Hexachlorobenzene treatment on hepatic mitochondrial function parameters and intracellular coproporphyrinogen oxidase location
These studies try to elucidate why isocoproporphyrin appears in hexachlorobenzene-poisoned rats' feces. Chronic exposure of hexachlorobenzene to rats produces an experimental model for human porphyria cutanea tarda. After 8 weeks of treatment, rats showed high porphyrin excreta and 50% inhibiti...
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| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_10915818_v27_n6_p455_Sopena |
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todo:paper_10915818_v27_n6_p455_Sopena2023-10-03T16:04:57Z Hexachlorobenzene treatment on hepatic mitochondrial function parameters and intracellular coproporphyrinogen oxidase location Sopena, Y.E. Ferramola De Sancovich, A.M. Sancovich, H.A. Coproporphyrinogen Oxidase Experimental Porphyria Hexachlorobenzene Isocoproporphyrin Mitochondria adenosine diphosphate albumin coproporphyrin coproporphyrinogen oxidase digitonin heptacarboxyporphyrin hexachlorobenzene isocoproporphyrin oxygen pentacarboxylic porphyrinogen III porphyrin derivative porphyrinogen trypsin unclassified drug uroporphyrin uroporphyrinogen decarboxylase coproporphyrinogen oxidase digitonin porphyrin trypsin animal experiment animal tissue article cellular distribution controlled study decarboxylation disease model elasticity enzyme activity enzyme inhibition feces female liver mitochondrion long term exposure membrane damage membrane fluidity membrane permeability nonhuman oscillation outer membrane oxidative phosphorylation permeability barrier porphyria cutanea tarda rat respiration control urine animal drug effect metabolism physiology Wistar rat Rattus Animals Coproporphyrinogen Oxidase Digitonin Feces Female Hexachlorobenzene Mitochondria, Liver Porphyrins Rats Rats, Wistar Trypsin These studies try to elucidate why isocoproporphyrin appears in hexachlorobenzene-poisoned rats' feces. Chronic exposure of hexachlorobenzene to rats produces an experimental model for human porphyria cutanea tarda. After 8 weeks of treatment, rats showed high porphyrin excreta and 50% inhibition of liver uroporphyrinogen decarboxylase activity. Uroporphyrin plus heptacarboxylic porphyrin exceeded coproporphyrin in urine, whereas in feces, isocoproporphyrin, from abnormal pentacarboxylic porphyrinogen III oxidative decarboxylation by liver coproporphyrinogen oxidase, became the main porphyrin. Trypsin-treated mitochondria showed that the outer and inner membrane permeability barrier was highly conserved after hexachlorobenzene intoxication. In digitonin-treated hexachlorobenzene mitochondria, coproporphyrinogen oxidase was free in the mitochondrial intermembrane space, whereas in normal mitochondria, 30% to 50% remained anchored to the inner membrane. Hexachlorobenzene led to a decrease in respiratory control and ADP/O ratios (uncoupled mitochondria). Albumin restored oxidative phosphorylation, indicating no irreversible inner membrane damage. Normal and hexachlorobenzene mitochondria oscillatory studies exhibited similar damping factor values, showing that hexachlorobenzene had no significant effect on membrane fluidity and elasticity. Mitochondrial uncoupling could explain the free state of the enzyme within the intermembrane space. The free state of the enzyme makes it more flexible and would allow pentacarboxylic porphyrinogen III, whose levels are increased, to compete with coproporphyrinogen III and being transformed into dehydroisocoproporphyrinogen, the liver forerunner of fecal isocoproporphyrin. © American College of Toxicology. Fil:Ferramola De Sancovich, A.M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Sancovich, H.A. 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_10915818_v27_n6_p455_Sopena |
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Universidad de Buenos Aires |
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I-28 |
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R-134 |
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Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Coproporphyrinogen Oxidase Experimental Porphyria Hexachlorobenzene Isocoproporphyrin Mitochondria adenosine diphosphate albumin coproporphyrin coproporphyrinogen oxidase digitonin heptacarboxyporphyrin hexachlorobenzene isocoproporphyrin oxygen pentacarboxylic porphyrinogen III porphyrin derivative porphyrinogen trypsin unclassified drug uroporphyrin uroporphyrinogen decarboxylase coproporphyrinogen oxidase digitonin porphyrin trypsin animal experiment animal tissue article cellular distribution controlled study decarboxylation disease model elasticity enzyme activity enzyme inhibition feces female liver mitochondrion long term exposure membrane damage membrane fluidity membrane permeability nonhuman oscillation outer membrane oxidative phosphorylation permeability barrier porphyria cutanea tarda rat respiration control urine animal drug effect metabolism physiology Wistar rat Rattus Animals Coproporphyrinogen Oxidase Digitonin Feces Female Hexachlorobenzene Mitochondria, Liver Porphyrins Rats Rats, Wistar Trypsin |
| spellingShingle |
Coproporphyrinogen Oxidase Experimental Porphyria Hexachlorobenzene Isocoproporphyrin Mitochondria adenosine diphosphate albumin coproporphyrin coproporphyrinogen oxidase digitonin heptacarboxyporphyrin hexachlorobenzene isocoproporphyrin oxygen pentacarboxylic porphyrinogen III porphyrin derivative porphyrinogen trypsin unclassified drug uroporphyrin uroporphyrinogen decarboxylase coproporphyrinogen oxidase digitonin porphyrin trypsin animal experiment animal tissue article cellular distribution controlled study decarboxylation disease model elasticity enzyme activity enzyme inhibition feces female liver mitochondrion long term exposure membrane damage membrane fluidity membrane permeability nonhuman oscillation outer membrane oxidative phosphorylation permeability barrier porphyria cutanea tarda rat respiration control urine animal drug effect metabolism physiology Wistar rat Rattus Animals Coproporphyrinogen Oxidase Digitonin Feces Female Hexachlorobenzene Mitochondria, Liver Porphyrins Rats Rats, Wistar Trypsin Sopena, Y.E. Ferramola De Sancovich, A.M. Sancovich, H.A. Hexachlorobenzene treatment on hepatic mitochondrial function parameters and intracellular coproporphyrinogen oxidase location |
| topic_facet |
Coproporphyrinogen Oxidase Experimental Porphyria Hexachlorobenzene Isocoproporphyrin Mitochondria adenosine diphosphate albumin coproporphyrin coproporphyrinogen oxidase digitonin heptacarboxyporphyrin hexachlorobenzene isocoproporphyrin oxygen pentacarboxylic porphyrinogen III porphyrin derivative porphyrinogen trypsin unclassified drug uroporphyrin uroporphyrinogen decarboxylase coproporphyrinogen oxidase digitonin porphyrin trypsin animal experiment animal tissue article cellular distribution controlled study decarboxylation disease model elasticity enzyme activity enzyme inhibition feces female liver mitochondrion long term exposure membrane damage membrane fluidity membrane permeability nonhuman oscillation outer membrane oxidative phosphorylation permeability barrier porphyria cutanea tarda rat respiration control urine animal drug effect metabolism physiology Wistar rat Rattus Animals Coproporphyrinogen Oxidase Digitonin Feces Female Hexachlorobenzene Mitochondria, Liver Porphyrins Rats Rats, Wistar Trypsin |
| description |
These studies try to elucidate why isocoproporphyrin appears in hexachlorobenzene-poisoned rats' feces. Chronic exposure of hexachlorobenzene to rats produces an experimental model for human porphyria cutanea tarda. After 8 weeks of treatment, rats showed high porphyrin excreta and 50% inhibition of liver uroporphyrinogen decarboxylase activity. Uroporphyrin plus heptacarboxylic porphyrin exceeded coproporphyrin in urine, whereas in feces, isocoproporphyrin, from abnormal pentacarboxylic porphyrinogen III oxidative decarboxylation by liver coproporphyrinogen oxidase, became the main porphyrin. Trypsin-treated mitochondria showed that the outer and inner membrane permeability barrier was highly conserved after hexachlorobenzene intoxication. In digitonin-treated hexachlorobenzene mitochondria, coproporphyrinogen oxidase was free in the mitochondrial intermembrane space, whereas in normal mitochondria, 30% to 50% remained anchored to the inner membrane. Hexachlorobenzene led to a decrease in respiratory control and ADP/O ratios (uncoupled mitochondria). Albumin restored oxidative phosphorylation, indicating no irreversible inner membrane damage. Normal and hexachlorobenzene mitochondria oscillatory studies exhibited similar damping factor values, showing that hexachlorobenzene had no significant effect on membrane fluidity and elasticity. Mitochondrial uncoupling could explain the free state of the enzyme within the intermembrane space. The free state of the enzyme makes it more flexible and would allow pentacarboxylic porphyrinogen III, whose levels are increased, to compete with coproporphyrinogen III and being transformed into dehydroisocoproporphyrinogen, the liver forerunner of fecal isocoproporphyrin. © American College of Toxicology. |
| format |
JOUR |
| author |
Sopena, Y.E. Ferramola De Sancovich, A.M. Sancovich, H.A. |
| author_facet |
Sopena, Y.E. Ferramola De Sancovich, A.M. Sancovich, H.A. |
| author_sort |
Sopena, Y.E. |
| title |
Hexachlorobenzene treatment on hepatic mitochondrial function parameters and intracellular coproporphyrinogen oxidase location |
| title_short |
Hexachlorobenzene treatment on hepatic mitochondrial function parameters and intracellular coproporphyrinogen oxidase location |
| title_full |
Hexachlorobenzene treatment on hepatic mitochondrial function parameters and intracellular coproporphyrinogen oxidase location |
| title_fullStr |
Hexachlorobenzene treatment on hepatic mitochondrial function parameters and intracellular coproporphyrinogen oxidase location |
| title_full_unstemmed |
Hexachlorobenzene treatment on hepatic mitochondrial function parameters and intracellular coproporphyrinogen oxidase location |
| title_sort |
hexachlorobenzene treatment on hepatic mitochondrial function parameters and intracellular coproporphyrinogen oxidase location |
| url |
http://hdl.handle.net/20.500.12110/paper_10915818_v27_n6_p455_Sopena |
| work_keys_str_mv |
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