title: Toxicity of inhaled cadmium chloride: early responses of the antioxidant and surfactant systems in rat lungs.
abstract: 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.
authors.affiliation: Département des Sciences Biologiques, Université du Québec à Montréal, Canada.
authors.forename: J
authors.initials: J
authors.lastname: Boudreau
authors.forename: R
authors.initials: R
authors.lastname: Vincent
authors.forename: D
authors.initials: D
authors.lastname: Nadeau
authors.forename: B
authors.initials: B
authors.lastname: Trottier
authors.forename: M
authors.initials: M
authors.lastname: Fournier
authors.forename: K
authors.initials: K
authors.lastname: Krzystyniak
authors.forename: G
authors.initials: G
authors.lastname: Chevalier
mesh_terms: D000118:Acetylglucosaminidase / Q000032:analysis; D000135:Acid Phosphatase / Q000032:analysis; D000280:Administration, Inhalation; D000469:Alkaline Phosphatase / Q000032:analysis; D000818:Animals; D000975:Antioxidants / Q000032:analysis; D001992:Bronchoalveolar Lavage Fluid / Q000032:analysis; D002104:Cadmium / Q000633:toxicity*; D019256:Cadmium Chloride; D005954:Glucosephosphate Dehydrogenase / Q000032:analysis; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D010743:Phospholipids / Q000032:analysis; D011506:Proteins / Q000032:analysis; D011663:Pulmonary Surfactants / Q000032:analysis*; D051381:Rats
chemical_list: D000975:Antioxidants; D010743:Phospholipids; D011506:Proteins; D011663:Pulmonary Surfactants; D002104:Cadmium; D005954:Glucosephosphate Dehydrogenase; D000469:Alkaline Phosphatase; D000135:Acid Phosphatase; D000118:Acetylglucosaminidase; D019256:Cadmium Chloride