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2014 | 58 | 1 |

Tytuł artykułu

Adriamycin activity's durational governance of different cell death types and zonality in rat liver acinus. Immunohistochemical studies

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
The aim of this study was to develop and examine a model of apoptosis and necrosis of hepatocytes induced by a damaging factor - adriamycin, correlating time after its administration with cell death type, and to investigate the localisation within the liver acinus of hepatocytes dying in these two ways. The results obtained in the present and previous studies were compared in order to make a map of cell death localisation in the liver acinus, showing the effect of time in action and dose of adriamycin. The experiment was performed on 32 female Wistar rats, divided into four groups: I and II - experimental, and III and IV - control. Adriamycin (3 mg/kg b.w.) was administered intraperitoneally to rats in groups I and II, and the rats were decapitated after four (group I) and eight (group II) weeks. Animals in control groups III and IV were given 0.5 mL of 0.9% NaCl solution, and decapitated after four and eight weeks respectively. Sections of the liver were examined with a three-stage immunohistochemical method. This method allowed to examine hepatocytes qualitatively and quantitatively for the presence of proteins involved in three types of apoptosis: induced by the mitochondrial pathway (caspase 3, 9), the intrinsic pathway related to endoplasmic reticulum stress (caspase 3, 12), and the extrinsic pathway (caspase 3, 8). One of the inflammatory markers, caspase 1, was also examined. The zonal localisation of all three types of apoptosis was assessed in the liver tissue. More oxidated hepatocytes indicated only signs of the internal mitochondrial pathway, whereas less oxidated hepatocytes induced the internal reticular pathway and the external apoptotic pathway. The period between adriamycin administration and hepatic cell investigation was a main factor of the process. A longer period post insult resulted in a more pronounced effect of the activation of apoptosis. Sections explored eight weeks after treatment with different doses of the drug (3 and 5 mg/kg in the previous study) showed a similar intensity of apoptosis.

Słowa kluczowe

Wydawca

-

Rocznik

Tom

58

Numer

1

Opis fizyczny

p.125-133,fig.,ref.

Twórcy

autor
  • Department of Histology and Embryology with Laboratory of Experimental Cytology, Medical University of Lublin, 20-080 Lublin, Poland
  • Department of Animal Anatomy and Histology, Faculty of Veterinary Medicine, University of Life Sciences Lublin, 20-950 Lublin, Poland
  • Department of Maritime and Hyperbaric Medicine, Military Institute of Medicine, 81-103 Gdynia, Poland
autor
  • Lublin Oncology Centre, 20-090 Lublin, Poland
autor
  • Centre for Diagnosis and Therapy of Digestive System Diseases, 80-210 Gdansk, Poland
  • Department of Integrated Medical Care Medical University of Bialystok, 15-096 Bialystok, Poland

Bibliografia

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  • 4. Faubel S., Ljubanovic D., Reznikow L., Somerset H., Dinarello C.A.: Caspase-1-deficient mice are protected against cisplatin induced apoptosis and acute tubular necrosis. Kidney Int 2004, 66, 2202-2213.
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  • 6. Halicka H.D., Bedner E., Darżynkiewicz Z.: Segregation of RNA and separate packing of DNA and RNA in apoptotic bodies during apoptosis. Exp Cell Res 2000, 260. 248-256.
  • 7. Ho J.A., Fan N.C., Jou A.F., Wu L.C., Sun T P.: Monitoring the subcellular localization of doxombicin in CHO-K1 using MEKC-LIF: liposomal carrier for enhanced drug delivery. Talanta 2012, 99, 683-688.
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  • 9. Jang Y.M., Kendaiah S., Drew B., Philips T., Selman C., Julian D., Leeuwenburgh C.: Doxorubicin treatment in vivo activates caspase-12 mediated cardiac apoptosis in both male and female rats. FEBS 2004, 577, 483-490.
  • 10. Kaufmann S.H., Hengartner M.O.: Programmed cell death: alive and well in the new millennium. Trends Cell Biol 2001,11, 526 534.
  • 11. Mehmet H.: Caspases find a new place to hide. Nature 2000, 403, 29-30.
  • 12. Mendocha J.: Localisation of different types of cell death in hepatic acinus depending on dose and time of adriamycin action. Thesis. Medical University in Lublin, Poland, 2009.
  • 13. Muraoka S., Miura T.: Inactivation of mitochondrial succinatedehydrogenase by adriamycin activated by horseradish peroxidase and hydrogen peroxide. Chem Biol Interact 2003, 145, 67-75.
  • 14. Pedrycz A., Boratyński Z., Mendocha J.: Immunolocalization of different types of adriamycin-induced cell death in the portal acinus of the liver depending on time. Med Weter 2014, 70, 98-106.
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  • 16. Riedl S.J., Salvesen G S.: The apoptosome: signallingplatform of cell death. Nat Rev Mol Cell Biol 2007, 8, 405-413.
  • 17. Serafino A., Sinibaldi - Vallebona P., Lazzarino G., Tavazzi B., Di Pierro D., Rasi G., Ravagnan G.: Modifications of mitochondria in human tumor cells during anthracycline induced apoptosis. Anticancer Res 2000, 20, 3383-3394.
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Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

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