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- W2140656979 endingPage "F477" @default.
- W2140656979 startingPage "F465" @default.
- W2140656979 abstract "Kidney proximal tubules exhibit decreased ATP and reduced, but not absent, mitochondrial membrane potential (Δψ m ) during reoxygenation after severe hypoxia. This energetic deficit, which plays a pivotal role in overall cellular recovery, cannot be explained by loss of mitochondrial membrane integrity, decreased electron transport, or compromised F 1 F 0 -ATPase and adenine nucleotide translocase activities. Addition of oleate to permeabilized tubules produced concentration-dependent decreases of Δψ m measured by safranin O uptake (threshold for oleate = 0.25 μM, 1.6 nmol/mg protein; maximal effect = 4 μM, 26 nmol/mg) that were reversed by delipidated BSA (dBSA). Cell nonesterified fatty acid (NEFA) levels increased from <1 to 17.4 nmol/mg protein during 60- min hypoxia and remained elevated at 7.6 nmol/mg after 60 min reoxygenation, at which time ATP had recovered to only 10% of control values. Safranin O uptake in reoxygenated tubules, which was decreased 85% after 60-min hypoxia, was normalized by dBSA, which improved ATP synthesis as well. dBSA also almost completely normalized Δψ m when the duration of hypoxia was increased to 120 min. In intact tubules, the protective substrate combination of α-ketoglutarate + malate (α-KG/MAL) increased ATP three- to fourfold, limited NEFA accumulation during hypoxia by 50%, and lowered NEFA during reoxygenation. Notably, dBSA also improved ATP recovery when added to intact tubules during reoxygenation and was additive to the effect of α-KG/MAL. We conclude that NEFA overload is the primary cause of energetic failure of reoxygenated proximal tubules and lowering NEFA substantially contributes to the benefit from supplementation with α-KG/MAL." @default.
- W2140656979 created "2016-06-24" @default.
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- W2140656979 date "2006-02-01" @default.
- W2140656979 modified "2023-09-30" @default.
- W2140656979 title "Accumulation of nonesterified fatty acids causes the sustained energetic deficit in kidney proximal tubules after hypoxia-reoxygenation" @default.
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