Enhancement of aminolevulinic acid based photodynamic therapy by adriamycin

This paper reports on studies that evaluate the interaction between δ-aminolevulinic acid (ALA)-based photodynamic therapy (PDT) and adriamycin (ADM) in an animal model system. Two groups of mice bearing a transplantable mammary adenocarcinoma received ADM i.p. in a single dose of 5 mg (low dose) an...

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Autor principal: Casas, A.
Otros Autores: Fukuda, H., Riley, P., Del C. Batlle, A.M
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 1997
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Acceso en línea:Registro en Scopus
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024 7 |2 scopus  |a 2-s2.0-0030833018 
024 7 |2 cas  |a DNA, 9007-49-2; aminolevulinic acid, 106-60-5; doxorubicin, 23214-92-8, 25316-40-9; hydroxyl radical, 3352-57-6; malonaldehyde, 542-78-9; peroxide, 14915-07-2; porphobilinogen synthase, 9036-37-7; porphyrin, 24869-67-8; semiquinone, 60766-01-0; Aminolevulinic Acid, 106-60-5; Ammonia-Lyases, 4.3.1.-; Doxorubicin, 23214-92-8; Porphobilinogen Synthase, 4.2.1.24; Porphyrins; porphobilinogenase, 5.- 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a CALED 
100 1 |a Casas, A. 
245 1 0 |a Enhancement of aminolevulinic acid based photodynamic therapy by adriamycin 
260 |c 1997 
270 1 0 |m Riley, P.; Department of Molecular Pathology, University College London Med. Sch., Division of Pathology, 46 Cleveland Street, London W1P 6DB, United Kingdom; email: rebc900@ucl.ac.uk 
506 |2 openaire  |e Política editorial 
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520 3 |a This paper reports on studies that evaluate the interaction between δ-aminolevulinic acid (ALA)-based photodynamic therapy (PDT) and adriamycin (ADM) in an animal model system. Two groups of mice bearing a transplantable mammary adenocarcinoma received ADM i.p. in a single dose of 5 mg (low dose) and 30 mg (high dose) per kg body weight. Sixteen or 40 h after administration of the drug, mice were sacrificed, tumours, livers and hearts were removed and porphyrins, enzyme activities and malondialdehyde content were determined. Tumour explants of ADM-treated mice were incubated with ALA and irradiated with an He-Ne laser. Re-implantation of these in vitro PDT-treated explants into test animals showed that inhibition of tumour growth was significantly enhanced by combined treatment when the low dose of ADM was used. There were no significant changes in porphyrin content, ALA dehydratase and porphobilinogenase activities in the tissues analyzed after ADM treatment as compared with control values. ADM toxicity is thought to be related to semiquinone free radical formation with subsequent generation of reactive oxygen species such as peroxide and hydroxyl radical. These species are considered to initiate lipid peroxidation (LPO) and cause DNA damage. In the case of low-dose treatment with ADM a significant increase in the LPO product, malondialdehyde, was observed after PDT whereas with the high-dose regimen no changes were observed. In the case of explants of (non-irradiated) cardiac tissue malondialdehyde production was also found to be dependent on the dose and time of administration of adriamycin. In our in vivo/in vitro model system we have shown that pre-treatment with ADM increased the cytotoxicity of ALA-PDT at a dosage level of ADM which did not raise LPO levels in heart tissue. The mechanism of this effect has not been clearly elucidated but our data suggest that the observed enhancement of PDT may be attributed in part to the weakening of cellular defence mechanisms by the pre-treatment involving free radical generation by ADM.  |l eng 
536 |a Detalles de la financiación: National Council for Scientific Research 
536 |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas 
536 |a Detalles de la financiación: This research was supported by grants from the Argentine National Research Council (CONICET). The authors are very grateful to Raffo S.A. for providing Doxorubicina Asofarma, to Mrs Victoria Castillo for technical assistance and to Miss M. Malacos for typing the manuscript. A.M. del C.B. and H.F. hold the posts of Superior and Associate Researchers at the CONICET. A.C. is a CONICET Research Fellow. The work presented in this paper forms part of a Doctoral Thesis submitted to the University of Buenos Aires by A.C. 
593 |a Ctro. Invest. Sobre Porfirinas Y P., Cd. Univ., Pabellon II, 2do P., Buenos Aires, Argentina 
593 |a Department of Molecular Pathology, Univ. Coll. London Med. Sch., D., London, United Kingdom 
690 1 0 |a Δ-AMINOLEVULINIC ACID 
690 1 0 |a ADRIAMYCIN 
690 1 0 |a ANTITUMOUR DRUGS 
690 1 0 |a COMBINATION THERAPY 
690 1 0 |a PHOTODYNAMIC THERAPY 
690 1 0 |a AMINOLEVULINIC ACID 
690 1 0 |a DNA 
690 1 0 |a DOXORUBICIN 
690 1 0 |a FREE RADICAL 
690 1 0 |a HYDROXYL RADICAL 
690 1 0 |a MALONALDEHYDE 
690 1 0 |a PEROXIDE 
690 1 0 |a PORPHOBILINOGEN SYNTHASE 
690 1 0 |a PORPHYRIN 
690 1 0 |a REACTIVE OXYGEN METABOLITE 
690 1 0 |a SEMIQUINONE 
690 1 0 |a ANIMAL EXPERIMENT 
690 1 0 |a ANIMAL MODEL 
690 1 0 |a ANIMAL TISSUE 
690 1 0 |a ARTICLE 
690 1 0 |a BREAST ADENOCARCINOMA 
690 1 0 |a CANCER INHIBITION 
690 1 0 |a CANCER TRANSPLANTATION 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a CYTOTOXICITY 
690 1 0 |a DNA DAMAGE 
690 1 0 |a DRUG MECHANISM 
690 1 0 |a DRUG TOXICITY 
690 1 0 |a ENZYME ACTIVITY 
690 1 0 |a HEART 
690 1 0 |a INTRAPERITONEAL DRUG ADMINISTRATION 
690 1 0 |a LIPID PEROXIDATION 
690 1 0 |a LIVER 
690 1 0 |a MALE 
690 1 0 |a MOUSE 
690 1 0 |a NONHUMAN 
690 1 0 |a PHOTODYNAMIC THERAPY 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a ADENOCARCINOMA 
690 1 0 |a AMINOLEVULINIC ACID 
690 1 0 |a AMMONIA-LYASES 
690 1 0 |a ANIMALS 
690 1 0 |a DOXORUBICIN 
690 1 0 |a DRUG THERAPY, COMBINATION 
690 1 0 |a LIPID PEROXIDATION 
690 1 0 |a LIVER 
690 1 0 |a MALE 
690 1 0 |a MAMMARY NEOPLASMS, EXPERIMENTAL 
690 1 0 |a MICE 
690 1 0 |a MICE, INBRED BALB C 
690 1 0 |a MYOCARDIUM 
690 1 0 |a NEOPLASM TRANSPLANTATION 
690 1 0 |a PHOTOCHEMOTHERAPY 
690 1 0 |a PORPHOBILINOGEN SYNTHASE 
690 1 0 |a PORPHYRINS 
690 1 0 |a ANIMALIA 
650 1 7 |2 spines  |a LASER 
700 1 |a Fukuda, H. 
700 1 |a Riley, P. 
700 1 |a Del C. Batlle, A.M. 
773 0 |d 1997  |g v. 121  |h pp. 105-113  |k n. 1  |p CANCER LETT.  |x 03043835  |w (AR-BaUEN)CENRE-4108  |t Cancer Letters 
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856 4 0 |u https://hdl.handle.net/20.500.12110/paper_03043835_v121_n1_p105_Casas  |y Handle 
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