Alicja Krasowska

Photoperiod affects hepatic and renal cadmium accumulation, metallothionein induction, and cadmium toxicity in the wild bank vole (Clethrionomys glareolus).

The objective of this study was to examine the toxic effects of dietary cadmium (Cd) on bank voles, being the F1 offspring of a wild-caught population. For 6 weeks, the rodents were provided with diets containing 0.05 (control), 40, 80, and 120 microg Cd/g dry wt of diet under moderate (12 h) and long (16 h) photoperiods. Histological examinations and analyses of metallothionein (MT), Cd, Cd bound and not bound to MT, iron and lipid peroxidation in the liver and kidneys were carried out. Histopathological changes occurred in the liver (infiltrations of leukocytes) and kidneys (hemorrhage, glomerular injury, tubular cell degeneration) of bank voles fed the highest dose of dietary Cd only under the moderate photoperiod. The same voles also exhibited the highest values of hepatic and renal Cd, Cd not bound to MT, and renal lipid peroxidation. It seems that under the long photoperiod the liver and kidneys of bank voles were protected against Cd-induced injury through decreasing Cd accumulation and increasing synthesis of MT.

An iron-rich diet protects the liver and kidneys against cadmium-induced injury in the bank vole (Clethrionomys glareolus)

The objective of this study was to determine whether supplemental dietary iron (Fe) would protect against cadmium (Cd)-induced injury in the liver and kidneys of bank voles. The rodents were provided, for 6 weeks, Fe-adequate (60-80 microg/g) and Fe-enriched (250-270 microg/g) diets containing 0.05 (control), 40, and 80 microg Cd/g. Histological examinations and analyses of Cd, Cd bound and not bound to metallothionein (MT), Fe, and lipid peroxidation in liver and kidneys were carried out. The Fe-enriched diet prevented Cd-induced histopathological changes as well as deprivation of tissue Fe and lipid peroxidation. Also, supplemental Fe significantly decreased hepatic and renal Cd burden. However, in the Cd-80 bank voles fed the Fe-enriched diet, the non-MT-bound Cd, considered a toxic species, reached 4.7 microg/g liver and 13.7 microg/g kidney, these values being similar to those at which histopathological changes occurred in the voles fed Cd diets not supplemented with Fe. The data indicate that the protective effect of supplemental Fe in the bank vole may be due to the prevention of Cd-induced deprivation of tissue Fe and Fe-dependent oxidative processes rather than to reduction of cadmium accumulation.

Dietary cadmium induces histopathological changes despite a sufficient metallothionein level in the liver and kidneys of the bank vole (Clethrionomys glareolus)

The objective of this study was to correlate hepatic and renal cadmium (Cd) accumulation, Cd-binding capacity of metallothionein (MT) and lipid peroxidation with the tissue injury in the male bank voles raised under short (8 h light/16 h dark) and long (16 h light/8 h dark) photoperiods that affect differently Cd accumulation and MT induction in these rodents. The animals were exposed to dietary Cd (0, 40 and 80 microg/g) for 6 weeks. The accumulation of Cd in the liver and kidneys appeared to be dose-dependent in bank voles from the two photoperiod groups; however, the short-photoperiod animals exhibited significantly higher concentrations of Cd in both organs than the long-photoperiod bank voles. Cd-Binding capacity of MT in the liver and kidneys of bank voles from the long photoperiod was sufficiently high to bind and detoxify all Cd ions, while in the animals fed 80 microg Cd/g under the short photoperiod, the concentrations of Cd in both organs exceeded (by about 10 microg/g) the MT capacity. However, similar histopathological changes in the liver (a focal hepatocyte swelling and granuloma) and kidneys (a focal degeneration of proximal tubules) occurred in Cd-80 bank voles from the two photoperiods. Likewise, in either photoperiod group, dietary Cd brought about a similar, dose-dependent decrease in the hepatic and renal lipid peroxidation, which paralleled closely that of the iron (Fe) concentrations. These data indicate that: (1) MT does not protect the liver and kidneys against Cd-induced injury in the bank vole exposed to the higher level of dietary Cd; and (2) lipid peroxidation cannot be responsible for the tissue damage. It is hypothesized that dietary Cd produces histopathological changes indirectly, through depressing the tissue Fe and Fe-dependent oxidative processes.

Subcellular distribution of metallothionein and cadmium in the liver and kidneys of bank voles (Clethrionomys glareolus) exposed to dietary cadmium

Metallothionein (MT) and cadmium (Cd) contents were determined in the subcellular fractions of the liver and kidneys of bank voles exposed for 6 weeks to elevated levels of dietary Cd-40 and 80 μg g-1 dry weight. Hepatic and renal MT was detected exclusively in the cytosol, while Cd was found in the cytosol (73–79% of the total content), nuclei (14–18%) and particulates (4–9%). The concentration of MT in the cytosol as well as Cd content in the particular subcellular fractions appeared to be a dose-dependent. The absence of MT in the nuclear and particulate fractions implied that Cd present in these compartments was not bound to the protein that is considered to provide protection against the toxic metal. Therefore, it is assumed that this component of intracellular Cd could be responsible for the histopathological changes that occurred in the liver (granuloma and focal hepatocyte swelling) and kidneys (focal degeneration of proximal tubules) of bank voles exposed to the higher level of dietary Cd.

Dietary cadmium decreases lipid peroxidation in the liver and kidneys of the bank vole (Clethrionomys glareolus)

The effect of elevated levels of dietary cadmium on lipid peroxidation in the liver and kidneys of a small rodent, the bank vole, was determined in the present study. Males and females, aged 1 month, were given diets containing 0.40 and 80 mg Cd per kg; liver and kidneys were removed for TBA-RS as well as iron, copper, zinc, cadmium and metallothionein analyses at the end of 6 weeks. Dietary Cd significantly decreased the TBA-RS level in the liver and kidneys of both sexes; however, this effect appeared to be dose-dependent only for the male liver. The changes in hepatic and renal TBA-RS paralleled closely those of tissue iron. Copper concentration decreased significantly only in the male liver, while hepatic and renal zinc were not influenced by dietary Cd. The concentrations of Cd and metallothionein in the liver and kidneys increased significantly in a dose-dependent fashion. Regression analysis confirmed that TBA-RS in both organs correlated closely with iron. The data suggest that dietary Cd decreases hepatic and renal lipid peroxidation indirectly, through lowering the tissue iron concentration.