The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
Differential interaction of porphyrins used in photoradiation therapy with ferrochelatase
Open accessAbstract
The mechanism of porphyrin accumulation by tumours is not yet established. If metabolism aids porphyrin elimination, tumours, unlike normal tissues, may not metabolize porphyrins used clinically, such as proto-, haemato-, OO'-diacetyl-haemato- and monohydroxyethyl-monovinyl-deutero-porphyrin. Proto-, haemato- and monohydroxyethyl-monovinyl-deutero-porphyrin are substrates for the mitochondrial enzyme ferrochelatase (EC 4.99.1.1), which can form haem analogues from exogenous porphyrins. The Km values for proto-, haemato- and monohydroxyethyl-monovinyl-deutero-porphyrin are 11, 22 and 23 microM respectively. However, OO'-diacetyl-haematoporphyrin is an effective competitive inhibitor with Ki of 11 microM. Hepatic ferrochelatase specific activity is 5.9 and 5.5 nmol of haem/h per mg of protein respectively in normal Buffalo rat and in those bearing the extrahepatic Morris 7288C hepatoma, and is only 0.13 nmol/h per mg in the hepatomas. Therefore low ferrochelatase activity in cancerous cells may provide one means whereby some porphyrins accumulate in tumours, and the ability of certain porphyrins to act as ferrochelatase inhibitors may provide another.
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“Although the uptake of ALA is non-selective, accumulation of PpIX in tumor cells may occur selectively because of alterations in enzymatic activity in the heme synthesis pathway.”
From Photodynamic Therapy for Non-Melanoma Skin Cancers (2016) · cites this paper as [10]
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“The accumulation of PpIX in neoplastic tissue is further supplemented by decreased activity of ferrochelatase (FC), which converts PpIX to heme [9,10].”
From Photodynamic Therapy for Non-Melanoma Skin Cancers (2016) · cites this paper as [10]
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Cited by
Sorted by citations
5-Aminolevulinic Acid-Based Photodynamic Therapy: Principles and Experimental Research
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“Dailey and Smith (1984) studied the interaction of some of the porphyrins present in HPD with ferrochelatase and found that these porphyrins were either substrates for this enzyme to form hemes or effective competitive inhibitors.”
BackgroundMitochondria-based photodynamic anti-cancer therapy
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Metadata
- Authors
- Dailey, H. A., & Smith, A.
- ORCID
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 1984-10-15
- Volume
- 223
- Issue
- 2
- Pages
- 441-445
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- PMC
- PMC1144316
- OpenAlex
- W2170447022
- Cited by
- 140
- References
- 30
- Citations by year
- 2025: 1 · 2023: 1 · 2022: 3 · 2020: 3 · 2019: 3 · 2018: 1 · 2017: 4 · 2016: 3 · 2015: 4 · 2014: 1 · 2012: 3
- FWCI
- 6.75
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biochemical Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- British Sedimentological Research Group
- National Institutes of Health
- U.S. Public Health Service
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Photodynamic Therapy Research Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Porphyrin Metabolism and Disorders
- Physical Sciences › Materials Science › Materials Chemistry › Porphyrin and Phthalocyanine Chemistry
- Keywords
- porphyrins, ferrochelatase, photodynamic therapy, hematoporphyrin, deuteroporphyrin, competitive inhibition, enzyme kinetics, hepatocellular carcinoma
- MeSH terms
- Animals, Ferrochelatase, Hematoporphyrins, Kinetics, Liver, Liver Neoplasms, Experimental, Lyases, Male, Porphyrins, Rats, Inbred BUF, Rats, In Vitro Techniques
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