Abstract
Hypoxia is one of the important factors in formation of reactive oxygen species (ROS). Ghrelin is a peptide hormone that reduces oxidative stress. However, antioxidant effect of ghrelin on blood and brain in normobaric hypoxia condition has not yet been investigated. thirty-two animals were randomly divided into four (n=8) experimental groups: Control (C), ghrelin (Gh), hypoxia (H), hypoxic animals that received ghrelin (H+Gh). Normobaric systemic hypoxia (11% O2) was induced in rats for 48 hours. Effect of ghrelin (80 μg/kg, i.p) on serum TAC and MDA and brain SOD, CAT, GPx and MDA were assessed. Hypoxia significantly (p<0.001) increased both blood and brain MDA Levels. Ghrelin treatment significantly (p<0.001) decreased blood MDA levels both in control and hypoxia, and brain MDA levels in hypoxia conditions. Brain SOD, CAT and GPx variations were not significant in two days of hypoxia. Ghrelin treatment also could not significantly increase activity of SOD, CAT and GPx in brain. Total antioxidant capacity of serum increased in ghrelin treatment both in control and hypoxic conditions, although it was only significant (p<0.01) in control conditions. Our findings showed that administration of ghrelin may be useful in reducing blood and brain oxidative stress in normobaric hypoxia condition.
Highlights
Hypoxia is a decrease in tissue oxygen concentration, normally caused by a reduction in the partial pressure of atmospheric oxygen.[1]
Our findings showed that administration of ghrelin may be useful in reducing blood and brain oxidative stress in normobaric hypoxia condition
Effect of ghrelin on blood malonyl dialaldehyde (MDA) level in normobaric hypoxia The effect of two days of ghrelin (80 μg/kg/day) treatment on blood MDA level in animals showed that administration of ghrelin significantly (p
Summary
Hypoxia is a decrease in tissue oxygen concentration, normally caused by a reduction in the partial pressure of atmospheric oxygen.[1] Hypoxia is an important pathogenic factor in different injuries of CNS such as cerebral ischemia, tumorigenesis, head injury, acute mountain sickness, and in pulmonary disease such as COPD.[2,3,4,5] Due to the exposition to hypoxia, reactive oxygen species are continuously generated.[6] The rate of ROS production from mitochondria is increased in a variety of pathologic conditions including ischemia, reperfusion, aging and chemical inhibition of mitochondrial respiration.[7] Reactive oxygen species (ROS) such as superoxide anion, hydrogen peroxide, and hydroxyl radical are generated continuously in cells grown aerobically.[8] These free radicals can interact with bimolecules such as DNA, carbohydrates, protein, and lipids and damage various cellular components.[9] An increase in free radicals causes overproduction of malonyl dialaldehyde (MDA) in oxidative stress conditions.[10]
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