El-Bacha 2007 Biochim Biophys Acta

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El-Bacha T, Midlej V, Pereira da Silva AP, Silva da Costa L, Benchimol M, Galina A, Da Poian AT (2007) Mitochondrial and bioenergetic dysfunction in human hepatic cells infected with dengue 2 virus. Biochim Biophys Acta 1772:1158-66.

» PMID: 17964123 Open Access

El-Bacha T, Midlej V, Pereira da Silva AP, Silva da Costa L, Benchimol M, Galina A, Da Poian AT (2007) Biochim Biophys Acta

Abstract: Dengue virus infection affects millions of people all over the world. Although the clinical manifestations of dengue virus-induced diseases are known, the physiopathological mechanisms involved in deteriorating cellular function are not yet understood. In this study we evaluated for the first time the associations between dengue virus-induced cell death and mitochondrial function in HepG2, a human hepatoma cell line. Dengue virus infection promoted changes in mitochondrial bioenergetics, such as an increase in cellular respiration and a decrease in ΔΨm. These alterations culminated in a 20% decrease in ATP content and a 15% decrease in the energy charge of virus-infected cells. Additionally, virus infected cells showed several ultrastructural alterations, including mitochondria swelling and other morphological changes typical of the apoptotic process. The alterations in mitochondrial physiology and energy homeostasis preceded cell death. These results indicate that HepG2 cells infected with dengue virus are under metabolic stress and that mitochondrial dysfunction and alterations in cellular ATP balance may be related to the pathogenesis of dengue virus infection.

Keywords: Dengue virus infection; Mitochondrial dysfunction; Metabolism; Energy charge; Apoptosis; HepG2 cell

O2k-Network Lab: BR Rio de Janeiro Galina A, BR Rio de Janeiro Da Poian AT


Labels: MiParea: Respiration 

Stress:Cell death  Organism: Human  Tissue;cell: Liver  Preparation: Intact cells, Permeabilized cells 


Coupling state: LEAK, ROUTINE, OXPHOS, ET  Pathway: N, S, ROX