title: The effect of maternal low-protein diet on the heart of adult offspring: role of mitochondria and oxidative stress.
abstract: Protein restriction during perinatal and early postnatal development is associated with a greater incidence of disease in the adult, such arterial hypertension. The aim in the present study was to investigate the effect of maternal low-protein diet on mitochondrial oxidative phosphorylation capacity, mitochondrial reactive oxygen species (ROS) formation, antioxidant levels (enzymatic and nonenzymatic), and oxidative stress levels on the heart of the adult offspring. Pregnant Wistar rats received either 17% casein (normal protein, NP) or 8% casein (low protein, LP) throughout pregnancy and lactation. After weaning male progeny of these NP or LP fed rats, females were maintained on commercial chow (Labina-Purina). At 100 days post-birth, the male rats were sacrificed and heart tissue was harvested and stored at -80 °C. Our results show that restricting protein consumption in pregnant females induced decreased mitochondrial oxidative phosphorylation capacity (51% reduction in ADP-stimulated oxygen consumption and 49.5% reduction in respiratory control ratio) in their progeny when compared with NP group. In addition, maternal low-protein diet induced a significant decrease in enzymatic antioxidant capacity (37.8% decrease in superoxide dismutase activity; 42% decrease in catalase activity; 44.8% decrease in glutathione-S-transferase activity; 47.9% decrease in glutathione reductase; 25.7% decrease in glucose-6 phosphate dehydrogenase) and glutathione level (34.8% decrease) when compared with control. From these findings, we hypothesize that an increased production of ROS and decrease in antioxidant activity levels induced by protein restriction during development could potentiate the progression of metabolic and cardiac diseases in adulthood.
authors.affiliation: a Laboratory of Biochemistry and Exercise Biochemistry, Department of Physical Education and Sports Science, CAV-Federal University of Pernambuco, Brazil.
authors.forename: Luciana
authors.initials: L
authors.lastname: Nascimento
authors.forename: Cristiane M
authors.initials: CM
authors.lastname: Freitas
authors.forename: Reginaldo
authors.initials: R
authors.lastname: Silva-Filho
authors.forename: Ana Catarina R
authors.initials: AC
authors.lastname: Leite
authors.forename: Alessandra B
authors.initials: AB
authors.lastname: Silva
authors.forename: Aline Isabel
authors.initials: AI
authors.lastname: da Silva
authors.forename: Diorginis Soares
authors.initials: DS
authors.lastname: Ferreira
authors.forename: Anderson Apolonio
authors.initials: AA
authors.lastname: Pedroza
authors.forename: Maria Bernadete Souza
authors.initials: MB
authors.lastname: Maia
authors.forename: Mariana P
authors.initials: MP
authors.lastname: Fernandes
authors.forename: Claudia
authors.initials: C
authors.lastname: Lagranha
mesh_terms: D000367:Age Factors; D000818:Animals; D018753:Diet, Protein-Restricted; D005260:Female; D008297:Male; D008928:Mitochondria / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*; D018384:Oxidative Stress; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar
keywords: bioénergétique mitochondriale; developmental plasticity; diet; mitochondrial bioenergetics; oxidative stress; plasticité développementale; régime alimentaire; stress oxydatif