Heme biosynthesis pathway regulation in a model of hepatocarcinogenesis pre-initiation
1. 1. Heme regulation before the appearance of hyperplastic nodules was investigated in mice models of hepatocarcinogenesis. 2. 2. With this aim 5-aminolaevulinate synthetase (ALA-S), microsomal heme-oxygenase (MHO), mitochondrial and cytoplasmic rhodanese activities were examined throughout a perio...
Guardado en:
| Autores principales: | , , , , |
|---|---|
| Formato: | JOUR |
| Materias: | |
| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_03050491_v103_n1_p251_Polo |
| Aporte de: |
| id |
todo:paper_03050491_v103_n1_p251_Polo |
|---|---|
| record_format |
dspace |
| spelling |
todo:paper_03050491_v103_n1_p251_Polo2023-10-03T15:21:13Z Heme biosynthesis pathway regulation in a model of hepatocarcinogenesis pre-initiation Polo, C.F. Vazquez, E.S. Caballero, F. Gerez, E. Batlle, A.M.d.C. 4 dimethylaminoazobenzene 5 aminolevulinate synthase heme oxygenase thiosulfate sulfurtransferase animal experiment animal model animal tissue article heme synthesis liver carcinogenesis mouse nonhuman priority journal 5-Aminolevulinate Synthetase Animal Cytoplasm Heme Heme Oxygenase (Decyclizing) Kinetics Liver Liver Neoplasms, Experimental Male Mice Microsomes, Liver Mitochondria, Liver p-Dimethylaminoazobenzene Support, Non-U.S. Gov't Thiosulfate Sulfurtransferase Animalia 1. 1. Heme regulation before the appearance of hyperplastic nodules was investigated in mice models of hepatocarcinogenesis. 2. 2. With this aim 5-aminolaevulinate synthetase (ALA-S), microsomal heme-oxygenase (MHO), mitochondrial and cytoplasmic rhodanese activities were examined throughout a period of 35 days in animals exposed to dietary p-dimethylaminoazobenzene (DAB). 3. 3. ALA-S activity was significantly diminished (50%) on day 14, then showing a sharply rising profile from day 28 onwards, and reaching 350% on day 35. 4. 4. A similar profile was observed for mitochondrial rhodanese activity. 5. 5. Changes in MHO and cytoplasmic rhodanese activities were almost the opposite to those observed for ALA-S. 6. 6. The distinctive alteration in mitochondrial and cytoplasmic rhodanese would suggest that it plays a subtle role in ALA-S regulation during carcinogenesis initiation through a mechanism that appears to involved subcellular localization controls perhaps by means of the breakage of cystine trisulphide postulated to act as an ALA-S activator. 7. 7. Taking into account the present results, we suggest a probable mechanism for the onset of hepatocarcinogenesis that includes a primary activating liver status, provoking biochemical aberration leading to the stage of initiation of hepatocarcinogenesis involving the whole organ. © 1992. Fil:Vazquez, E.S. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Gerez, E. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Batlle, A.M.d.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_03050491_v103_n1_p251_Polo |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
4 dimethylaminoazobenzene 5 aminolevulinate synthase heme oxygenase thiosulfate sulfurtransferase animal experiment animal model animal tissue article heme synthesis liver carcinogenesis mouse nonhuman priority journal 5-Aminolevulinate Synthetase Animal Cytoplasm Heme Heme Oxygenase (Decyclizing) Kinetics Liver Liver Neoplasms, Experimental Male Mice Microsomes, Liver Mitochondria, Liver p-Dimethylaminoazobenzene Support, Non-U.S. Gov't Thiosulfate Sulfurtransferase Animalia |
| spellingShingle |
4 dimethylaminoazobenzene 5 aminolevulinate synthase heme oxygenase thiosulfate sulfurtransferase animal experiment animal model animal tissue article heme synthesis liver carcinogenesis mouse nonhuman priority journal 5-Aminolevulinate Synthetase Animal Cytoplasm Heme Heme Oxygenase (Decyclizing) Kinetics Liver Liver Neoplasms, Experimental Male Mice Microsomes, Liver Mitochondria, Liver p-Dimethylaminoazobenzene Support, Non-U.S. Gov't Thiosulfate Sulfurtransferase Animalia Polo, C.F. Vazquez, E.S. Caballero, F. Gerez, E. Batlle, A.M.d.C. Heme biosynthesis pathway regulation in a model of hepatocarcinogenesis pre-initiation |
| topic_facet |
4 dimethylaminoazobenzene 5 aminolevulinate synthase heme oxygenase thiosulfate sulfurtransferase animal experiment animal model animal tissue article heme synthesis liver carcinogenesis mouse nonhuman priority journal 5-Aminolevulinate Synthetase Animal Cytoplasm Heme Heme Oxygenase (Decyclizing) Kinetics Liver Liver Neoplasms, Experimental Male Mice Microsomes, Liver Mitochondria, Liver p-Dimethylaminoazobenzene Support, Non-U.S. Gov't Thiosulfate Sulfurtransferase Animalia |
| description |
1. 1. Heme regulation before the appearance of hyperplastic nodules was investigated in mice models of hepatocarcinogenesis. 2. 2. With this aim 5-aminolaevulinate synthetase (ALA-S), microsomal heme-oxygenase (MHO), mitochondrial and cytoplasmic rhodanese activities were examined throughout a period of 35 days in animals exposed to dietary p-dimethylaminoazobenzene (DAB). 3. 3. ALA-S activity was significantly diminished (50%) on day 14, then showing a sharply rising profile from day 28 onwards, and reaching 350% on day 35. 4. 4. A similar profile was observed for mitochondrial rhodanese activity. 5. 5. Changes in MHO and cytoplasmic rhodanese activities were almost the opposite to those observed for ALA-S. 6. 6. The distinctive alteration in mitochondrial and cytoplasmic rhodanese would suggest that it plays a subtle role in ALA-S regulation during carcinogenesis initiation through a mechanism that appears to involved subcellular localization controls perhaps by means of the breakage of cystine trisulphide postulated to act as an ALA-S activator. 7. 7. Taking into account the present results, we suggest a probable mechanism for the onset of hepatocarcinogenesis that includes a primary activating liver status, provoking biochemical aberration leading to the stage of initiation of hepatocarcinogenesis involving the whole organ. © 1992. |
| format |
JOUR |
| author |
Polo, C.F. Vazquez, E.S. Caballero, F. Gerez, E. Batlle, A.M.d.C. |
| author_facet |
Polo, C.F. Vazquez, E.S. Caballero, F. Gerez, E. Batlle, A.M.d.C. |
| author_sort |
Polo, C.F. |
| title |
Heme biosynthesis pathway regulation in a model of hepatocarcinogenesis pre-initiation |
| title_short |
Heme biosynthesis pathway regulation in a model of hepatocarcinogenesis pre-initiation |
| title_full |
Heme biosynthesis pathway regulation in a model of hepatocarcinogenesis pre-initiation |
| title_fullStr |
Heme biosynthesis pathway regulation in a model of hepatocarcinogenesis pre-initiation |
| title_full_unstemmed |
Heme biosynthesis pathway regulation in a model of hepatocarcinogenesis pre-initiation |
| title_sort |
heme biosynthesis pathway regulation in a model of hepatocarcinogenesis pre-initiation |
| url |
http://hdl.handle.net/20.500.12110/paper_03050491_v103_n1_p251_Polo |
| work_keys_str_mv |
AT polocf hemebiosynthesispathwayregulationinamodelofhepatocarcinogenesispreinitiation AT vazquezes hemebiosynthesispathwayregulationinamodelofhepatocarcinogenesispreinitiation AT caballerof hemebiosynthesispathwayregulationinamodelofhepatocarcinogenesispreinitiation AT gereze hemebiosynthesispathwayregulationinamodelofhepatocarcinogenesispreinitiation AT batlleamdc hemebiosynthesispathwayregulationinamodelofhepatocarcinogenesispreinitiation |
| _version_ |
1782029231567405056 |