Exposure To Cadmium Chloride Research Articles

Oxidant radical release by alveolar macrophages after cadmium chloride exposure in vitro.

Chronic exposure to cadmium can cause lung emphysema, the mechanism of which is unknown. Current concepts on the pathogenesis of emphysema largely emphasize the role of a protease-antiprotease imbalance. The aim of this work was to study the effects of cadmium on the regulation of antiprotease activity and the release of oxidant radicals from alveolar macrophages. Guinea pig alveolar macrophages (AM) were exposed overnight to cadmium chloride (CdCl2) in vitro. To define the cytolytic threshold dose, cell lysis was evaluated by trypan blue exclusion and lactate dehydrogenase release. Non-cytolytic concentrations were then used (0.1, 0.4 and 0.8 ppm) to simulate chronic exposure conditions. Overnight exposure to 0.1, 0.4 and 0.8 ppm CdCl2 decreased intracellular ATP (mean +/- SD: 91 +/- 8%, 72 +/- 7%, 50 +/- 8% of control cells, respectively), suggesting that even at non-cytolytic doses, Cd2+ can cause cell injury. The assessment of oxygen radical release from AM after overnight exposure to CdCl2 showed a dose-dependent decrease to 54.3 +/- 8.2%, 32.2 +/- 4.3% and 25 +/- 3% of control after exposure to 0.1, 0.4 and 0.8 ppm Cd2+, respectively. At non-cytolytic concentrations (0.1, 0.4 and 0.8 ppm) CdCl2 did not decrease alpha 1-proteinase inhibitor activity either in the absence of AM or in the presence of AM and myeloperoxidase. In conclusion, our in vitro results do not suggest that a protease-antiprotease imbalance is involved in the pathogenesis of cadmium-induced emphysema.(ABSTRACT TRUNCATED AT 250 WORDS)

Responses of hemocytes and gill tissues to sublethal cadmium chloride poisoning in the crab Paratelphusa hydrodromous (Herbst).

The hemocytic and gill tissue responses of the crab Paratelphusa hydrodromous (Herbst) to a wide range of sublethal concentrations of cadmium chloride (0.02-0.50 microM/L) were examined after a 30-day exposure using hemocyte counts (THC and DHC) and lamellar pathology. A continued reduction in the hemocyte counts and selective changes in the numbers of hyalinocytes and eosinophilic granulocytes was evident in the toxified crabs. Under sublethal stress, the hyalinocytes developed eccentric nuclei, granular cytoplasm and membrane blebs. Atypical shape, lobate nucleus, dense cytoplasmic deposits and granuloplasmic vacuoles were frequently observed in the granulocytes. Greater proliferation of prohemocytes and abnormal hemocyte morphology indicated cadmium-induced neoplastic transformation of hemocytopoietic organs. No major structural changes in the gills were noted at 0.02 microM CdCl2. Nodular gill disease (NGD), hemocytic hyperplasia and sloughing of walled off hemocytes were prominent lesions after 0.50 microM cadmium chloride exposure.

Age-related dose response of selected reproductive parameters to acute cadmium chloride exposure in the male Long-Evans rat.

Groups of male Long-Evans rats 30, 50, or 70 d old were injected subcutaneously (sc) with a single dose of 0, 5.5, 11.5, or 24.6 mumol Cd/kg as cadmium chloride. All animals were killed 60 d after treatment. At 2 h prior to sacrifice, the rats were injected sc with 100 IU human chorionic gonadotrophin (hCG) to maximally stimulate serum testosterone concentrations. After sacrifice the testes, epididymides and seminal vesicles were removed and weighed. Cardiac blood was taken, and serum concentrations of testosterone (sT) and follicle-stimulating hormone (sFSH) were determined. Sperm concentration in luminal fluid collected from the vas deferens was determined. Significant (p less than 0.01) dose-dependent effects for all measured reproductive parameters were noted in the 70-d-old animals, while no effects were seen in the 30- or 50-d-old rats in either seminal vesicles weight or hCG-stimulated sT concentration. In the absence of significant (p greater than 0.05) changes in body weight gain, effects were seen in testes and epididymides weight, sperm concentration, and sFSH in the 70-d-old rats at Cd doses that were lower than those necessary to bring about similar changes in the 30- or 50-d-old animals. The sensitive indicators of Cd exposure in all age groups were testicular weight greater than epididymal weight greater than vas deferens sperm concentration greater than sFSH concentration. Seminal vesicle weight and sT concentration were found to be the least sensitive. Regression analyses indicated a significant interaction of age with dose; the 70-d-old rats required 30-61% less Cd/kg to cause a 50% change in a measured parameter than did the 30-d-old animals, while the 50-d-old rats required 15-47% less.

Biochemical and physiologic changes in lungs of rats exposed to a cadmium chloride aerosol.

The purpose of this study was to examine the in vivo effects of acute exposure to a cadmium chloride aerosol on the activity of pulmonary enzymes and selected physiologic parameters that are altered by exposure to oxidant agents. Male rats were exposed for 1 hour to 0.5 per cent aerosol of cadmium chloride. At 1,5, and 11 days after exposure to cadmium chloride, exposed rats compared to control rats (data expressed as per cent of control values) had lung-to-body weight ratios of 192, 174, and 140 per cent; lung glucose-6-phosphate dehydrogenase activities of 90, 107, and 135 per cent; lung superoxide dismutase activities of 96, 101, and 132 per cent; tidal volumes of 62, 63, and 89 per cent; respiratory frequencies of 170, 145, and 108 per cent; and lung weight-specific static deflation volumes at 30 cm water of 30, 13, and 31 per cent. A zero-order clearance of cadmium from whole lung was observed, with a half-time of 27.4 days. Light microscopic examination of lung tissue revealed initial pulmonary edema on day 1 that progressed to interstitial pneumonitis on day 5, with some recovery by 11 days after exposure. The cadmium induced biochemical, physiologic, and pathologic alterations were similar to the responses observed in lungs of rats exposed to a wide variety of pulmonary irritants; thus, the changes observed may represent a nonspecific response to tissue injury.