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The ion balance in the flounder ( Ptatichthys flesus L.) was studied after 4 and 9 wk of exposure to sublethal cadmium levels (5–500 μg Cd/l) in brackish water. The cadmium exposure had no effect on the major blood plasma electrolytes, sodium and chloride, indicating an intact osmoregulation. In contrast, cadmium seriously affected the regulation of other ions. Potassium and calcium concentrations showed a strong and dose-dependent depression in blood plasma, whereas the plasma concentrations of inorganic phosphate and magnesium were significantly elevated. It is suggested that these ion disturbances might be associated with cadmium-induced pathological changes in ion-regulating tissues. The reduced concentrations of plasma calcium and potassium might be responsible for neuromuscular disturbances, such as hyperexcitability, spasms and tetanic body contractions, observed in some flounders exposed to the highest cadmium concentration (500 μg Cd/l). In spite of the pronounced disturbance of the calcium metabolism, the spinal columns of the cadmiumexposed flounders did not show any signs of demineralization, fractures or other deformations. This might be due to the fact that the flounder probably has an acellular bone tissue, which only to a small degree seems to be affected by the disturbed calcium balance. It is suggested that fish species with acellular bone tissue run a minor risk of suffering from skeletal damage after cadmium exposure than fish species with an active cellular bone tissue.

The effects on hematology, blood plasma ion balance and carbohydrate metabolism were studied in rainbow trout, Salmo gairdneri, kept in brackish water, and after 18 and 30 wk of exposure to sublethal levels of cadmium (10 and 100 μg Cd/liter), after 25 and 57 wk of subsequent recovery in clean water. Cadmium exposure caused anemia, hypocalcemia and hypermagnesemia. These effects have previously been observed in fish during shorter periods of exposure, but disappeared in the present study within 25 wk of recovery. This suggests that it is the presence of free cadmium ions during the exposure that is responsible for most of the hematological and biochemical effects. Contrary to these findings, the hyperglycemia, that was present during the exposure, persisted throughout the recovery period. Further evidence for a disturbed carbohydrate metabolism after cessation of the exposure was indicated by a dose-dependent decrease in muscle glycogen content after 25 wk of recovery, and by a dose-dependent increase in liver glycogen content after 57 wk of recovery. These effects on the carbohydrate metabolism could be mediated via the selective uptake of cadmium ions in the pancreas and an inhibitory effect on the insulin secretion, thus resulting in an abnormal endocrine control of the metabolism. Analyses of cadmium revealed a dose-dependent accumulation of cadmium in the muscle, that had reached equilibrium after 18 wk of exposure, while a continuing and dose-dependent accumulation was found in the liver throughout the exposure. The levels attained in the liver were about 100 times higher than in the muscle. The slow elimination from liver and kidney suggest a biological half-life for cadmium of more than 1 yr in these tissues. A close positive correlation was found between cadmium levels in liver and in kidney (r = 0.90) in fish after 57 wk of recovery.

The subcellular distribution of cadmium, copper and zinc in the liver, and the binding of these heavy metals to metallothionein (MT) were studied in a wild population of perch ( Perca fluviatilis ). The fish were caught in two areas of the cadmium-contaminated river Eman in the southeast of Sweden. The livers were analyzed for zinc, copper and cadmium and the subcellular distribution of the heavy metals in mitochondrial, microsomal and cytosolic fractions was determined. The cytosols were chromatographed on Sephadex G-75 columns to determine the partition of heavy metals between high molecular weight and MT fractions. Metallothionein was determined, in tissue extracts, by differential pulse polarography. The elevated hepatic cadmium levels found in perch from the contaminated region of the river did not significantly alter the distribution of zinc and copper in the liver. With increasing amounts of cadmium present in the liver cytosol, the distribution of cadmium was altered. The increased cadmium content correlated with an increased MT level in the liver ( r =0.84). The relationship between cadmium and MT is described by the formula [MT] = 7.2 + 0.53 [Cd]. Chromatography of the liver revealed that all of the applied cadmium was bound to MT. The variations in zinc and copper showed low correlation to the MT content of the liver ( r =0.51 and r =−0.15, respectively).

The biliary excretion of an estrogen, 17β-[ 3 H]estradiol, in rainbow trout was studied. Significant amounts of intraperitoneally injected steroid were found in the bile and most of the radioactive material was identified as glucuronides. In response to the treatment of the fish with β-naphthoflavone, which is a potent inducer of cytochrome P -450 monooxygenases in fish, a two-fold increase in radioactivity in the bile was found. The glucuronidation reaction with 17β-estradiol as an aglycon substrate was studied and upon the activity of the microsomal UDP glucuronyl transferase, significant amounts of glucuronides were formed. In response to the treatment of the fish with β-naphthoflavone a two-fold increase in the activity of the UDP glucuronyl transferase was observed. It is suggested that the glucuronidation reaction may be the rate limiting step for the biliary excretion of the steroid. The physiological significance of the changed metabolism and excretion of the estrogen is discussed.

The effects of intraperitoneal administration of cadmium and exposure to cadmium in the water on rainbow trout, Salmo gairdneri , were studied. The results of intraperitoneal injection of cadmium indicate that this metal has the potential to inhibit phase I and phase II xenobiotic biotransformation activities in the liver and kidney. The exposure to cadmium through water resulted in different responses in the liver and kidney. The marked inhibition of the glucuronidation reaction is of toxicological importance, since this may potentiate the toxic action of organic xenobiotics biotransformed through this pathway. This response in the kidney was accompanied by histopathological changes in the proximal renal tubules, which are probably associated with the plasma hypocalcaemic response observed in cadmium-poisoned fish.