In order to identify sensitive and specific biochemical indicators of pulmonary damages caused by industrial contaminants, male Long-Evans rats were exposed to a cadmium chloride (CdCl2) aerosol (5 mg Cd/m3; MMAD = 1.4 microns; SDg = 1.8) for 1 hr. The rats were sacrificed at 1, 4, 8, and 16 days after treatment. The response of the pulmonary surfactant (SF) system, which prevents alveolar collapse during expiration by lowering the surface tension at the air-liquid interface, was of particular interest. The effect of CdCl2 inhalation on the SF system was monitored by assaying the alkaline phosphatase (AKP) activity and phospholipid (PL) content in an enriched surface active SF fraction purified from bronchoalveolar lavages. The AKP activity of the SF fraction was markedly decreased (99%) on Day 1, indicating an inhibition of AKP by Cd. The PL content remained at control level while the total protein content was significantly increased (199%). On day 4, the high recovery of PL (207%) and AKP activities (639%) may reflect an increased secretion caused by Type II cell hyperplasia. By Day 8 these parameters returned to baseline levels. On Day 16 both the AKP activity and the PL content of the SF fraction were decreased significantly. Concurrently, the activities of the acid phosphatase and the B-N-acetylglucosaminidase followed, but to a lesser extent, the response of the AKP activity on Days 1 and 4. They differed from AKP, however, in that their activities remained significantly elevated on Day 8 and in that they returned to baseline levels on Day 16.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗

PubMed1988

Toxicity of inhaled cadmium chloride: early responses of the antioxidant and surfactant systems in rat lungs.

In order to establish an animal model for assessing early and sensitive biochemical indicators of pulmonary damage, we studied the effects of inhaled CdCl2 (5 mg/m3.h; mass median aerodynamic diameter (MMAD) = 1.4 microns; SDg = 1.8) on the antioxidant defense and pulmonary surfactant systems of rat lungs. Rats were sacrificed 1, 4, 8, and 16 d after inhalation. Pulmonary edema (wet/dry weight) was observed on d 1. The total activities of the enzymes superoxide dismutase (SOD) and glucose-6-phosphate dehydrogenase (G6PD) in the lung homogenates of the treated animals were significantly throughout the 16-d period. Glutathione reductase (GR) was increased on d 4 and after. The general increases of SOD, GR, and the lysosomal enzymes acid phosphatase and beta-N-acetylglucosaminidase could be attributed to changes in the cellularity of the lung tissue. The significant increase in the specific activity of G6PD on d 4 suggested enzyme stimulation. Concurrently, the response of the surfactant system was measured by assaying the alkaline phosphatase (AKP) and the phospholipid content in the homogenates and in the cell-free bronchoalveolar lavage (BAL) fluids. The AKP activity in the homogenates decreased by 30%, while no activity was detected in the BAL on d 1, suggesting an inhibition of AKP by Cd. The secretion of surfactant seemed altered at this early time: phospholipid in the BAL decreased by 44%, although it increased by 61% in the tissue. The high recovery of phospholipid (312%) in the BAL on d 4 and the important changes in the AKP activity in the BAL from d 4 to 16 may reflect alterations in the processing of the surfactant. The effect of Cd on AKP makes this enzyme a potential marker of the metal redistribution in the pulmonary alveolar region, which could be a useful tool in long-term studies.

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