Hayes J A, Snider G L, Palmer K C
Am Rev Respir Dis. 1976 Feb;113(2):121-30. doi: 10.1164/arrd.1976.113.2.121.
Rats were exposed once to a polydisperse aerosol of 0.005 M cadmium chloride for 2 hours. Controls were saline-exposed rats and unexposed rats. Total extractable lipid, malate, lactate, isocitrate, and glucose-6-phosphate dehydrogenases were measured on the organelle-free cytosol from homogenized lungs at periods up to 10 days after exposure. The wet weight, dry weight, ribonucleic acid, and deoxyribonucleic acid content of the lungs were also determined. Ultrastructural appearances were studied at the same time intervals in a separate experiment. Total lipid content, lactate dehydrogenase, and glucose-6-phosphate dehydrogenase activities showed approximate doubling by the fourth day after exposure, this change coinciding with doubling of wet lung weight and total lung deoxyribonucleic acid content. Malate dehydrogenase activity showed a high peak 1 hour after exposure before decreasing to follow the pattern of lactate and glucose-6-phosphate dehydrogenase. The changes found may be a nonspecific reaction to lung injury, comparable with oxygen, ozone, and nitrogen dioxide. These results in Type II cell proliferation, which would enhance glucose-6-phosphate dehydrogenase content and resistance to peroxidation. Lipid accumulation could be a similar response. However, the initial elevation in malate dehydrogenase activity is more in keeping with a specific mitochondrial injury (with some ultrastructural support), perhaps with leakage of mitochondrial enzymes. This suggests that there may be more than one mechanism at work in the injury. It is significant that despite the marked structural and functional changes, none of the rats died after the exposure, which makes the injury a model worthy of further investigation.
