Tadeusz Włostowski

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.

Tissue Trace Elements and Lipid Peroxidation in Breeding Female Bank Voles Myodes glareolus

Recent studies have demonstrated that reproduction reduces oxidative damage in various tissues of small mammal females. The present work was designed to determine whether the reduction of oxidative stress in reproductive bank vole females was associated with changes in tissue trace elements (iron, copper, zinc) that play an essential role in the production of reactive oxygen species. Lipid peroxidation (a marker of oxidative stress) and iron concentration in liver, kidneys, and skeletal muscles of reproducing bank vole females that weaned one litter were significantly lower than in non-reproducing females; linear regression analysis confirmed a positive relation between the tissue iron and lipid peroxidation. The concentrations of copper were significantly lower only in skeletal muscles of reproductive females and correlated positively with lipid peroxidation. No changes in tissue zinc were found in breeding females when compared with non-breeding animals. These data indicate that decreases in tissue iron and copper concentrations may be responsible for the reduction of oxidative stress in reproductive bank vole females.

Orally Administered Melatonin and the Accumulation and Toxicity of Cadmium in the Bank Vole (Myodes Glareolus)

Orally Administered Melatonin and the Accumulation and Toxicity of Cadmium in the Bank Vole (Myodes Glareolus) Animal gender and age significantly influence the accumulation and toxicity of heavy metals, including cadmium (Cd). The aim of this study was to determine the effect of orally administered melatonin (6 μg/ml), a known antioxidant and metal chelator, on Cd accumulation and toxicity in one month old females and males (young) and five months old bank voles (old) exposed to dietary Cd (100 μg/g) for six weeks. Compared to the Cd alone group, melatonin co-treatment brought about a decrease of Cd concentration in the liver (17% and 20%) and kidneys (39% and 36%) of young female and male bank voles, respectively, while in old animals increased Cd accumulation in liver (65%) and kidneys (81%) and enhanced consumption of Cd-contaminated food (136%) without any effect on their body mass. The results suggest that orally administered melatonin together with cadmium in young bank voles reduces tissue Cd accumulation possibly through forming stable complexes with this metal but in older rodents, melatonin increases concentration of the metal through increasing consumption of Cd-contaminated food. Melatonina Podawana Doustnie a Akumulacja i Toksyczność Kadmu u Nornicy Rudej (Myodes Glareolus) Wiek oraz płeć zwierząt są istotnymi czynnikami wpływającymi na akumulację i toksyczność metali ciężkich, w tym kadmu. Celem pracy było sprawdzenie wpływu doustnie podawanej melatoniny, znanego antyoksydanta i chelatora metali, na akumulację i toksyczność kadmu u jednomiesięcznych (młodych) oraz pięciomiesięcznych (starych) nornic rudych spożywających pokarm zawierający kadm (100 μg/g). Po sześciu tygodniach eksperymentu nastąpiło obniżenie akumulacji kadmu w wątrobie (17 i 20%) i nerkach (39 i 36%) odpowiednio u młodych samic i samców spożywających melatoninę i kadm w porównaniu do zwierząt spożywających wyłącznie kadm, natomiast u dorosłych zwierząt wzrosła akumulacja kadmu w wątrobie (65%) i nerkach (81%) oraz spożycie pokarmu skażonego kadmem (136%) bez istotnych zmian w ciężarze ciała. Uzyskane wyniki wskazują, że melatonina podawana wraz z kadmem per os u młodych nornic obniża akumulację kadmu w tkankach prawdopodobnie poprzez tworzenie kompleksów z metalem, natomiast u dorosłych zwierząt zwiększa koncentrację tego metalu stymulując spożycie pokarmu zawierającego kadm.