Differential temporal response of hippocampus, cortex and cerebellum to hypobaric hypoxia: a biochemical approach.
Hypobaric hypoxia is known to cause cognitive dysfunctions and memory impairment. The present study aimed at exploring the occurrence of oxidative stress in hypobaric hypoxia and the differential temporal response of the hippocampus, cerebellum following hypobaric hypoxia. Animals were divided into control, 3 days, 7 days and 14 days exposure groups and were exposed to an altitude of 25,000 ft. Our study revealed an increase in lactate dehydrogenase activity along with increase in free radical generation and lipid peroxidation. We also noted depletion in the antioxidants and decrease in glutathione reductase and superoxide dismutase activity. There was significant decrease in reduced glutathione levels in the exposure groups when compared to the control which was accompanied by a concomitant increase in oxidized glutathione levels. Increase in glutamate dehydrogenase activity was observed coinciding with the decrease in glutathione levels which was accompanied with an increase in expression of vesicular glutamate transporter. The hippocampus was found to be more vulnerable to hypobaric hypoxia-induced oxidative stress in comparison to the cortex and cerebellum. An interesting observation was the onset of acclimatization on prolonged exposure to hypobaric hypoxia for a period of 14 days. Hypobaric hypoxia was found to affect various regions of the brain differentially and the response of each region varied as a function of time.
Hota
Sunil K
SK
Defence Institute of Physiology and Allied Sciences, Lucknow Road, Timarpur, Delhi 110054, India.
Barhwal
Kalpana
K
Singh
Shashi B
SB
Ilavazhagan
G
G
D000532:Altitude Sickness / Q000378:metabolism* / Q000503:physiopathology; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001274:Atmospheric Pressure; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D001923:Brain Chemistry / Q000502:physiology*; D002531:Cerebellum / Q000378:metabolism / Q000503:physiopathology; D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology; D005609:Free Radicals / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology; D002534:Hypoxia, Brain / Q000378:metabolism* / Q000503:physiopathology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors; D050598:Vesicular Glutamate Transport Protein 1 / Q000378:metabolism
D000975:Antioxidants; D005609:Free Radicals; D050598:Vesicular Glutamate Transport Protein 1; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione