Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Growth, regression and cell death in rat liver as related to tissue levels of the hepatomitogen cyproterone acetate (1986)
    Springer
    Archives of toxicology 59 (1986), S. 221-227 
    Details
    ISSN: 1432-0738
    Keywords: Apoptosis ; Cell death ; Liver hyperplasia regression ; Cyproterone acetate ; α-Hexachlorocyclohexane ; nafenopin ; Pharmacokinetics ; Serum glutamate pyruvate transaminase ; Serum alkaline phosphatase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previous studies have shown that “xenobiotic” compounds such as the environmental pollutant α-hexa-chlorocyclohexane (α-HCH) and the synthetic sex steroid cyproterone acetate (CPA) induce growth of rat liver by hypertrophy and hyperplasia. After withdrawal of the growth stimuli, liver hypertrophy was usually found to be readily reversible. Conflicting observations were made concerning the fate of liver hyperplasia: hepatic hyperplasia persisted when induced by α-HCH but was found to be partially reversible when induced by CPA. The present study confirms the reversibility of hepatic hyperplasia induced by CPA in rats: about 30% of liver DNA present at maximal liver enlargement disappeared within 6 days after cessation of CPA treatment. Simultaneously, a dramatic increase in the rate of cell elimination by apoptosis was found. Glutamate-pyruvate transaminase and alkaline phosphatase in serum did not show major increases, suggesting that cell death was not due to lytic membrane damage. Furthermore, if treatment with CPA was continued or resumed, the enhanced DNA content persisted and the number of apoptotic bodies was greatly reduced. These observations suggest that the occurrence of cell death is due to withdrawal of the growth stimulus CPA. It may reflect a regulatory phenomenon serving to maintain homeostasis of cell number. Further studies showed that CPA is rapidly eliminated from rat liver and serum: t 1/2 in the liver is about 11 h. In contrast, α-HCH was previously found to be eliminated more slowly: t 1/2 approximately 144 h. The present study revealed that α-HCH, CPA and nafenopin lower the number of apoptotic bodies. This suggests that inducers of liver growth can inhibit hepatocellular death by apoptosis. It is concluded that the regression of hyperplasia after CPA withdrawal may be due to its rapid elimination. On the other hand the relatively long persistence of α-HCH may result in inhibition of cell death and thereby stabilize hepatic hyperplasia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00290542
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Expression of clusterin (testosterone-repressed prostate message-2) mRNA during growth and regeneration of rat liver (1995)
    Springer
    Archives of toxicology 69 (1995), S. 253-258 
    Details
    ISSN: 1432-0738
    Keywords: Key words Clusterin ; Liver ; Apoptosis ; Mitosis ; Necrosis ; Cyproterone acetate ; Carbon tetrachloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Clusterin has been used as a marker for apoptosis (often denoted “active”“or programmed” cell death) in the prostate, mammary gland and other solid organs. The protein is thought to be involved in membrane remodelling during separation of apoptotic cells from their vital neighbours and fragmentation into apoptotic bodies. In the present study, we have looked at the expression of clusterin during the growth and regression of rat liver induced by short term administration of the hepatomitogen, cyproterone acetate. The steady state level of clusterin mRNA, as measured by Northern and slot blot analysis, is low in control hepatocytes. Following administration of cyproterone acetate, the clusterin mRNA level is increased during both liver growth and regression. In situ hybridization reveals that clusterin is expressed in all hepatocytes, indicating that it is not confined to cell death by apoptosis. These results suggest that the gene product may be involved in maintaining membrane integrity, which is necessary during both mitosis and apoptosis. To determine whether clusterin mRNA is induced by membrane remodelling independent of either mitosis or apoptosis, we examined the expression of clusterin mRNA in the liver after a necrogenic dose of carbon tetrachloride. During the first 24–48 h of this time period, necrosis is the predominant form of cell death and liver regeneration starts after approximately 24 h. Elevated levels of clusterin mRNA are found as early as 12 h after carbon tetrachloride administration and persist for at least 72 h. Clusterin expression in tissues such as the prostate and mammary gland appears to be confined to the apoptotic pathway; however, our results suggest that in hepatocytes, the expression of the gene is induced in processes other than apoptosis, including mitosis and necrosis. These processes involve substantial membrane remodelling, suggesting that clusterin expression may be induced by perturbations in the normal membrane structure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050167
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Apoptosis in the liver and its role in hepatocarcinogenesis (1997)
    Springer
    Cell biology and toxicology 13 (1997), S. 339-348 
    Details
    ISSN: 1573-6822
    Keywords: apoptosis ; hepatocarcinogenesis ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Apoptosis seems to be the predominant type of active cell death in the liver (type I), while in other tissues cells may die via biochemically and morphologically different pathways (type II, type III). Active cell death is under the control of growth factors and death signals. In the liver, endogenous factors, such as transforming growth factor β1 (TGF-β1), activin A, CD95 ligand, and tumor necrosis factor (TNF) may be involved in induction of apoptosis. Release and action of these death factors seems to be triggered by exogenous signals such as withdrawal of hepato-mitogens, food restriction, etc. During stages of hepatocarcinogenesis, not only DNA synthesis but also apoptosis gradually increase from normal to preneoplastic to adenoma and carcinoma tissue. Also, in human carcinomas, birth and death rates of cells are several times higher than in surrounding liver. (Pre)neoplastic liver cells are more susceptible than normal hepatocytes to stimulation of cell replication and of cell death. Consequently, tumor promoters may act as survival factors, i.e., inhibit apoptosis preferentially in preneoplastic and even in malignant liver cells, thereby stimulating selective growth of (pre)neoplastic lesions. On the other hand, regimens favoring apoptosis and lowering cell replication may result in selective elimination of (pre)neoplastic cell clones from the liver. Finally, we have studied the first stage of carcinogenesis, namely the appearance of putatively initiated cells after a single dose of the genotoxic carcinogen N-nitrosomorpholine (NNM). Most of these cells were found to be eliminated by apoptosis, suggesting that initiation, at the organ level, can be reversed at least partially by preferential elimination of initiated cells. These events may be regulated by autocrine or paracrine actions of survival factors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007495626864
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...