Cachexia induced by Walker 256 tumor growth causes rat lymphocyte death

Death induction by Walker 256 tumor cachexia in non-tumor-infiltrating lymphocytes was investigated. Lymphocytes from cachectic tumor-bearing rats presented a higher proportion of cells with ruptured membranes, indicating necrotic cell death. The cachexia induced by Walker 256 tumor also increased b...

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Bibliographic Details
Published in:Cancer Immunology, Immunotherapy Immunotherapy, 2005-02, Vol.54 (2), p.179-186
Main Authors: MARTINS DE LIMA, Thais, RAMOS LIMA, Manuela M, ALMEIDA, Débora C. G, MENDONCA, José Roberto, CURI, Rui
Format: Article
Language:English
Subjects:
Animals
Antigens
Antineoplastic agents
Apoptosis
bcl-2-Associated X Protein
bcl-X Protein
Biological and medical sciences
Body Weight
Cachexia - etiology
Cancer
Carcinoma 256, Walker - immunology
Carcinoma 256, Walker - metabolism
Carcinoma 256, Walker - pathology
Caspase 3
Caspases - metabolism
Cell death
Lymphocytes
Lymphocytes - immunology
Lymphocytes - metabolism
Lymphocytes - pathology
Male
Medical sciences
Membrane Potentials
Mitochondria
Original
Pharmacology. Drug treatments
Proto-Oncogene Proteins c-bcl-2 - genetics
Proto-Oncogene Proteins c-bcl-2 - metabolism
Rats
Rats, Wistar
Signal transduction
Tumor Cells, Cultured - transplantation
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
Tumors
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Summary:Death induction by Walker 256 tumor cachexia in non-tumor-infiltrating lymphocytes was investigated. Lymphocytes from cachectic tumor-bearing rats presented a higher proportion of cells with ruptured membranes, indicating necrotic cell death. The cachexia induced by Walker 256 tumor also increased by 3.6-fold the percentage of cells with fragmented DNA, suggestive of apoptotic cell death. The mitochondria involvement was examined by analysis of mitochondria transmembrane potential using rhodamine 123. Lymphocytes from cachectic tumor-bearing rats presented a more pronounced depolarization of mitochondrial transmembrane potential in comparison with cells from the control group. The expression of important proapoptotic (Bcl-xs, Bax, p53, caspase-3) and antiapoptotic genes (Bcl-2 and Bcl-xL) was also altered by tumor cachexia. These results suggest that the immunosuppression induced by Walker 256 tumor cachexia is at least in part a result of lymphocyte death. Evidence was found for the involvement of mitochondria and important proapoptotic genes in the process of lymphocyte death by Walker 256 tumor cachexia.
ISSN:0340-7004
1432-0851
DOI:10.1007/s00262-004-0570-4