Activities of respiratory chain complexes and pyruvate dehydrogenase in isolated muscle mitochondria in premature neonates

Honzík, Tomáš; Wenchich, László; Böhm, M.; Hansı́ková, Hana; Pejznochova, Martina; Zapadlo, M; Plavka, R; Zeman, Jiřı́

doi:10.1016/j.earlhumdev.2006.07.008

Cited by 31 publications

(23 citation statements)

References 37 publications

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“…In murine heart, kidney, and muscle, the activity of C-I was reported to be the highest in young animals with a gradual reduction with the age (31)(32)(33). In humans, C-I activity in muscle mitochondria was greater in premature neonates compared with older infants and children (34). Of note, in our model a dramatic surge in C-I activity coincided with active alveolar redevelopment during recovery from hyperoxic stress.…”

Section: Discussionsupporting

confidence: 46%

Mitochondrial Dysfunction Contributes to Alveolar Developmental Arrest in Hyperoxia-Exposed Mice

Ratner¹,

Starkov²,

Matsiukevich³

et al. 2009

Am J Respir Cell Mol Biol

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This study investigated whether mitochondrial dysfunction contributes to alveolar developmental arrest in a mouse model of bronchopulmonary dysplasia (BPD). To induce BPD, 3-day-old mice were exposed to 75% O 2 . Mice were studied at two time points of hyperoxia (72 h or 2 wk) and after 3 weeks of recovery in room air (RA). A separate cohort of mice was exposed to pyridaben, a complex-I (C-I) inhibitor, for 72 hours or 2 weeks. Alveolarization was quantified by radial alveolar count and mean linear intercept methods. Pulmonary mitochondrial function was defined by respiration rates, ATP-production rate, and C-I activity. At 72 hours, hyperoxic mice demonstrated significant inhibition of C-I activity, reduced respiration and ATP production rates, and significantly decreased radial alveolar count compared with controls. Exposure to pyridaben for 72 hours, as expected, caused significant inhibition of C-I and ADP-phosphorylating respiration. Similar to hyperoxic littermates, these pyridaben-exposed mice exhibited significantly delayed alveolarization compared with controls. At 2 weeks of exposure to hyperoxia or pyridaben, mitochondrial respiration was inhibited and associated with alveolar developmental arrest. However, after 3 weeks of recovery from hyperoxia or 2 weeks after 72 hours of exposure to pyridaben alveolarization significantly improved. In addition, there was marked normalization of C-I and mitochondrial respiration. The degree of hyperoxia-induced pulmonary simplification and recovery strongly (r 2 5 0.76) correlated with C-I activity in lung mitochondria. Thus, the arrest of alveolar development induced by either hyperoxia or direct inhibition of mitochondrial oxidative phosphorylation indicates that bioenergetic failure to maintain normal alveolar development is one of the fundamental mechanisms responsible for BPD.

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Section: Discussionsupporting

confidence: 46%

Mitochondrial Dysfunction Contributes to Alveolar Developmental Arrest in Hyperoxia-Exposed Mice

Ratner¹,

Starkov²,

Matsiukevich³

et al. 2009

Am J Respir Cell Mol Biol

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“…These results are consistent with studies showing a functional respiratory chain (post-mortem) in muscle of premature neonates (59,89), heart, liver, brain, and kidney of human fetuses (90,91). Little is known regarding the kinetics of mitochondrial complex assembly during human embryonic and fetal life.…”

Section: Energy Deficiency Typesupporting

confidence: 89%

“…Little is known regarding the kinetics of mitochondrial complex assembly during human embryonic and fetal life. Investigating postmortem isolated muscle mitochondria in premature neonates, activities of RC-complexes III, IV, and the marker enzyme citratesynthase were found to be markedly lower in comparison with older children (59,89).…”

Section: Energy Deficiency Typementioning

confidence: 97%

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Impact of selected inborn errors of metabolism on prenatal and neonatal development

Illsinger

2010

IUBMB Life

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SummaryIn general, data regarding maturational processes of different metabolic pathways in the very vulnerable fetal and neonatal period are rare. This review is to substantiate the impact of selected inborn errors of metabolism on this critical period of life and their clinical manifestation. Significant adaptation of mitochondrial/energy-, carbohydrate-, lysosomal-, and amino acid-metabolism occurs during early prenatal and neonatal development. In utero, metabolic environment has an impact on the development of the fetus as well as fetal organ maturation.

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“…39,40 Indicaciones de la ventilación mecánica La decisión de iniciar la VM debe basarse en un adecuado juicio clínico, el cual debe considerar la evaluación de síntomas, signos y exámenes de laboratorio. La indicación depende de los objetivos clínicos que se desee cumplir.…”

Section: ¿Por Qué Los Niños Son Diferentes?unclassified

Ventilación mecánica invasiva. Puesta al día para el médico pediatra

et al. 2013

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Arch Argent Pediatr 2013;111(5): 428-436 / 428 Ventilación mecánica invasiva. Puesta al día para el médico pediatra Invasive mechanical ventilation. Update for the pediatrician RESUMENEn esta revisión se recogen los conceptos fundamentales del uso de la ventilación mecánica (VM) invasiva, principalmente en la insuficiencia respiratoria aguda. La VM es una práctica común en la unidad de cuidados intensivos (UCI) y debe ser entendida como una terapia de sostén destinada a sustituir el trabajo respiratorio mientras se restablece el balance entre la demanda ventilatoria y la capacidad del paciente para sostenerla. Se debe reconocer que el objetivo de la VM no es la normalización de los gases sanguíneos, sino obtener un intercambio gaseoso razonable, sin sobrepasar los umbrales de seguridad, lo que permite limitar el daño inducido por su uso. Palabras clave: ventilación mecánica, ventilación con presión positiva, ventilación protectora pulmonar, falla respiratoria aguda. SUMMARYIn this review, we collect the fundamental concepts of the use of invasive mechanical ventilation (MV) in children, particularly in acute respiratory failure. MV is a common practice in the ICU and must be understood as a therapeutic intervention to replace the work of breathing while restores the balance between ventilatory demand and the patient's ability to sustain it. It is essential for the clinician to recognize that the goal of mechanical ventilatory support is not to normalize the patient's blood gases but providing a reasonable gas exchange; the benefits are obtained if the safety thresholds are not exceeded. Thus, this strategy has become the only tool available to limit the development of ventilator-induced lung injury (VILI). INTRODUCCIÓNEl soporte ventilatorio artificial es una de las prácticas más comunes en las unidades de cuidados intensivos (UCI) pediátricas. Hasta un 50% de los pacientes que ingresan en esas unidades la reciben; la falla respiratoria aguda es la indicación más

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Activities of respiratory chain complexes and pyruvate dehydrogenase in isolated muscle mitochondria in premature neonates

Cited by 31 publications

References 37 publications

Mitochondrial Dysfunction Contributes to Alveolar Developmental Arrest in Hyperoxia-Exposed Mice

Mitochondrial Dysfunction Contributes to Alveolar Developmental Arrest in Hyperoxia-Exposed Mice

Impact of selected inborn errors of metabolism on prenatal and neonatal development

Ventilación mecánica invasiva. Puesta al día para el médico pediatra

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