The effects of zinc deficiency on turnover of cadmium-metallothionein in rat liver

The object of this experiment was to determine the effects of Zn deficiency on the turnover of Cd-induced metallothionein (MT) in rat liver. Male rats were fed a purified Zn-deficient or Zn-adequate diet. After 13 days, the rats were given three daily injections of Cd2+ totaling 1.5 or 3.0 (Zn-deficient) and 3.0 or 6.0 (Zn-adequate) mg Cd/kg body weight. The MT was labeled by injecting the rats with [35S]cystine 2 hours after the final Cd injection. One, 3 or 5 days after labeling, the rats were killed, and their livers were assayed for MT 35S and metal content. The metal composition of MT (mole %) was 41-42% Cd, 51-54% Zn and 4-7% Cu in the Zn-adequate groups and 64% Cd, 27-31% Zn and 6-9% Cu in the Zn-deficient groups. The half-lives of Cd-induced MT in the Zn-deficient rats were 2.6 days (1.5 mg Cd/kg) and 2.8 days (3.0 mg Cd/kg). In the Zn-adequate rats, the half-lives were 3.6 days (3.0 mg Cd/kg) and 3.1 days (6.0 mg Cd/kg). The half-lives of general, soluble hepatic proteins were 4.1 to 4.3 days in all groups. Despite the stabilizing effect of the higher Cd content, the half-life of hepatic MT in the Zn-deficient rats was significantly shorter than in the Zn-adequate rats. These results indicate that hepatic MT degradation is faster in Zn-deficient animals.     

Decreased preference for sucrose in rats fed a low protein diet and its intensification by zinc-deficiency

This study examined whether protein concentrations in the diet of rats fed adequate Zn or deficient Zn affect their preference for disaccharides of sucrose and maltose. Sucrose and maltose were used as a source of carbohydrate and the selection patterns of rats were analyzed for 28 d by a two-choice selection method. Diets provided as a set of two either Zn-adequate or Zn-deficient diets containing 10, 20 and 40% protein each were changed in position daily. For the first 24 h, both the control Zn-adequate and Zn-deficient rats preferred sucrose to maltose and then gradually selected the maltose diet. Protein in the diet affected the selection of the disaccharides for both the control and Zn-deficient rats. The decrease order of the ratio of consumed sucrose to maltose over 28 d was 10% > 20% > 40% protein diet group, and Zn-deficiency emphasized the decrease. These results suggest that sucrose has a stronger taste effect than maltose in rats, but that the selection of sucrose is decreased by the post-ingestive effect which is stimulated in low-protein and Zn-deficient diets.     

Tissue-specific cadmium accumulation, metallothionein induction, and tissue zinc and copper levels during chronic sublethal cadmium exposure in juvenile rainbow trout

Juvenile rainbow trout, on 3% of body weight daily ration, were exposed to 0 (control) or 3 μg/L Cd (as Cd(NO₃)₂· 4H₂O) in moderately hard (140 mg/L as CaCO₃), alkaline (95 mg/L as CaCO₃, pH 8.0) water for 30 days. Particular attention focused on Cd burden in tissues (gills, liver, kidney, and whole body) and induction of metallothionein (MT) in gills, liver, and kidney during chronic Cd exposure. Mortality in Cd-exposed fish was minimal (∼10%), and no growth effects occurred over the 30-day exposure. Cd accumulated in a time-dependent fashion to 9 times (gills), 3 times (liver), 20 times (kidney), 2 times (carcass), and 2 times (whole body) control levels by 30 days; absolute concentrations were in the order kidney > gill > liver > whole body > carcass. Tissue (gills, liver, and kidney) Zn and Cu burdens were not altered by chronic exposure to 3 μg/L Cd. MT concentrations in all tissues increased over the 30 days of Cd exposure, but the increases were much less than those of Cd on a molar binding site basis. Absolute MT concentrations were in the order liver > kidney > gill, but relative increases were greatest in kidney (fourfold), followed by gills (twofold) and liver (1.3-fold). MT levels were sufficient to bind all Cd in gill, liver, and kidney under control conditions, and after chronic Cd exposure remained sufficient in liver and kidney, but not in gills. Total metal levels (Cd + Zn + Cu) greatly exceeded MT binding capacity in all tissues under all conditions. Received: 20 February 2001/Accepted: 20 May 2001     

Protective effects of selenium (Se) and zinc (Zn) on cadmium (Cd) toxicity in the liver of the rat: Effects on the oxidative stress

Cadmium (Cd) is a very harmful environmental pollutant that transfers between various levels of the food chain. To study the protective effect of Se and Zn on Cd-induced oxidative stress in livers, male rats received either, tap water, Cd, Cd+Zn, Cd+Se or Cd+Zn+Se in their drinking water, for 35 days. The activities of total superoxide dismutase (SOD), copper, zinc-superoxide dismutase (CuZn SOD), glutathione peroxidase (GPx) and catalase (CAT), malondialdehyde (MDA) level and the ratio of CuZn SOD to GPx activity, were determined in the liver. Exposure to Cd lowered total SOD, CuZn SOD, GPx and CAT activities, while it increased MDA level and the ratio of CuZn SOD to GPx activity, in the organ studied. With Se or Zn administration during exposure to Cd, only partial corrective effects on Cd-induced oxidative stress in the liver have been observed, while Se and Zn together assured a more efficient protection of the organ against the observed oxidative stress.     

Differential Susceptibility to Cadmium-Induced Liver and Kidney Injury in Wild and Laboratory-Bred Bank Voles Myodes glareolus

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.     

Tissue-Specific Cadmium and Metallothionein Levels in Rainbow Trout Chronically Acclimated to Waterborne or Dietary Cadmium

Rainbow trout were exposed to a sublethal concentration of waterborne Cd (0 or 3 g/L) or dietary Cd (0 or 500 mg/kg dry wt) for 30 days to induce acclimation, and tissue Cd and metallothionein (MT) levels were examined. The greatest Cd concentrations were observed in the kidney followed by the gills and liver of the fish exposed to Cd via water, but in the gut tissues followed by the kidney, liver, and gills for dietary-exposed fish, reflecting a variation depending on the route of Cd exposure. Some MT was found in the nonacclimated naïve fish with no experience of elevated Cd exposure, and these background MT levels were quite high in the posterior intestine (480 g/g), cecae (257 g/g), and liver (248 g/g) relative to other tissues (7–50 g/g). With exposure to both waterborne and dietary Cd, MT levels rose significantly in all observed tissues. The increases relative to the control levels of MT in naïve fish were in the order: kidney (5.4 times) > gills (4.6) > liver (1.3) for the waterborne exposure group, and in the order kidney (19.3 times) >> cecae and posterior intestine (6.5 times) > liver and stomach (5 times) > midintestine (4.3 times) > gills (2.1 times) for the dietary exposure group. At 24 hours after an acute gastrointestinal dose of Cd (276 g/kg) infused into the stomach of dietary exposure groups, large increases of total Cd but not MT levels were found in the gut tissues of nonacclimated fish; in the Cd-acclimated fish, the posterior intestine was greatly affected with decreases in Cd (71%), Zn (33%), Cu (70%) and MT (46%) levels, suggesting an enhanced sloughing of tissue materials after infusion. Exposure to Cd did not cause any notable decrease of Zn or Cu in any tissue, except that found in the posterior intestine. However, a molar analysis indicated that although Cd levels remained less than MT binding capacity in both waterborne and dietary exposure groups, the total metal levels (Cd + Zn + Cu) greatly exceeded MT binding capacity in all tissues of Cd-exposed fish, suggesting a potential competition of Cd with other metals for binding sites on MT and non-MT proteins in the tissues.     

The effect of dietary zinc depletion and repletion on rats: Zn concentration in various tissues and activity of pancreatic gamma-glutamyl hydrolase (EC 3.4.22.12) as indices of Zn status

Unlike severe zinc deficiency, marginal Zn deficiency is difficult to identify in rats because no reliable indicator of suboptimal Zn status is currently available. We have previously observed reduced pancreatic gamma-glutamyl hydrolase (EC 3.4.22.12) activity and impaired pteroylpolyglutamate absorption in Zn-deficient rats. In the present study the effect of Zn depletion and repletion on the Zn concentration of various tissues and on the activity of this enzyme was investigated. The objective was to determine the sensitivity of these variables to Zn depletion and to evaluate their usefulness as indices of Zn status. Male Wistar rats (about 180 g), maintained from weanling on a purified Zn-adequate diet, were randomly allocated into twelve groups. A pretreatment control group was killed immediately. The remaining eleven groups were fed on a Zn-deficient diet and a group killed daily for 7 d (Zn-depleted groups). The remaining four groups were re-fed the Zn-adequate diet and a group killed daily (Zn-repleted groups). On analysis, pancreas and spleen Zn levels responded most rapidly to reduced Zn intake, followed by tibia, liver, kidney and plasma. Zn concentration was maintained in testes. Reduced plasma folate levels were also observed. A significant reduction in pancreatic gamma-glutamyl hydrolase activity before the depletion of many tissue Zn stores confirms the Zn sensitivity of the enzyme. It was concluded that future investigation into the inter-relationship between Zn and folate metabolism may be useful in identifying a sensitive, biochemical index of Zn status.     

Mitochondrial effects of low-level cadmium in rats: Interaction with zinc

Male Sprague-Dawley rats were treated with sodium or cadmium (Cd) 4 acetate (25 g Cd per kg body weight) orally 5 times a week for 6 weeks. A second group of animals was repeatedly injected with zinc sulphate (6 and 12 mg zinc (Zn) per kg ip) with or without Cd gavage. Cadmium treatment alone yielded no obvious toxic effects as evidenced by serum constituents or animal weight gain. Similarly, Zn injection did not affect these criteria. Zinc injection increased metallothionein in liver and kidneys and increased renal Cd. Cytosolic sorbitol dehydrogenase was not influenced by either cadmium, Zn or Cd + Zn exposure. However, individual Cd gavage decreased mitchochondrial cytochrome c oxidase in liver by 50%. This was partly protected by Zn. Hepatic adenosine triphosphatase (ATPase) was not affected by any of the treatment regimens. However, renal ATPase was inhibited by combined Cd + Zn administration. The data suggest subcellular toxic effects due to treatment with low Cd doses as evidenced by the decrease in hepatic cytochrome c oxidase. Simultaneous Zn injection may reduce this effect of Cd in liver. However, the treatment of rats by low level Cd gavage combined with zinc administration impairs the animals' health as shown by weight loss.Abbreviations Cd cadmium - Zn zinc - ATP adenosine triphosphate - ATPase adenosine triphosphatase - MT metallo thionein - NADH nicotinamide adenine dinucleotide, reduced Parts of this study have been presented at the 20th Annual Meeting of the Australasian Society for Clinical and Experimental Pharmacologists (ASCEP), Dec 8–10, 1986, Melbourne.     

Dietary zinc deficiency and repletion modulate metallothionein immunolocalization and concentration in small intestine and liver of rats

Metallothionein (MT) functions in zinc (Zn) homeostasis and dietary Zn affects tissue MT concentration. The objective of this study was to investigate the effects of dietary Zn deficiency and 24-h Zn repletion on MT immunolocalization and concentration in the small intestine and liver of growing rats. Three-week-old rats fed Zn-deficient diet (< 1 mg Zn/kg) for 16 d had no MT staining in either small intestine or liver. After 24-h Zn repletion with control diet (30 mg Zn/kg), strong MT staining was observed in intestinal Paneth cells and surface epithelial cells in the proliferative regions of villi. Pair-fed control rats had strong MT staining in liver that was localized around central veins. After 24-h energy repletion, the hepatic MT staining diminished. Furthermore, Zn-deficient rats had significantly reduced intestinal (57%) and hepatic (61%) MT concentrations but unaffected Zn concentrations compared with controls that consumed food ad libitum. Zn repletion for 24 h restored intestinal and hepatic MT concentrations and reduced hepatic Zn concentration. Pair-fed control rats had elevated MT concentration in liver that was normalized by energy repletion. There was a significant positive correlation between tissue Zn and MT concentrations in liver (r = 0.60, P = 0.0001), but not in small intestine. In summary, MT immunolocalization and concentration in rat small intestine and liver were responsive to changes in Zn status, supporting the role of MT in Zn metabolism. Cell-type-specific localization of MT in small intestine after dietary Zn manipulations indicates a function of Zn and MT in gut immunity and intestinal mucosal turnover, and the pattern of hepatic MT distribution with energy restriction may be linked to detoxification processes.     

必需脂肪酸对大鼠实验性缺锌的影响

以饱和脂肪(椰子油)配制缺锌(1.4～1.5ppm)饲料,从第二周起即有死亡,三周时死亡达55％。存活动物有严重缺锌症状。给存活鼠以含锌水(100ppm),症状很快消失,体重增长迅速。以红花油替代椰子油,动物到第四周时仍无缺锌表现,血锌、毛锌与正常近似。调正脂肪酸组成,使亚油酸约占总脂肪酸的20％,实验鼠可在两周后出现缺锌症状,血锌、毛锌低于正常,无死亡。动物可以供作缺锌实验用。     

Metallothionein Gene Expression in Liver of Rats Exposed to Cadmium and Supplemented with Zinc and Selenium

Cadmium (Cd), one of the most widely distributed heavy metals, is highly toxic to humans and animals. It is well known that zinc (Zn) and selenium (Se) administration reduce the Cd-induced toxicity and that metallothioneins can have a protective effect to mitigate Cd toxicity in biological systems. In this study we report the expression analysis of the two metallothioneines gene classes MT-1 and MT-2 as well as the total metalloprotein content in the liver of rats exposed to Cd (200 ppm), Cd + Zn (200 ppm + 500 ppm), Cd + Se (200 ppm + 0.1 ppm) or Cd + Zn + Se (200 ppm + 500 ppm + 0.1 ppm) in their drinking water for 35 days. Metals accumulation was quantified in rat liver. Cd decreased significantly the hepatic concentrations of Se and increased those of Zn. The treatment of Cd-exposed rats with Se alone or combined with Zn reversed the Cd-induced depletion of Se concentrations in the liver. However, Zn or Zn + Se administration significantly increased the liver Cd uptake and had no effect on the Cd-induced increase in hepatic concentrations of Zn. The molecular assay showed a decreasing trend of MT-1 relative gene expression levels in animals supplemented with Zn (6.87-fold), Se (3.58-fold), and their combination (1.69-fold) when compared to Cd-treated animals (16.22-fold). Upregulation of the MT-2 expression were recorded in all conditions, although fold induction levels were less pronounced than MT-1 expressions. Our data suggest that the well-established protective effect of Zn and Se against Cd-induced toxicity passes through non-MT gene expression mechanisms, being more dependent on the oxidative stress status of the cell.     

Rats allowed to self-select zinc-deficient lard and fish-oil diets did not develop a preference for fish-oil diet

Zinc (Zn)-deficiency causes a reduction in food intake and alters adipose metabolism. The effect of zinc restriction in rats on the selection of fish-oil and lard was studied during a period of reduced appetite. The reduction of appetite was caused by an experimentally induced Zn-deficiency. Four-week-old male rats were divided into three dietary treatment groups: Zn-adequate (ZnA, 30.9 mg Zn/kg), marginal Zn-deficient (ZnM, 5.9 mg Zn/kg) or Zn-deficient (ZnD, 0.9 mg Zn/kg). The three groups were placed on a self-selection regimen of the ZnA-fish-oil diet (ZnA-FD) and the ZnA-lard diet (ZnA-LD), the ZnM-FD and the ZnM-LD or the ZnD-FD and the ZnD-LD, respectively for 24 d. The amount of the FD intake in the ZnD group decreased to 0.5 g/d after day 4-6 of self-selecting on the LD and the FD and no significant increase in the FD intake in the group was observed during the self-selection period. However, after day 7-9 and 13-15, the FD intake of the ZnA and the ZnM groups increased, respectively, and at the end of the self-selection period the ZnM and the ZnA rats consumed about 2.0 g FD/d and 4.5 g FD/d, respectively. The FD intake ratio [FD intake (g)/total intake (g)] in the ZnD rats during the self-selection period was the lowest and that in the ZnA rats was the highest of three groups. In conclusion, we showed that zinc status alters fish-oil and lard selection patterns and ZnD rats did not show a preference for fish-oil.     

Sephadex G-75凝胶柱层析法测定金属硫蛋白

应用Sephadex G-75凝胶柱层祈技术分离出大鼠肝、肾、血液和尿液中金属硫蛋白(MT),通过测定该蛋白质所结合的金属含量来计算MT含量。此法不但能较灵敏地反映镉等重金属中毒情况下MT的体内变化,也能测出正常机体肝、肾等组织中MT含量。若样品加以浓缩亦可检出正常血、尿中MT的含量。     

Influence of copper and iron on subacute cadmium intoxication in protein-malnourished rats

Male albino rats maintained on low-protein (9%) diets were dosed intraperitoneally with 0.75 mg Cd/kg, as cadmium chloride, for 20 days. Groups of these animals were provided with diets supplemented with 40 ppm Cu, 400 ppm Fe or a combination of both during the exposure period. Hepatic and renal distribution of Cd, Zn, Cu, and Fe along with activity of acid and alkaline phosphatases and ribonuclease and glutathione content were studied. Uptake of Cd both in liver and in kidney was significant and was accompanied by increased Zn and depletion of Fe concentration. The Cu level remained unaltered. Dietary supplementation of Cu or Fe interacted effectively and influenced the metal distribution. Acid and alkaline phosphatases in both liver and kidney were inhibited by Cd exposure. However, Cu and/or Fe supplements could to a varying degree offset the Cd-induced inhibition. Cadmium exposure did not, however, elicit any effect on hepatic and renal ribonuclease activity of low-protein-fed animals. The glutathione concentration registered profound increase on Cd exposure, possibly to act as a defence mechanism.     

Preference for glucose in Zn-deficient rats selecting from glucose and fructose diets

Glucose and fructose selection patters of rats were analyzed for 28 d by a 2-choice selection in either Zn-adequate or Zn-deficient status. In this paper, we describe the following serial studies: (1) For the first 24 h, rats fed a Zn-deficient diet preferred a fructose-diet compared with a glucose-diet. On and after the third day, rats fed both Zn-adequate and Zn-deficient diets preferred the glucose-diet. (2) Throughout the experimental period, many of the rats fed a Zn-adequate and Zn-deficient diet continuously selected one diet. (3) Some of the rats fed a Zn-adequate and Zn-deficient diet suddenly changed preference for the glucose-diet or the fructose-diet. (4) The sum of daily glucose- and fructose-diet intake in rats fed a Zn-deficient diet showed a characteristic variation with the cyclic period of 3.9 +/- 0.4 d.     

The effect of low doses of dietary cadmium oxide on the disposition of trace elements (zinc,copper, iron), hematological parameters,and liver function in rats

The Zn, Cu, and Fe concentrations in selected organs, tissues and in the excreta of male Wistar rats, exposed to dietary CdO (2.80 and 7.15 ppm) for 40 and 60 days, were investigated. Concomitantly hematological values and serum enzyme activities were recorded. Zn levels of spleen, kidney, testes, muscle and feces were not affected by the Cd treatment. After 40 days of Cd exposure, the Zn concentration in the hair decreased, while the Zn level of the lung slightly increased. During the feeding trial, Cd produced an increase of liver Zn by about 24%. Femur Zn decreased and Zn in urine increased after 60 days of exposure to 7.15 ppm Cd. Except in hair and urine, the Cu concentration in all organs and tissues investigated remained unchanged. Hair Cu levels decreased after 40 days of Cd exposure but increased after 60 days. At this time, elevated Cu concentration in urine was recorded. After exposure to 7.15 ppm Cd, the Fe content of the lung, liver, spleen, testes, muscle, femur and blood decreased significantly. After 60 days on the 7.15 ppm diet, highest reductions (30%–60%) of Fe content were recorded in the lung, liver, and spleen. Similar to Zn and Cu, the Fe concentration in urine increased at that time. No changes were found in the Fe content of hair, kidney, and feces. In spite of a disturbed Fe metabolism, an anaemic response of Cd-treated rats was not observed. Hematocrit and hemoglobin remained unchanged and the number of red blood cells slightly increased after 40 days of Cd exposure. While the activity of serum alkaline phosphatase was not affected by dietary Cd, the activities of serum-GOT and serum-GPT increased after exposure to 7.15 ppm Cd indicating disturbed hepatic functions.     

Interrelationships between cadmium, zinc and antioxidants in the liver of the rat exposed orally to relatively high doses of cadmium and zinc

Zinc (Zn) reduces cadmium (Cd)-induced toxicity in the liver although it increases Cd tissue burden in some conditions; hence, the present study is designed to study the relationships between Cd, Zn and antioxidants in the liver of rats exposed to Cd. Livers of male rats which received orally relatively high doses of Cd (200 mg Cd/L as Cd chloride or Cd (200 mg/L)+Zn (500 mg Zn as Zn chloride) during five weeks, were investigated. Cd induced an accumulation of Cd and Zn in parallel to depletion in important variables (GSH, GSH/GSSG, CuZn-SOD and GPx activities) and to elevation in others (Cd/Zn and GSSG). Cd, did not affect CuZn SOD/GPx, nor Mn-SOD in the liver. Cd accumulation, Cd/Zn, CuZn SOD activity and CuZn SOD/GPx, was increased remarkably under Zn action. Zn supply ameliorated GSH level and partially reversed the decrease in GSH/GSSG, but it did not ameliorate GPx activity. Analysis showed high correlations between Cd and the majority of the variables, while Zn was positively correlated with only GSSG. We suggest from our results that Zn has indirect ameliorative effects on Cd-induced toxicity in the liver and that the increase in Cd retention is probably the key mechanism modulating, in the case of relatively high doses of Cd, the antioxidant response during exposure to Cd and Zn.     

Metal and Metallothionein Concentrations in Scoter (Melanitta spp.) from the Pacific Northwest of Canada, 1989–1994

Eighty-six surf (Melanitta perspicillata) and nine white winged (M. fusca) scoters were collected from 1989–1994 at 11 locations in British Columbia and the Yukon. Their kidney and liver tissues were analyzed for cadmium (Cd), copper (Cu), zinc (Zn), and metallothionein (MT) concentrations. Individual kidney Cd values ranged from 2.4 μg/g dry weight (DW) in birds from northern Vancouver Island to 390.2 μg/g (DW) in birds from the Queen Charlotte Islands, which is in the range of values potentially associated with kidney damage. Birds from the Queen Charlotte Islands also had high kidney Zn concentrations, which were significantly higher than values in birds from Naniamo and Westham Island on the south coast of BC. Cd values were significantly (p < 0.001) correlated with both Zn and MT concentrations in kidney tissue (r = 0.66 and 0.62, respectively). Male surf scoters had significantly higher kidney Cd and Zn levels than females, with mean Cd values of 47.3 and 19.7 μg/g DW (p < 0.002) for males and females, respectively. Mean Zn values were 120.8 and 108.0 μg/g DW (p < 0.05) for males and females, respectively. However, no sex differences were observed for either Cu or MT concentrations in kidney tissue. Individual MT values ranged from 2.7 to 416.8 μg/g wet weight (WW). Individual kidney Cu values ranged from 15.1 to 48.4 μg/g DW for both sexes. Kidney and liver Cd concentrations were significantly correlated (r = 0.90, p < 0.05) with kidney levels almost always higher than liver values. Although Cd accumulation by the Skidegate scoters was high, comparable tissue Cd values have been documented in other seabirds collected from the same general area, indicating elevated Cd concentrations in marine food chains around the Queen Charlotte Islands (Haida Gwaii) region of the Pacific coast. Received: 17 January 2002/Accepted: 2 June 2002     

Modulation of maltose preference by selection from dextrin, maltose and glucose diets in zinc-deficient rats

This study examined whether the chain length of glucose in the diet could affect the selection of foods by Zn-adequate and Zn-deficient rats. Dextrin, maltose and glucose were used as sources of carbohydrate in the diet and the selection patterns of the rats were analyzed for 28 d by a 3-choice selection. Diets provided as a set of three either Zn-adequate or Zn-deficient diets were rotated daily. The Zn-adequate control rats selected widely from the three diets throughout the 28 d. In contrast, rats fed a Zn-deficient diet selected exclusively and continuously the dextrin diet or dextrin and glucose diets from the three diets over the experimental periods. The average daily total food intakes of rats fed a Zn-deficient diet were very significantly decreased. The selections of dextrin, maltose and glucose diets in the 3-choice methods of the control rats were 5.7+/-1.6(b), 5.8+/-2.0(b) and 2.7+/-0.9(a) g/d, respectively (p<0.05), and those of the Zn-deficient rats were 6.4+/-2.5(c), 0.8+/-1.3(a) and 2.6+/-1.4(b) g/d, respectively (p<0.05). The ratios of the selected maltose-diet in the Zn-adequate control and the Zn-deficient rats were 40.8+/-13.8 and 9.0+/-15.6%, respectively (p<0.01) and those of the dextrin-diet were 40.3+/-11.4 and 63.0+/-22.3%, respectively (p<0.05). The decreased preference for the maltose-diet in the Zn-deficient rats may reflect the increased selection of the dextrin-diet.     

Metallothionein levels in liver and kidney of Canadians--a potential indicator of environmental exposure to cadmium

Liver and kidney cortex samples were obtained from 89 human autopsies for the determination of metallothionein (MT), cadmium (Cd), zinc (Zn), and copper (Cu). An age-dependent increase of Cd, Zn, and Cd/Zn was observed in the kidney; increases peaked at mid-age and were followed by a decline. Cadmium was present at a low constant level in the liver at all ages. The mean concentrations of Cd and Zn were 18.0 and 40.1 micrograms/g wet weight, respectively, in the kidney, and for the liver the values for Cd and Zn were 2.0 and 79.0 micrograms/g wet weight, respectively. A positive linear relationship was observed between Cd or Zn and MT in the kidney and between Zn and MT in the liver. No other correlation was found between Cu and MT in either organs. Similar values were obtained for MT when estimated by Ag-hem and Cd-hem methods.