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Protein undernutrition during development and oxidative impairment in the central nervous system (CNS): potential factors in the occurrence of metabolic syndrome and CNS disease

Published online by Cambridge University Press:  08 June 2016

D. J. S. Ferreira
Affiliation:
Neuropsychiatry and Behavior Science Graduate Program, Federal University of Pernambuco, Vitória de Santo Antão, Brazil
D. F. Sellitti
Affiliation:
Department of Medicine, Uniformed Service University of Health Science (USUHS), Bethesda, MD, USA
C. J. Lagranha*
Affiliation:
Neuropsychiatry and Behavior Science Graduate Program, Federal University of Pernambuco, Vitória de Santo Antão, Brazil Laboratory of Biochemistry and Exercise Biochemistry, Department of Physical Education and Sports Science, Federal University of Pernambuco, Vitória de Santo Antão, Brazil
*
*Address for correspondence: C. J. Lagranha, Rua Alto do Reservatório, s/n, Núcleo de Educação Física e Ciências do Esporte, Bela Vista, Vitória de Santo Antão 55608-680, PE, Brazil. (Email lagranha@hotmail.com)

Abstract

Mitochondria play a regulatory role in several essential cell processes including cell metabolism, calcium balance and cell viability. In recent years, it has been postulated that mitochondria participate in the pathogenesis of a number of chronic diseases, including central nervous system disorders. Thus, the concept of mitochondrial function now extends far beyond the common view of this organelle as the ‘powerhouse’ of the cell to a new appreciation of the mitochondrion as a transducer of early metabolic insult into chronic disease in later life. In this review, we have attempted to describe some of the associations between nutritional status and mitochondrial function (and dysfunction) during embryonic development with the occurrence of neural oxidative imbalance and neurogenic disease in adulthood.

Type
Review
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2016 

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