Deferoxamine administration in septic animals

Improved survival and altered apoptotic gene expression

Evangelos Messaris, Pantelis T. Antonakis, Nicholaos Memos, Emmy Chatzigianni, Emanuel Leandros, Manousos M. Konstadoulakis

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Background: Oxidative damage is one of the major factors that lead to cell damage, organ dysfunction and death in sepsis. Thus, an attractive candidate for the pharmacologic treatment of the septic syndrome is desferoxamine (DFX), an antioxidant iron chelator used for the removal of iron and a potential free radical scavenger. Objective: The impact of DFX administration on the survival of septic animals. The effect on cell integrity and cycle of vital organs. Methods: Sepsis was induced in 40 rats using the cecal ligation and puncture method (CLP) and 20 rats randomly received twice subcutaneously DFX (total dose: 40 mg/kg). Rats were monitored for 36 h and all vital organs were harvested for pathology examination and immunohistochemical detection of Bax, Bcl-2, cytochrome c and caspase-8 apoptosis regulating proteins. Results: Mean survival in the DFX group was 34.2 h (median 36.0, S.D. 4.4) and 30.2 h (median 36.0, S.D. 9.1) in the control group (p=0.04), while 36 h after follow up 85% of the DFX-treated rats and 55% of placebo rats were alive (p=0.04). Expression of pro-apoptotic bax protein was significantly increased in the heart, liver and kidney of animals in the DFX group compared to the control group. Conclusions: Treatment with the polymeric iron chelator DFX significantly increases survival of septic subjects and alters the expression of bax, an apoptosis regulating protein in certain organs (heart, liver and kidney).

Original languageEnglish (US)
Pages (from-to)455-459
Number of pages5
JournalInternational Immunopharmacology
Volume4
Issue number3
DOIs
StatePublished - Mar 1 2004

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Deferoxamine
Gene Expression
Iron
Chelating Agents
Sepsis
Apoptosis
Kidney
bcl-2-Associated X Protein
Control Groups
Free Radical Scavengers
Apoptosis Regulatory Proteins
Caspase 8
Liver
Cytochromes c
Punctures
Ligation
Cell Cycle
Proteins
Antioxidants
Placebos

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Pharmacology

Cite this

Messaris, E., Antonakis, P. T., Memos, N., Chatzigianni, E., Leandros, E., & Konstadoulakis, M. M. (2004). Deferoxamine administration in septic animals: Improved survival and altered apoptotic gene expression. International Immunopharmacology, 4(3), 455-459. https://doi.org/10.1016/j.intimp.2004.01.012
Messaris, Evangelos ; Antonakis, Pantelis T. ; Memos, Nicholaos ; Chatzigianni, Emmy ; Leandros, Emanuel ; Konstadoulakis, Manousos M. / Deferoxamine administration in septic animals : Improved survival and altered apoptotic gene expression. In: International Immunopharmacology. 2004 ; Vol. 4, No. 3. pp. 455-459.
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Messaris, E, Antonakis, PT, Memos, N, Chatzigianni, E, Leandros, E & Konstadoulakis, MM 2004, 'Deferoxamine administration in septic animals: Improved survival and altered apoptotic gene expression', International Immunopharmacology, vol. 4, no. 3, pp. 455-459. https://doi.org/10.1016/j.intimp.2004.01.012

Deferoxamine administration in septic animals : Improved survival and altered apoptotic gene expression. / Messaris, Evangelos; Antonakis, Pantelis T.; Memos, Nicholaos; Chatzigianni, Emmy; Leandros, Emanuel; Konstadoulakis, Manousos M.

In: International Immunopharmacology, Vol. 4, No. 3, 01.03.2004, p. 455-459.

Research output: Contribution to journalArticle

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T1 - Deferoxamine administration in septic animals

T2 - Improved survival and altered apoptotic gene expression

AU - Messaris, Evangelos

AU - Antonakis, Pantelis T.

AU - Memos, Nicholaos

AU - Chatzigianni, Emmy

AU - Leandros, Emanuel

AU - Konstadoulakis, Manousos M.

PY - 2004/3/1

Y1 - 2004/3/1

N2 - Background: Oxidative damage is one of the major factors that lead to cell damage, organ dysfunction and death in sepsis. Thus, an attractive candidate for the pharmacologic treatment of the septic syndrome is desferoxamine (DFX), an antioxidant iron chelator used for the removal of iron and a potential free radical scavenger. Objective: The impact of DFX administration on the survival of septic animals. The effect on cell integrity and cycle of vital organs. Methods: Sepsis was induced in 40 rats using the cecal ligation and puncture method (CLP) and 20 rats randomly received twice subcutaneously DFX (total dose: 40 mg/kg). Rats were monitored for 36 h and all vital organs were harvested for pathology examination and immunohistochemical detection of Bax, Bcl-2, cytochrome c and caspase-8 apoptosis regulating proteins. Results: Mean survival in the DFX group was 34.2 h (median 36.0, S.D. 4.4) and 30.2 h (median 36.0, S.D. 9.1) in the control group (p=0.04), while 36 h after follow up 85% of the DFX-treated rats and 55% of placebo rats were alive (p=0.04). Expression of pro-apoptotic bax protein was significantly increased in the heart, liver and kidney of animals in the DFX group compared to the control group. Conclusions: Treatment with the polymeric iron chelator DFX significantly increases survival of septic subjects and alters the expression of bax, an apoptosis regulating protein in certain organs (heart, liver and kidney).

AB - Background: Oxidative damage is one of the major factors that lead to cell damage, organ dysfunction and death in sepsis. Thus, an attractive candidate for the pharmacologic treatment of the septic syndrome is desferoxamine (DFX), an antioxidant iron chelator used for the removal of iron and a potential free radical scavenger. Objective: The impact of DFX administration on the survival of septic animals. The effect on cell integrity and cycle of vital organs. Methods: Sepsis was induced in 40 rats using the cecal ligation and puncture method (CLP) and 20 rats randomly received twice subcutaneously DFX (total dose: 40 mg/kg). Rats were monitored for 36 h and all vital organs were harvested for pathology examination and immunohistochemical detection of Bax, Bcl-2, cytochrome c and caspase-8 apoptosis regulating proteins. Results: Mean survival in the DFX group was 34.2 h (median 36.0, S.D. 4.4) and 30.2 h (median 36.0, S.D. 9.1) in the control group (p=0.04), while 36 h after follow up 85% of the DFX-treated rats and 55% of placebo rats were alive (p=0.04). Expression of pro-apoptotic bax protein was significantly increased in the heart, liver and kidney of animals in the DFX group compared to the control group. Conclusions: Treatment with the polymeric iron chelator DFX significantly increases survival of septic subjects and alters the expression of bax, an apoptosis regulating protein in certain organs (heart, liver and kidney).

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