrolysis of fluorescein diacetate. It is concluded that the cells are killed by processes that involve at least two steps. In each type of injury, disruption of the integrity of the plasma membrane by widely differing mechanisms is followed by a common functional consequence involving extracellular calcium, and most likely representing an influx of calcium across the damaged plasma membrane and down a steep concentration gradient. This later step represents, or at least initiates, a final common pathway for the toxic death of these cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schanne, F A -- Kane, A B -- Young, E E -- Farber, J L -- New York, N.Y. -- Science. 1979 Nov 9;206(4419):700-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/386513" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcimycin/pharmacology ; Calcium/*physiology ; Cell Membrane/drug effects ; Cell Membrane Permeability/drug effects ; *Cell Survival/drug effects ; Drug Interactions ; Liver/cytology ; Lysophosphatidylcholines/pharmacology ; Membrane Potentials/drug effects ; Rats ; Toxins, Biological/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
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