Adaptability to hypobaric hypoxia is facilitated through mitochondrial bioenergetics: an in vivo study.

ABSTRACT:

Background and purpose

High-altitude pulmonary oedema (HAPE) experienced under high-altitude conditions is attributed to mitochondrial redox distress. Hence, hypobaric hypoxia (HH)-induced alteration in expression of mitochondrial biogenesis and dynamics genes was determined in rat lung. Further, such alteration was correlated with expression of mitochondrial DNA (mtDNA)-encoded oxidative phosphorylation (mtOXPHOS) genes. The prophylactic effect of dexamethasone (DEX) in counteracting the HH-induced mitochondrial distress was used as control to understand adaptation to high-altitude exposure.

Experimental approach

Rats pretreated with DEX were exposed to normobaric normoxia (NN) or HH. HH-induced injury was assessed as an increase in lung water content, tissue damage and oxi

SUBMITTER: Chitra L 

PROVIDER: S-EPMC3696327 | biostudies-literature | 2013 Jul

REPOSITORIES: biostudies-literature