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(Hypertension. 2009;53:885.)
© 2009 American Heart Association, Inc.

Brief Review

Mitochondria and Reactive Oxygen Species

From the Departments of Medicine and Pharmacology (F.A., M.S.G.), Renal Research Institute, New York Medical College, Valhalla; and the Department of Pharmacology and Human Physiology (F.A., M.M.), University of Bari Medical School, Bari, Italy.

Correspondence to Michael S. Goligorsky, Renal Research Unit, Department of Medicine and Pharmacology, New York Medical College, 95 Grasslands Rd, Valhalla, NY 10595. E-mail Michael_goligorsky@nymc.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Fascination by the mitochondria, "the colonial posterity of migrant prokaryocytes, probably primitive bacteria that swam into ancestral precursors of our eukaryotic cells and stayed there,"¹ stems from the above-mentioned nebulous endosymbiotic theory of their origin, as well as from the growing realization of a very special role that they play in the pathogenesis of diverse diseases.

These organelles generate energy primarily in the form of the electrochemical proton gradient (µH+), which fuels ATP production, ion transport, and metabolism.² Generation of this universal energy currency, µH+, occurs through the series of oxidative reactions conducted by the respiratory chain complexes at the ion-impermeable, almost cholesterol-free inner membrane. Reduced nicotinamide adenine dinucleotide represents the entry point to the complex I (reduced nicotinamide adenine dinucleotide:ubiquinone reductase), whereas the reduced ubiquinol enters the respiratory chain in the complex III (ubiquinol:cytochrome c [cyt-c] reductase) to reduce cyt-c, the electron carrier to the complex IV, cyt-c oxidase. Each of these steps generates µH+ by electrogenic pumping of protons from the mitochondrial matrix to the intermembrane space and is coupled to electron flow, thus generating the electric membrane potential of –180 to –220 mV and a pH gradient of 0.4 to 0.6 U across the inner mitochondrial membrane resulting in the negatively charged matrix side of the membrane and alkaline matrix. Ultimately, accumulated µH+ is converted into the influx of protons into the matrix driving ATP synthesis or protein transport. In addition, these end points are necessary for the execution of 2 major enzymatic metabolic pathways within . . . [Full Text of this Article]

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