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• W3149773905 abstract "Hypoxia leads to Ca 2? overload and results in mitochondrial uncoupling, decreased ATP synthesis, and neuronal death. Inhibition of mitochondrial Ca 2? overload protects mitochondrial function after hypoxia. The present study was aimed to investigate the effect of intermittent hypoxia on mitochondrial function and mitochondrial tol- erance to Ca 2? overload. Wistar rats were divided into control and intermittent hypoxia (IH) groups. The IH group was subject to hypoxia for 4 h daily in a hypobaric cabin (5,000 m) for 7 days. Brain mitochondria were isolated on day 7 following hypoxia. The baseline mitochondrial functions, such as ST3, ST4, and respiratory control ratio (RCR = ST3/ST4), were measured using a Clark-type oxygen electrode. Mitochondrial adenine nucleotide con- centrations were measured by HPLC. Mitochondrial membrane potential was determined by measuring rhoda- mine 123 (Rh-123) fluorescence in the absence and pre- sence of high Ca 2? concentration (0.1 M), which simulates Ca 2? overload. Our results revealed that IH did not affect mitochondrial respiratory functions, but led to a reduction in AMP and an increase in ADP concentrations in mito- chondria. Both control and IH groups demonstrated decreased mitochondrial membrane potential in the pre- sence of high Ca 2? (0.1 M), while the IH group showed a relative higher mitochondrial membrane potential. These results indicated that the neuroprotective effect of intermittent hypoxia was resulted partly from preserving mitochondrial membrane potential, and increasing mito- chondrial tolerance to high calcium levels. The increased ADP and decreased AMP in mitochondria following intermittent hypoxia may be a mechanism underlying this protection." @default.
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• W3149773905 date "2013-01-01" @default.
• W3149773905 modified "2023-09-26" @default.
• W3149773905 title "Intermittent hypoxia protects cerebral mitochondrial function from calcium overload" @default.
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