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Adult and juvenile rainbow trout, Oncorhynchus mykiss, were exposed for 30 days to CdCl2 in water (10 and 25 micrograms Cd/L for adults, and 1 and 5 micrograms Cd/L for juveniles) to investigate effects of subchronic exposures to Cd on the hypothalamo-pituitary-interrenal and the hypothalamo-pituitary-thyroid axis, and on metabolic status. liver size and glycogen content and body mass gain were significantly reduced in the exposed adult fish and similar changes were detected in the juveniles. Plasma cortisol levels increased after exposure to the lower dose but decreased at the higher dose. Plasma T3 and T4 tended to decrease in the exposed adult fish. No significant differences in plasma glucose or cholesterol levels were detected between the controls and the exposed fish, plasma calcium levels were lower in the exposed fish. The results indicate that long-term exposures to Cd at sublethal doses have adverse effects on the physiological status of the fish and that these effects are mediated partly through alterations of endocrine function.

Lipid peroxidation (LPO), measured as thiobarbituric acid reactive substances (TBARS), was evaluated in lungs of rats 24 h after intraperitoneal injection of 50, 250, and 1000 micrograms Cd/kg body weight as CdCl2. In order to gain some insight into possible causative factors responsible for these oxidative phenomena, the redox-active elements iron (Fe) and copper (Cu), and total lung protein content (an indication of pulmonary inflammatory processes) were also measured. Results obtained demonstrate a similar dose-related, non-linear evolution of total lung TBARS and total lung protein as a function of increasing lung Cd concentrations. Standardization of total lung TBARS to lung protein content further resulted in a linear relationship with lung Cd concentrations, thus suggesting a possible cause-effect relationship between these parameters. No statistically significant association was observed between the dose-related evolution of lung TBARS, and iron (Fe) and copper (Cu) after Cd exposure. The results obtained provide support for the possible involvement of inflammatory phenomena as the most likely events responsible for the generation of LPO in lung tissue following acute exposure to Cd salts.

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