Response of glucose metabolism enzymes in an acute porphyria model: Role of reactive oxygen species
Acute hepatic porphyrias are human metabolic diseases characterized by the accumulation of heme precursors, such as 5-aminolevulinic acid (ALA). The administration of glucose can prevent the symptomatology of these diseases. The aim of this work was to study the relationship between glucose metaboli...
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2005
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0300483X_v216_n1_p49_Lelli http://hdl.handle.net/20.500.12110/paper_0300483X_v216_n1_p49_Lelli |
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paper:paper_0300483X_v216_n1_p49_Lelli |
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dspace |
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Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Acute porphyria model Glucose metabolism Rat liver Reactive oxygen species 1,4 dihydro 2,4,6 trimethyl 3,5 pyridinedicarboxylic acid diethyl ester 5 aminolevulinate synthase allylisopropylacetamide aminolevulinic acid carbonyl derivative catalase corn oil ferrochelatase glycogen phosphorylase liver protein phosphoenolpyruvate carboxykinase (GTP) porphobilinogen reactive oxygen metabolite sodium chloride superoxide dismutase acute intermittent porphyria animal experiment animal model animal tissue article chemoluminescence controlled study enzyme activity enzyme induction female glucose metabolism lipid peroxidation liver level nonhuman oxidative stress priority journal rat Allylisopropylacetamide Animals Chemiluminescent Measurements Dicarbethoxydihydrocollidine Disease Models, Animal Female Glucose Heme Lipid Peroxidation Liver Porphyria, Acute Intermittent Rats Rats, Wistar Reactive Oxygen Species Urine Animalia Rattus norvegicus Zea mays |
| spellingShingle |
Acute porphyria model Glucose metabolism Rat liver Reactive oxygen species 1,4 dihydro 2,4,6 trimethyl 3,5 pyridinedicarboxylic acid diethyl ester 5 aminolevulinate synthase allylisopropylacetamide aminolevulinic acid carbonyl derivative catalase corn oil ferrochelatase glycogen phosphorylase liver protein phosphoenolpyruvate carboxykinase (GTP) porphobilinogen reactive oxygen metabolite sodium chloride superoxide dismutase acute intermittent porphyria animal experiment animal model animal tissue article chemoluminescence controlled study enzyme activity enzyme induction female glucose metabolism lipid peroxidation liver level nonhuman oxidative stress priority journal rat Allylisopropylacetamide Animals Chemiluminescent Measurements Dicarbethoxydihydrocollidine Disease Models, Animal Female Glucose Heme Lipid Peroxidation Liver Porphyria, Acute Intermittent Rats Rats, Wistar Reactive Oxygen Species Urine Animalia Rattus norvegicus Zea mays Lelli de Angeletti, Sandra Marcela Mazzetti, Marta Blanca Response of glucose metabolism enzymes in an acute porphyria model: Role of reactive oxygen species |
| topic_facet |
Acute porphyria model Glucose metabolism Rat liver Reactive oxygen species 1,4 dihydro 2,4,6 trimethyl 3,5 pyridinedicarboxylic acid diethyl ester 5 aminolevulinate synthase allylisopropylacetamide aminolevulinic acid carbonyl derivative catalase corn oil ferrochelatase glycogen phosphorylase liver protein phosphoenolpyruvate carboxykinase (GTP) porphobilinogen reactive oxygen metabolite sodium chloride superoxide dismutase acute intermittent porphyria animal experiment animal model animal tissue article chemoluminescence controlled study enzyme activity enzyme induction female glucose metabolism lipid peroxidation liver level nonhuman oxidative stress priority journal rat Allylisopropylacetamide Animals Chemiluminescent Measurements Dicarbethoxydihydrocollidine Disease Models, Animal Female Glucose Heme Lipid Peroxidation Liver Porphyria, Acute Intermittent Rats Rats, Wistar Reactive Oxygen Species Urine Animalia Rattus norvegicus Zea mays |
| description |
Acute hepatic porphyrias are human metabolic diseases characterized by the accumulation of heme precursors, such as 5-aminolevulinic acid (ALA). The administration of glucose can prevent the symptomatology of these diseases. The aim of this work was to study the relationship between glucose metabolism disturbances and the development of experimental acute hepatic porphyria, as well as the role of reactive oxygen species (ROS) through assays on hepatic key gluconeogenic and glycogenolytic enzymes; phosphoenolpyruvate carboxykinase (PEPCK) and glycogen phosphorylase (GP), respectively. Female Wistar rats were treated with three different doses of the porphyrinogenic drug 2-allyl-2-isopropylacetamide (AIA) and with a single dose of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC). Thus, rats were divided into the following groups: group L (100 mg AIA + 50 mg DDC/kg body wt.); group M (250 mg AIA + 50 mg DDC/kg body wt.) and group H (500 mg AIA + 50 mg DDC/kg body wt.). The control group (group C) only received vehicles (saline solution and corn oil). Acute hepatic porphyria markers ALA-synthase (ALA-S) and ferrochelatase, heme precursors ALA and porphobilinogen (PBG), and oxidative stress markers superoxide dismutase (SOD) and catalase (CAT) were also measured in hepatic tissue. On the other hand, hepatic cytosolic protein carbonyl content, lipid peroxidation and urinary chemiluminescence were determined as in vivo oxidative damage markers. All these parameters were studied in relation to the different doses of AIA/DDC. Results showed that enzymes were affected in a drug-dose-dependent way. PEPCK activity decreased about 30% in group H with respect to groups C and L, whereas GP activity decreased 53 and 38% in group H when compared to groups C and L, respectively. On the other hand, cytosolic protein carbonyl content increased three-fold in group H with respect to group C. A marked increase in urinary chemiluminescence and a definite increase in lipid peroxidation were also detected. The activity of liver antioxidant enzyme SOD showed an induction of about 235% in group H when compared to group C, whereas CAT activity diminished due to heme depletion caused by both drugs. Based on these results, we can speculate that the alterations observed in glucose metabolism enzymes could be partly related to the damage caused by ROS on their enzymatic protein structures, suggesting that they could be also linked to the beneficial role of glucose administration in acute hepatic porphyria cases. © 2005 Elsevier Ireland Ltd. All rights reserved. |
| author |
Lelli de Angeletti, Sandra Marcela Mazzetti, Marta Blanca |
| author_facet |
Lelli de Angeletti, Sandra Marcela Mazzetti, Marta Blanca |
| author_sort |
Lelli de Angeletti, Sandra Marcela |
| title |
Response of glucose metabolism enzymes in an acute porphyria model: Role of reactive oxygen species |
| title_short |
Response of glucose metabolism enzymes in an acute porphyria model: Role of reactive oxygen species |
| title_full |
Response of glucose metabolism enzymes in an acute porphyria model: Role of reactive oxygen species |
| title_fullStr |
Response of glucose metabolism enzymes in an acute porphyria model: Role of reactive oxygen species |
| title_full_unstemmed |
Response of glucose metabolism enzymes in an acute porphyria model: Role of reactive oxygen species |
| title_sort |
response of glucose metabolism enzymes in an acute porphyria model: role of reactive oxygen species |
| publishDate |
2005 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0300483X_v216_n1_p49_Lelli http://hdl.handle.net/20.500.12110/paper_0300483X_v216_n1_p49_Lelli |
| work_keys_str_mv |
AT lellideangelettisandramarcela responseofglucosemetabolismenzymesinanacuteporphyriamodelroleofreactiveoxygenspecies AT mazzettimartablanca responseofglucosemetabolismenzymesinanacuteporphyriamodelroleofreactiveoxygenspecies |
| _version_ |
1768544502051504128 |
| spelling |
paper:paper_0300483X_v216_n1_p49_Lelli2023-06-08T15:27:16Z Response of glucose metabolism enzymes in an acute porphyria model: Role of reactive oxygen species Lelli de Angeletti, Sandra Marcela Mazzetti, Marta Blanca Acute porphyria model Glucose metabolism Rat liver Reactive oxygen species 1,4 dihydro 2,4,6 trimethyl 3,5 pyridinedicarboxylic acid diethyl ester 5 aminolevulinate synthase allylisopropylacetamide aminolevulinic acid carbonyl derivative catalase corn oil ferrochelatase glycogen phosphorylase liver protein phosphoenolpyruvate carboxykinase (GTP) porphobilinogen reactive oxygen metabolite sodium chloride superoxide dismutase acute intermittent porphyria animal experiment animal model animal tissue article chemoluminescence controlled study enzyme activity enzyme induction female glucose metabolism lipid peroxidation liver level nonhuman oxidative stress priority journal rat Allylisopropylacetamide Animals Chemiluminescent Measurements Dicarbethoxydihydrocollidine Disease Models, Animal Female Glucose Heme Lipid Peroxidation Liver Porphyria, Acute Intermittent Rats Rats, Wistar Reactive Oxygen Species Urine Animalia Rattus norvegicus Zea mays Acute hepatic porphyrias are human metabolic diseases characterized by the accumulation of heme precursors, such as 5-aminolevulinic acid (ALA). The administration of glucose can prevent the symptomatology of these diseases. The aim of this work was to study the relationship between glucose metabolism disturbances and the development of experimental acute hepatic porphyria, as well as the role of reactive oxygen species (ROS) through assays on hepatic key gluconeogenic and glycogenolytic enzymes; phosphoenolpyruvate carboxykinase (PEPCK) and glycogen phosphorylase (GP), respectively. Female Wistar rats were treated with three different doses of the porphyrinogenic drug 2-allyl-2-isopropylacetamide (AIA) and with a single dose of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC). Thus, rats were divided into the following groups: group L (100 mg AIA + 50 mg DDC/kg body wt.); group M (250 mg AIA + 50 mg DDC/kg body wt.) and group H (500 mg AIA + 50 mg DDC/kg body wt.). The control group (group C) only received vehicles (saline solution and corn oil). Acute hepatic porphyria markers ALA-synthase (ALA-S) and ferrochelatase, heme precursors ALA and porphobilinogen (PBG), and oxidative stress markers superoxide dismutase (SOD) and catalase (CAT) were also measured in hepatic tissue. On the other hand, hepatic cytosolic protein carbonyl content, lipid peroxidation and urinary chemiluminescence were determined as in vivo oxidative damage markers. All these parameters were studied in relation to the different doses of AIA/DDC. Results showed that enzymes were affected in a drug-dose-dependent way. PEPCK activity decreased about 30% in group H with respect to groups C and L, whereas GP activity decreased 53 and 38% in group H when compared to groups C and L, respectively. On the other hand, cytosolic protein carbonyl content increased three-fold in group H with respect to group C. A marked increase in urinary chemiluminescence and a definite increase in lipid peroxidation were also detected. The activity of liver antioxidant enzyme SOD showed an induction of about 235% in group H when compared to group C, whereas CAT activity diminished due to heme depletion caused by both drugs. Based on these results, we can speculate that the alterations observed in glucose metabolism enzymes could be partly related to the damage caused by ROS on their enzymatic protein structures, suggesting that they could be also linked to the beneficial role of glucose administration in acute hepatic porphyria cases. © 2005 Elsevier Ireland Ltd. All rights reserved. Fil:Lelli, S.M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Mazzetti, M.B. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2005 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0300483X_v216_n1_p49_Lelli http://hdl.handle.net/20.500.12110/paper_0300483X_v216_n1_p49_Lelli |