The objective of the study was to compare the sensitivity of wild and laboratory-bred bank voles to cadmium (Cd)-induced histopathological changes in the liver and kidneys. For 4 weeks, the male bank voles—both wild and laboratory-bred—were provided with diet containing Cd in quantities <0.1 (control), 30, and 60 μg/g dry weight. At the end of exposure period, histopathology and analyses of Cd, metallothionein (MT), glutathione (GSH), zinc (Zn), copper (Cu), iron (Fe), and lipid peroxidation—all considered to be critical factors during the development of Cd toxicity in the liver and kidneys—were carried out. Histopathological changes (focal hepatocyte swelling, vacuolation and inflammation [leukocyte infiltration] in the liver, and focal proximal tubule degeneration [including epithelial cell swelling] in the kidneys) occurred only in the wild bank voles fed a diet containing 60 μg Cd/g. There were no differences in concentrations of Cd, MT, GSH, Zn, and Cu in liver and kidney between the respective groups of wild and laboratory-bred animals. However, a decrease of hepatic Fe and lipid peroxidation was observed in the wild voles exhibiting histopathological changes. These data indicate the following: (1) wild bank voles are more susceptible to Cd-induced liver and kidney injury than those bred and raised in the laboratory; (2) the difference in sensitivity may be associated with a distinct decrease of hepatic Fe in response to Cd exposure between the two groups of bank voles; and (3) dietary Cd may produce histopathological changes indirectly through decreasing the hepatic Fe and Fe-dependent oxidative processes. These results also suggest that histopathology in the liver and kidney of wild bank voles living in a contaminated environment may occur at relatively low levels of tissue Cd.

The objective of this study was to examine relations between basal metabolic rate (BMR) and cadmium (Cd) accumulation in the liver, kidneys, and duodenum in mice. The 5-month-old mice selected for high (H) and low (L) BMR were exposed for 8 weeks to 0, 10, and 100 μg Cd/mL of drinking water. The H-BMR mice showed significantly higher concentrations of Cd in the liver (47-79%), kidneys (61-70%), and duodenum (74-100%) than L-BMR animals. The tissue Cd accumulation also positively correlated with the duodenal iron which, in turn, was positively associated with BMR (Spearman R (s) = 0.81, P = 0.0004). The data indicate that tissue accumulation of Cd in mice is linked to BMR; the correlation between tissue Cd and duodenal iron suggests an involvement of iron transport pathway in the accumulation of Cd.

Bank voles free living in a contaminated environment have been shown to be more sensitive to cadmium (Cd) toxicity than the rodents exposed to Cd under laboratory conditions. The objective of this study was to find out whether benzo(a)pyrene (BaP), a common environmental co-contaminant, increases Cd toxicity through inhibition of metallothionein (MT) synthesis-a low molecular weight protein that is considered to be primary intracellular component of the protective mechanism. For 6 weeks, the female bank voles were provided with diet containing Cd [less than 0.1 μg/g (control) and 60 μg/g dry wt.] and BaP (0, 5, and 10 μg/g dry wt.) alone or in combination. At the end of exposure period, apoptosis and analyses of MT, Cd, and zinc (Zn) in the liver and kidneys were carried out. Dietary BaP 5 μg/g did not affect but BaP 10 μg/g potentiated rather than inhibited induction of hepatic and renal MT by Cd, and diminished Cd-induced apoptosis in both organs. The hepatic and renal Zn followed a pattern similar to that of MT, attaining the highest level in the Cd+BaP 10-μg/g group. These data indicate that dietary BaP attenuates rather than exacerbates Cd toxicity in bank voles, probably by potentiating MT synthesis and increasing Zn concentration in the liver and kidneys.

Bank voles free living in a contaminated environment are known to be more sensitive to cadmium (Cd) toxicity than the rodents exposed to Cd under laboratory conditions, but the reasons for this difference are poorly defined. The present work was designed to determine whether dietary lead (Pb), a common environmental co-contaminant, and/or animal density that affects various physiological processes, would influence susceptibility to Cd toxicity in the kidneys and liver of these animals. For 6 weeks, the female bank voles were kept individually or in a group of six and provided with diet containing environmentally relevant concentrations of Cd [<0.1 μg/g (control) and 60 μg/g dry wt] and Pb [<0.2 μg/g (control) and 300 μg/g dry wt] alone or in combination. At the end of exposure period, histopathology and analyses of metallothionein, glutathione and zinc that are linked to a protective effect against Cd toxicity, as well as Cd, Pb, copper, iron and lipid peroxidation were carried out. Histopathological changes in the kidneys (a focal glomerular swelling and proximal tubule degeneration) and liver (a focal hepatocyte swelling, vacuolation and inflammation) occurred exclusively in some bank voles kept in a group and exposed to Cd alone (2/6) or Cd + Pb (4/6). The observed toxicity in grouped bank voles appeared not to be based on altered (1) tissue disposition of Cd and/or Pb, (2) metallothionein, glutathione and zinc concentrations, or (3) tissue copper, iron and lipid peroxidation. The data indicate that high population density in combination with environmental Pb may be responsible for an increased susceptibility to Cd toxicity observed in bank voles free living in a contaminated environment; the mechanism by which animal density affects Cd toxicity deserves further study.

The objective of this study was to examine relations between body iron (Fe) status and cadmium (Cd) accumulation in a small rodent, the bank vole, caught from the wild population in late autumn (November) and early spring (March). The concentrations of Fe in the liver, kidneys, and duodenum in the bank voles from the spring were only 30%, 60%, and 70%, respectively, of those found in the animals from the autumn. An analysis of hematocrit and hemoglobin content of blood showed no significant effect of the season, suggesting that the animals from the spring were not anemic. The exposure to dietary Cd (10 microg/g) for 7 days resulted in 70% higher accumulation of Cd in the liver and kidneys of the spring than autumn bank voles, and the concentration of Cd in the duodenum was 3.5 times higher in the spring animals, despite the fact that relative Cd intake was significantly higher in the autumn bank voles. The data indicate that seasonal changes of body Fe status occurring in the wild bank voles may influence tissue accumulation of Cd.