Lipid Peroxidation in Rat Lungs Following an Acute Inhalation Exposure to Cadmium Chloride

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Abstract
Lipid peroxidation in the lungs was evaluated at 1, 4, 8, and 16 days following an acute inhalation exposure of rats to aerosolized cadmium chloride (5 mg Cd/m3; 1 hour; MMAD = 1.4 μm; σg= 1.8). The activities of antioxidant enzymes were significantly increased in the lung homogenates and were taken to reflect the cellular changes in the tissue following acute injury. Maximal values were measured on day 4 (total activity; mean % of controls ±SD; p < 0.05): Superoxide dismutase, 192±42%; catalase, 236±52%; glutathione peroxidase, 181±34%; glutathione reductase, 197±45%; and glucose-6-phosphate dehydrogenase, 248±73%. The activity of gamma-glutamyl transpeptidase was depressed on day 1 (71±9%; p<0.05), but rose above control values on the following days (day 4, 180±37%; p < 0.05). The early decrease of this activity in the lungs may possibly be related to membrane damage. Values of thiobarbituric acid (TBA) reactive material were elevated on day 1 (272±95%; p<0.05), indicating lipid peroxidation. However, the subsequent cellular and metabolic changes in the lungs were accompanied by normal (day 4, 91±33%) or decreased levels of TBA-reactants (day 8, 58±7%; p < 0.05). Two weeks after treatment, the TBA-reactants returned to control levels. The TBA-reactants did not parallel the proliferative and infiltrative cellular changes. The results indicate an early alteration of the oxidant-antioxidant balance in the lungs by cadmium.