Ultrastructural observations in copper-deficient guinea-pig lung cells.

Dietary copper deficiency is known to affect metabolism of neutral lipids, phospholipids, prostaglandins, Cu-Zn superoxide dismutase and crosslinks of connective tissues. To investigate the effects of copper deficiency on lung ultrastructure, dietary copper deficiency was induced by feeding female guinea-pigs a diet marginally deficient in copper (0.8 microgram Cu/g diet) and compared with those fed a diet sufficient in copper (5.8 micrograms Cu/g diet). After 10 months on the diets, at age 340 days, animals were killed and the lungs removed and processed for electron microscopy to study the changes in cellular morphology. Type II epithelial cells in lung alveoli of copper deficient guinea-pigs, revealed larger lamellar bodies, in comparison with lungs of copper supplemented guinea-pigs (2.1 +/- 0.67 vs 1.35 +/- 0.47 microns). Fusion of lamellar bodies had occurred. Lipid droplets were found in the cytoplasm, which, in 20% of these cells, was as a single large lipid droplet approximately 10 microns in diameter. Features of the bronchiolar Clara cells in response to copper deficiency included the formation of packed tubular structures, 50 nm diameter. These tubules resembled smooth endoplasmic reticulums, and occupied 35.6% of the cell profiles by stereologic analysis. Clara cells from copper deficient guinea-pigs also contained many uniform, hexagonal crystal structures, in greater concentration than reported previously. Residual macrophages and monocytes observed in the capillaries contained giant lipid inclusions, which were stained by Sudan Black, indicative of neutral lipids. In this study, we suggest that perturbations in protein, lipid and membrane metabolism resulting from dietary copper deficiency in the guinea-pig may have altered the synthesis or degradation of lipid and protein components of lung cells or prevented their normal secretion into the airways or extracellular spaces.