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. 2008 Dec 5;283(49):33927–33934. doi: 10.1074/jbc.M806654200

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FIGURE 5. — Relative subcellular distribution and activity of hypoxic reduction to NO within liver tissue. A, subcellular fractionation of hepatic tissue reveals that -dependent NO formation is nonuniformly distributed among cell compartments. B, specific activity of reduction to NO within subcellular fractions reveals that both cytosolic (S3) and mitochondrial (P2) compartments exhibit the highest specific reductase activities. C, pyridine nucleotide (NAD(P)H, 100 μm) enhances hypoxia-induced reduction to NO (70–110% increase from control) within the mitochondrial fraction (n = 2). D, upon supplying to microsomal fractions (containing cyt P₄₅₀), rapid formation of an iron-nitrite complex precedes formation of an ironnitrosyl (λ_max = 448 nm) prior to release of NO. Inset, microsomal NO generation from is concentration-dependent. Increasing (0.1–1.0 mm) in hepatic microsomes potentiates NO formation (n = 3).

Inline graphic — Relative subcellular distribution and activity of hypoxic reduction to NO within liver tissue. A, subcellular fractionation of hepatic tissue reveals that -dependent NO formation is nonuniformly distributed among cell compartments. B, specific activity of reduction to NO within subcellular fractions reveals that both cytosolic (S3) and mitochondrial (P2) compartments exhibit the highest specific reductase activities. C, pyridine nucleotide (NAD(P)H, 100 μm) enhances hypoxia-induced reduction to NO (70–110% increase from control) within the mitochondrial fraction (n = 2). D, upon supplying to microsomal fractions (containing cyt P₄₅₀), rapid formation of an iron-nitrite complex precedes formation of an ironnitrosyl (λ_max = 448 nm) prior to release of NO. Inset, microsomal NO generation from is concentration-dependent. Increasing (0.1–1.0 mm) in hepatic microsomes potentiates NO formation (n = 3).