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Mohammad G. Mustafa, PhD; Carroll E. Cross, MD; Walter S. Tyler, DVM, PhD

Arch Intern Med. 1971;127(6):1050-1058.

Abstract
The pulmonary alveolar macrophages possess metabolic pathways operative predominantly in the aerobic environment. These cells consume 0.15 to 0.2µmolar O₂/mg protein/sec in vitro. Mitochondria from these cells manifest a respiratory rate of 0.5 to 0.6µmolar O₂/mg protein/sec for succinate as a substrate. Mitochondrial oxidation is coupled to phosphorylation; adenosine diphosphate (ADP):oxygen (0) ratios are approximately 2 for flavin-linked and 3 for pyridine nucleotide-linked substrates. Cadmium ion adversely affects respiration of alveolar macrophages. It completely inhibits macrophage mitochondrial oxygen uptake at 50µmolar concentrations and uncouples oxidative phosphorylation at 5µmolar concentrations. This and several other divalent cations, like Cu⁺⁺, Hg⁺⁺, Sn⁺⁺ and Zn⁺⁺, also inhibit adenosine triphosphatase (ATPase) activity of alveolar macrophages. Since metal fumes and oxides are common air pollutants, a study of this sort might provide information on mechanisms at the biochemical level as to how toxic inhalants initiate pulmonary pathology.

Author Affiliations
Davis, Calif

From the departments of biological chemistry, human physiology, internal medicine, and anatomy, University of California School of Medicine and Veterinary Medicine, Davis.

Footnotes
Received for publication Oct 20, 1971; accepted Feb 11, 1971.

Read in part before the Tenth Annual Hanford Biology Symposium on Pollution and Lung Biochemistry, Richland, Wash, June 1970, jointly sponsored by the Battelle Memorial Institute-Pacific Northwest Laboratories, National Air Pollution Control Administration, National Institute of Environmental Health Sciences, and the US Atomic Energy Commission.

Reprint requests to Department of Biological Chemistry, University of California School of Medicine, Davis, Calif 95616 (Dr. Mustafa).

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