Effects of Selenium on Liver and Muscle Contents and Urinary Excretion of Zinc,Copper, Iron and Manganese

Selenium is a main component of glutathione peroxidase (GPX), a key antioxidant enzyme. Other elements, such as zinc, copper, manganese and iron, are also involved in the pathogenesis of oxidative damage as well as in other important metabolic pathways. The effects of selenium supplementation on the metabolism of these elements have yield controversial results .The aim of this study is to analyse the effects of selenium supplementation on liver, muscle and urinary excretion of zinc, copper, iron and manganese in a situation of oxidative stress, such as protein deficiency. The experimental design included four groups of adult male Sprague–Dawley rats, which received the Lieber–DeCarli control diet, an isocaloric 2 % protein-containing diet and another similar two groups to which selenomethionine (6 mg/l liquid diet) was added. After sacrifice (5 weeks later), muscle, liver and serum selenium were determined, as well as muscle, liver and urinary zinc, copper, manganese and iron and liver GPX activity and liver malondialdehyde. Selenium addition led to decreased liver copper, increased muscle copper, increased copper excretion and increased liver iron, whereas zinc and manganese parameters were essentially unaltered. Muscle, liver and serum selenium were all significantly correlated with liver GPX activity.     

Manganese and ammonia interactions in the brain of cirrhotic rats: effects on brain ammonia metabolism

Hepatic encephalopathy is a major complication of cirrhosis. Ammonia and manganese have been associated with hepatic encephalopathy underlying mechanisms. Motor impairment and brain edema are common signs of hepatic encephalopathy. In the present study a model of liver damage in rats was combined with ammonia and manganese exposure to evaluate the role of these substances separately and their interactions on brain glutamine, water content and motor coordination. Additionally, we explored brain levels of each substance -Mn and ammonia- in the presence or absence of the other. Liver damage was induced by bile duct ligation. Rats were exposed to MnCl₂ in drinking water (1 mg Mn/ml) and to ammonia in chow pellets containing 20% ammonium acetate (w/w). As expected, manganese and ammonia levels increased in the brain of cirrhotic rats exposed to these substances; in these animals, glutamine brain levels also increased and positively correlated with tissue water content in cortex. A three way-ANOVA showed that manganese favored ammonia and glutamine accumulation in brain, and possibly their subsequent deleterious effects, as evidenced by the fact that manganese and ammonia accumulation in the brain of cirrhotic rats severely affected motor function. These results suggest that even when controlling ammonia levels in cirrhotic patients, reduction of manganese intake is also a potential strategy to be considered in clinical practice.     

The Effects of Chromium Histidinate on Mineral Status of Serum and Tissue in Fat-Fed and Streptozotocin-Treated Type II Diabetic Rats

The present study was conducted to investigate the effects of chromium histidinate (CrHis) against experimentally induced type II diabetes and on chromium (Cr), zinc (Zn), selenium (Se), manganese (Mn), iron (Fe), and copper (Cu) in serum, liver, and kidney of diabetic rats. The male Wistar rats (n = 60, 8 weeks old) were divided into four groups. Group I received a standard diet (12% of calories as fat); group II were fed standard diet and received CrHis (110 mcg CrHis/kg body weight per day); group III received a high-fat diet (HFD; 40% of calories as fat) for 2 weeks and then were injected with streptozotocin (STZ) on day 14 (STZ, 40 mg/kg i.p.; HFD/STZ); group IV were treated as group III (HFD/STZ) but supplemented with 110 mcg CrHis/kg body weight per day. The mineral concentrations in the serum and tissue were determined by atomic absorption spectrometry. Compared to the HFD/STZ group, CrHis significantly increased body weight and reduced blood glucose in diabetic rats (p < 0.001). Concentrations of Cr, Zn, Se, and Mn in serum, liver, and kidney of the diabetic rats were significantly lower than in the control rats (p < 0.0001). In contrast, higher Fe and Cu levels were found in serum and tissues from diabetic versus the non-diabetic rats (p < 0.001). Chromium histidinate supplementation increased serum, liver, and kidney concentrations of Cr and Zn both in diabetic and non-diabetic rats (p < 0.001). Chromium supplementation increased Mn and Se levels in diabetic rats (p < 0.001); however, it decreased Cu levels in STZ-treated group (p < 0.001). Chromium histidinate supplementation did not affect Fe levels in both groups (p > 0.05). The results of the present study conclude that supplementing Cr to the diet of diabetic rats influences serum and tissue Cr, Zn, Se, Mn, and Cu concentrations.     

Effect of dietary antioxidant supplementation on fresh semen quality in stallion

In this study, the effect of dietary supplementation of organic selenium, vitamin E, and zinc on raw semen characteristics was evaluated. Ten stallions with normal fertility were divided into two groups: a control group (CG), in which standard diet was provided, and a treated group (TG), in which the standard diet was supplemented with 1500 mg of α-tocopherol acetate, 360 mg of zinc, and 2.5 mg of organic selenium on a daily basis. Semen parameters on fresh semen were evaluated three times in all stallions before antioxidant supplementation (T0) and 30 (T1), 60 (T2), and 90 (T3) d after supplementation. Dietary supplementation with experimental antioxidants resulted in a significant increase in average path velocity (121.9 ± 3.1 μm/sec in TG vs 118.9 ± 4.3 μm/sec in CG), straightness (86.2 ± 2.4 % vs 82.6 ± 3.9 % in TG and CG respectively), viability (75.6 ± 10.2 % in TG vs 72.3 ± 6.9 % in CG) and total seminal plasma antioxidants levels (2.7 ± 0.5 mmol/l vs 1.9 ± 0.4 mmol/l in TG and CG respectively) while progressive motility 69.7 ± 11 % vs 62.2 ± 9.3 % in TG and CG stallions respectively) and abnormal sperm morphology (8.2±1.5 % in TG vs 14.4±4 % in CG) significantly improved in treated stallions after 60 d of supplementation. In contrast with previously reported in other species, a negative effect of antioxidant supplementation on semen concentration was recorded in the TG. A positive correlation between progressive motility and total antioxidants in seminal plasma in both treated and control stallions suggested that motility is affected by oxidative-antioxidative status, and that dietary antioxidant supplementation could increase the ability of spermatozoa to contrast reactive oxygen species or the ability of seminal plasma to reduce the oxidative stress. The improvement of semen parameters after antioxidant supplementation was not linear, and after 30 d (or 60 d for some parameters), a further increase was not noted. This evidence suggested that in our standard conditions, dietary intake of these antioxidants could be slightly under the dietary requirement and further evaluation of the actual nutrition requirements of organic selenium, zinc, and vitamin E in the stallion are needed.     

Effect of Allopurinol on the Hepatic and Cerebellar Iron,Selenium, Zinc and Copper Status Following Acute Ethanol Administration to Rats

An acute ethanol load (50mmol/kg, i.p.) induces an increase in the total non-heme iron and in the low-molecular-weight non-heme iron complexes (LMW-Fe) content both in liver and cerebellum. This increase in LMW-Fe is associated with a decrease in some essential trace elements (selenium, zinc, copper) playing a role in the anti-oxidant system. These changes could contribute to the enhancement in lipid peroxidation which occurs at the hepatic and cerebellar level following the ethanol administration.

The administration of allopurinol prior to the ethanol load prevents the changes in non-heme iron and trace elements. This prevention may contribute to the protective effects of allopurinol on the ethanol-induced oxidative stress.     

Serum concentration of zinc, copper, manganese and magnesium in patients with liver cirrhosis

The role of trace elements in the pathogenesis of liver cirrhosis and its complications is still not clearly understood. Serum concentrations of zinc, copper, manganese and magnesium were determined in 105 patients with alcoholic liver cirrhosis and 50 healthy subjects by means of plasma sequential spectrophotometer. Serum concentrations of zinc were significantly lower (median 0.82 vs. 11.22 micromol/L, p < 0.001) in patients with liver cirrhosis in comparison to controls. Serum concentrations of copper were significantly higher in patients with liver cirrhosis (median 21.56 vs. 13.09 micromol/L, p < 0.001) as well as manganese (2.50 vs. 0.02 micromol/L, p < 0.001). The concentration of magnesium was not significantly different between patients with liver cirrhosis and controls (0.94 vs. 0.88 mmol/L, p = 0.132). There were no differences in the concentrations of zinc, copper, manganese and magnesium between male and female patients with liver cirrhosis. Only manganese concentration was significantly different between Child-Pugh groups (p = 0.036). Zinc concentration was significantly lower in patients with hepatic encephalopathy in comparison to cirrhotic patients without encephalopathy (0.54 vs. 0.96 micromol/L, p = 0.002). The correction of trace elements concentrations might have a beneficial effect on complications and maybe progression of liver cirrhosis. It would be recommendable to provide analysis of trace elements as a routine.     

Protective role of intraperitoneally administered vitamin E and selenium in rats anesthetized with enflurane

The aim of this investigation was to determine levels of liver vitamins A and E and blood biochemical and hematological parameters in the enflurane anesthesia of rats. Fifty adult male Wistar rats were used in this study. All rats were randomly divided into five groups. The first and second groups were used as the control and anesthesia control groups, respectively, and only the placebo was intraperitoneally injected. The third group was intraperitoneally administered with vitamin E (dl/-α-tocopheryl acetate, 100 mg/kg body weight), the fourth group with Se (Na₂SeO₃ 1.5 mg/kg body weight), and the fifth group with vitamin E and Se (dl-α-tocopheryl acetate, 100 mg/kg body weight + Na₂SeO₃ 1.5 mg/kg body weight). This administration was done for three times with overday intervals and the second, third, forth, and fifth group rats were taken to enflurane anesthetise for 2 h. The liver vitamin E level was slightly lower in the anesthesia control group than in control group. However, the liver vitamin E content was significantly (p < 0.05 andp < 0.01) increased in vitamin E, Se, and combination groups, whereas the vitamin A level in liver was not statistically different. In general, plasma levels of alanine aminotransferase, creatin kinase, total bilirubin, urea, red blood cell counts, packet cell volume, and hemoglobulin values were significantly (p < 0.05 andp < 0.001) increased during the anesthesia and returned to near control values after the vitamin E plus selenium injection. However, administration of vitamin E had less effect on the hematological and biochemical parameters compared to that of selenium and their combination with vitamin E. However, the white blood cell count and levels of alkaline phosphatase, aspartate aminotransferase, total cholesterol, triglycerides, total protein, and creatinine were not statistically influenced by the anesthesia. In conclusion, we observed that plasma levels of some enzymes and metabolites were significantly increased in the enflurane anesthesia of rats, whereas the liver vitamin E levels were slightly decreased. Therefore, we observed that vitamin E and selenium have a protective effect against anesthesia complication, but the effect of selenium appears to be much greater than the vitamin E.     

Role of zinc in regulating the levels of hepatic elements following nickel toxicity in rats

This study was designed to determine the protective effects of zinc on the hepatotoxicity induced by nickel in rats. Female Sprague-Dawley (SD) rats received either nickel sulfate alone in the dose of 800 mg/L nickel in drinking water, zinc sulfate alone in the dose of 227 mg/L zinc in drinking water, and nickel plus zinc or drinking water alone for a total duration of 8 wk. The effects of different treatments were studied on activities of rat liver marker enzymes like alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferases (AST) and on the status of essential elements in rat liver. The study revealed a significant increase in the activities of enzymes ALP and ALT in rats subjected to nickel treatment. Interestingly, zinc supplementation to rats treated with nickel brought back the raised activities of these enzymes to within normal limits. Further, the levels of elements in liver that include zinc, copper, selenium, and potassium were found to be significantly suppressed following nickel treatment, whereas the levels of iron and sulfur were elevated. However, zinc treatment alone did not cause any appreciable change in the concentration of these elements. To the contrary, when zinc was given to nickel-treated rats, the concentrations of zinc, copper, potassium, and phosphorus were not significantly different from that of normal controls, whereas the levels of iron, selenium, and sulfur were improved in comparison to nickel-treated rats but were not within the normal limits. The present study concludes that zinc has the ability to maintain the levels of hepatic elements and has bearing in regulating the liver functions by maintaining the activities of marker enzymes in conditions of nickel toxicity.     

Protective effects of zinc in chlorpyrifos induced hepatotoxicity

The toxicological literature is replete with studies attempting to explain the mechanism of action of organophosphorus (OP) insecticides to their anticholinesterase activities, but not much is known about the metabolism and detoxification of these compounds. The goal of this study was to ascertain the toxic effects of chlorpyrifos, one of the most widely used OPs, on the liver of male rats and also to evaluate the protective potential of zinc in mediating its toxic effects. It was observed that chlorpyrifos (13.5 mg/kg body weight) treatment resulted in significant inhibition (p < 0.001) of serum and hepatic acetylcholinesterase (AChE) activities after 8 wk. However, zinc-treated (227 mg/L drinking water) animals resulted in significant normalization of the inhibited AChE activities. Similarly, a significant increase in the levels of various serum and liver marker enzymes (viz. alkaline phosphatase, aspartate aminotransferase [AST], and alanine aminotransferase [ALT]) was observed following treatment with chlorpyrifos. However, coadministration of zinc to these animals restored these enzymes to within normal limits, even though some increase in the activity of serum ALT and hepatic alkaline phosphatase still persisted at the end of the study. Chlorpyrifos treatment diminished serum and hepatic zinc levels significantly (p < 0.01 to p < 0.001) compared to normal control animals. Serum iron concentrations also plummeted significantly following chlorpyrifos treatment. On the contrary, serum copper levels were significantly increased (p < 0.01) in chlorpyrifos-treated animals, but they were normalized following zinc supplementation to the rats in this group. Interestingly, chlorpyrifos treatment resulted in elevated hepatic levels of copper, iron, and selenium, but zinc treatment could only partially restore the raised elemental concentrations. These data clearly demonstrate the potential role of zinc in mediating the toxic effects of chlorpyrifos, presumably because of their antioxidant properties and also their possible interaction with other trace elements in maintaining the cellular harmony.     

Impact of zinc,selenium and lycopene on capsaicin induced mutagenicity and oxidative damage in mice

Capsaicin is employed as a condiment and colorant in the cosmetic and pharmaceutical industries. Metabolism of capsaicin produces reactive phenoxy radicals, which inflict damage to DNA. Micronutrients such as zinc and selenium facilitate the expression of tissue repair factors, and lycopene has natural antioxidant action. The current study investigated the possible protective role of zinc, selenium and lycopene singly and in combination in ameliorating capsaicin induced mutagenicity. Fifty four Swiss albino mice received the vehicle, zinc (10 mg/kg), selenium (2 mg/kg), lycopene (2 mg/kg) alone, capsaicin alone (2 mg/kg), and capsaicin along with zinc (10 mg/kg), selenium (2 mg/kg) and lycopene (2 mg/kg) in combination by the oral route for 32 days. Animals were killed 24 h after the last treatment, and micronuclei formation in bone marrow and peripheral blood were assessed. Antioxidant status in plasma, the total protein, nucleic acids, and DNA fragmentation was assessed in the liver homogenate. Capsaicin substantially damaged nuclear material and increased oxidative stress. Individual therapy with lycopene was most effective in reducing micronuclei formation, lipid peroxidation, and in augmenting ferric reducing ability of plasma. This was closely followed by zinc and selenium. Zinc protected against DNA fragmentation followed by lycopene and selenium. The combination therapy was effective over individual treatment against DNA fragmentation, micronuclei and malondialdehyde formation. The combination did not exert a substantial benefit over individual therapy in enhancing the total antioxidant ability of plasma. The risk of capsaicin induced mutagenicity was lowered with the combination by reducing the generation of free radicals and by enhancing tissue repair.     

Effects of Aluminum Exposure on Bone Mineral Density,Mineral, and Trace Elements in Rats

The purpose of the study was to investigate the effects of aluminum (Al) exposure on bone mineral elements, trace elements, and bone mineral density (BMD) in rats. One hundred Wistar rats were divided randomly into two groups. Experimental rats were given drinking water containing aluminum chloride (AlCl₃, 430 mg Al³⁺/L), whereas control rats were given distilled water for up to 150 days. Ten rats were sacrificed in each group every 30 days. The levels of Al, calcium (Ca), phosphorus (P), magnesium (Mg), zinc (Zn), iron (Fe), copper (Cu), manganese (Mn), selenium (Se), boron (B), and strontium (Sr) in bone and the BMD of femur were measured. Al-treated rats showed lower deposition of Ca, P, and Mg compared with control rats. Levels of trace elements (Zn, Fe, Cu, Mn, Se, B, and Sr) were significantly lower in the Al-treated group than in the control group from day 60, and the BMD of the femur metaphysis in the Al-treated group was significantly lower than in the control group on days 120 and 150. These findings indicate that long-term Al exposure reduces the levels of mineral and trace elements in bone. As a result, bone loss was induced (particularly in cancellous bone).     

The effects of di(2-ethylhexyl) phthalate and/or selenium on trace element levels in different organs of rats

Di(2-ethylhexyl)phthalate (DEHP), a widely used plasticizer for synthetic polymers, is known to have endocrine disruptive potential, reproductive toxicity, and induces hepatic carcinogenesis in rodents. Selenium (Se) is a component of several selenoenzymes which are essential for cellular antioxidant defense and for the functions of mammalian reproductive system. The present study was designed to investigate the effects of DEHP exposure on trace element distribution in liver, testis, and kidney tissues and plasma of Se-deficient and Se-supplemented rats. Se deficiency was produced by feeding 3-week old Sprague-Dawley rats with ≤0.05 mg Se/kg diet for 5 weeks, and supplementation group were on 1 mg Se/kg diet. DEHP treated groups received 1000 mg/kg dose by gavage during the last 10 days of feeding period. Se, zinc (Zn), copper (Cu), iron (Fe) and manganese (Mn) levels were measured by inductively coupled plasma mass spectrometry (ICP-MS). Se supplementation caused significant increases in hepatic, renal, and testicular Se levels. With DEHP exposure, plasma Se and Zn, kidney Se, Cu and Mn levels were significantly decreased. Besides, liver Fe decreased markedly in all the DEHP-treated groups. Liver and kidney Mn levels decreased significantly in DEHP/SeD group compared to both DEHP and SeD groups. These results showed the potential of DEHP exposure and/or different Se status to modify the distribution pattern of essential trace elements in various tissues, the importance of which needs to be further evaluated.     

3-Alkynyl selenophene protects against carbon-tetrachloride-induced and 2-nitropropane-induced hepatic damage in rats

The aim of this study was to investigate the protective effect of 3-alkynyl selenophene (3-ASP) on acute liver injury induced by carbon tetrachloride (CCl₄) and 2-nitropropane (2-NP) in rats. On the first day of treatment, the animals received 3-ASP (25 mg/kg, p.o.). On the second day, the rats received CCl₄ (1 mg/kg, i.p.) or 2-NP (100 mg/kg, p.o.). Twenty-four hours after CCl₄ or 2-NP administration, the animals were euthanized, and their plasma and liver were removed for biochemical and histological analyses. The histological analysis revealed extensive injury in the liver of CCl₄-exposed and 2-NP-exposed rats, which was attenuated by 3-ASP. 3-ASP significantly attenuated (1) the increase in plasmatic aspartate and alanine aminotransferase activities and lipid peroxidation levels induced by CCl₄ and 2-NP; (2) the inhibition of δ-aminolevulinic dehydratase activity caused by 2-NP; and (3) the decrease in ascorbic acid (AA) levels and catalase (CAT) activity caused by CCl₄. AA levels and CAT activity remained unaltered in the liver of rats exposed to 2-NP. The protective effect of 3-ASP on acute liver injury induced by CCl₄ and 2-NP in rats was demonstrated.     

Allopurinol Enhances Adenine Nucleotide Levels and Improves Myocardial Function in Isolated Hypoxic Rat Heart

Allopurinol, a competitive inhibitor of xanthine oxidase, was found to have a protective effect on ischemic myocardium. Its mechanism of action is still controversial. We used Langendorff isolated rat heart preparation to test the hypothesis that allopurinol could maintain a level of the adenine nucleotide pool (ATP, ADP, and AMP) that would protect and improve the functional activity of the heart during a period of hypoxia. Hearts were initially perfused for 30 min until steady state was attained. This was followed by 20 min of experimental perfusion divided into 5 min of control perfusion followed by 15 min of hypoxic perfusion with or without allopurinol in the perfusate. Hearts were quick-frozen and enzymatically analyzed for adenine nucleotides and creatine phosphate at the end of the hypoxic period. Left ventricular pressure, heart rate, and coronary flow were measured in all preparations. Allopurinol (0.1 mM) treated hearts had greater levels of ATP (12.3 ± 0.8 vs. 9.3 ± 0.8 µmol/g dry weight; p < 0.01). This improvement occurred in the presence as well as the absence of glucose. Total adenine nucleotides improved from 17 ± 1 to 20.3 ± 2.4 µmol/g dry weight (p < 0.01). This improvement also occurred in the presence as well as in the absence of glucose in the perfusate. It also improved cell energy state significantly in the presence as well as the absence of glucose. There was insignificant change in creatine phosphate. Allopurinol improved left ventricular pressure from 38 ± 7% to 55 ± 9% (p < 0.002) in the presence of glucose and from 8 ± 3% to 27 ± 6.3% (p < 0.001) in the absence of glucose. Coronary flow improved from 110 ± 5% to 120 ± 8% (p < 0.04) in the presence of glucose. These results support the suggestion that allopurinol at 0.1 mM exerts its protective effect on rat heart during hypoxia by enhancing the adenine nucleotide pool.     

Nitric Oxide Production in Striatum and Pallidum of Cirrhotic Rats

Ammonium and manganese are neurotoxic agents related to brain metabolic disturbances observed after prolonged liver damage. The aim of this study was to assess the production of nitric oxide (NO) in the brain of cirrhotic rats exposed to manganese. We induced cirrhosis by bile duct ligation for 4 weeks in rats. From brain, striatum and globus pallidus were dissected out, and NO synthase activity and the content of nitrites plus nitrates (NOx) were determined. In pallidum we found a diminished constitutive NO synthase activity from cirrhotic rats, independently of manganese exposure. This result was confirmed by low levels of NOx in the same brain area (P<0.05, two-way ANOVA). This finding was not related to protein expression of NO synthase since no differences were observed in immunoblot signals between cirrhotic and sham-operated animals. Results from present study suggest that the production of NO is reduced in basal ganglia during cirrhosis.     

Ceruloplasmin, Copper, Selenium, Iron, Zinc, and Manganese Levels in Normal and Sulfite Oxidase Deficient Rat Plasma: Effects of Sulfite Exposure

A noticeable effect of sulfite treatment was observed on the plasma ceruloplasmin ferroxidase activity of rats with normal sulfite oxidase activity when compared to normal controls. The plasma levels of selenium, iron, and zinc were unaffected by sulfite in normal and sulfite oxidase (SOX)-deficient rats. While plasma level of Mn was decreasing, plasma Cu level increased in SOX-deficient rats. Treating SOX-deficient groups with sulfite did not alter plasma level of Mn but made plasma level of Cu back to its normal level. This is the first evidence that Cu and Mn status were affected in experimental sulfite oxidase deficiency induced by low molybdenum diet with tungsten addition deserving further research to determine the underlying mechanisms of these observations in experimental sulfite oxidase deficiency.     

Differential effects of dietary selenium (Se) and folate on methyl metabolism in liver and colon of rats

A previous study compared the effects of folate on methyl metabolism in colon and liver of rats fed a selenium-deficient die (<3 μg Se/kg) to those of rats fed a diet containing supranutritional Se (2 mg selenite/kg). The purpose of this study was to investigate the effects of folate and adequate Se (0.2 mg/kg) on methyl metabolism in colon and liver. Weanling, Fischer-344 rats (n=8/diet) were fed diets containing 0 or 0.2 mg selenium (as selenite)/kg and 0 or 2 mg folic acid/kg in a 2×2 design. After 70 d, plasma homocysteine was increased (p<0.0001) by folate deficiency; this increase was markedly, attenuated (p<0.0001) in rats fed the selenium-deficient diet compared to those fed 0.2 mg Se/kg. The activity of hepatic glycine N-methyltransferase (GNMT), an enzyme involved in the regulation of tissue S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), was increased by folate deficiency (p<0.006) and decreased by selenium deprivation, (p<0.0003). Colon and liver SAH were highest (p<0.006) in rats fed deficient folate and adequate selenium. Although folate deficiency decreased liver SAM (p<0.001), it had no effect on colon SAM. Global DNA methylation was decreased (p<0.04) by selenium deficiency in colon but not liver; folate had no effect. Selenium, deficiency did not affect DNA methyltransferase (Dnmt) activity in liver but tended to decrease (p<0.06) the activity of the enzyme in the colon. Dietary folate did not affect liver or colon Dnmt. These results in rats fed adequate selenium are similar to previous results found in rats fed supranutritional selenium. This suggests that selenium deficiency appears to be a more important modifier of methyl metabolism than either adequate or supplemental selenium. The U.S. Department of Agriculture, Agriculture Research Service, Northern Plains Area, is an equal opportunity/affirmative action employer and all agency services are available without discrimination.     

Variability of selected trace elements of different meat cuts determined by ICP-MS and DRC-ICPMS

The aim of this study was to determine the levels of cadmium, lead, iron, zinc, selenium, manganese, copper and molybdenum in different cuts of beef, pork, lamb, chicken and foal collected from supermarkets and butcheries in Switzerland. The concentrations of manganese, copper, molybdenum, zinc, iron, selenium, cadmium and lead were determined by inductively coupled plasma mass spectrometry (ICP-MS) after microwave digestion. Mean values and their respective coefficients of variation were calculated from the measured concentrations. The concentrations found for cadmium and lead ranged from 0.6 to 3.9 μg/100 g and 1.0 to 2.1 μg/100 g, respectively. Concentrations ranged between 0.5 and 3.3 mg/100 g for iron, 0.7 and 5.1 mg/100 g for zinc, 9 and 44 μg/100 g for selenium, 3.1 and 16.7 μg/100 g for manganese, 0.3 and 132 μg/100 g for copper and 0.9 and 3.2 μg/100 g for molybdenum. Differences found for the concentrations in meat from different species as well as between the individual meat cuts were notable for iron, zinc, selenium and copper. Manganese concentrations were found to vary unsystematically within muscles and species. Molybdenum concentrations were higher in chicken meat in comparison with the mammalian meats. The highest coefficients of variation were found for manganese (13% to 142%) and copper (13% to 224%), while the lowest was found for zinc (4% to 45%). In conclusion, in order to provide an accurate overview and to be able to calculate reliable dietary intakes, it is important to include the variability in food composition data.     

Effects of iron deficiency and iron overload on manganese uptake and deposition in the brain and other organs of the rat

Managanese (Mn) is an essential trace element at low concentrations, but at higher concentrations is neurotoxic. It has several chemical and biochemical properties similar to iron (Fe), and there is evidence of metabolic interaction between the two metals, particularly at the level of absorption from the intestine. The aim of this investigation was to determine whether Mn and Fe interact during the processes involved in uptake from the plasma by the brain and other organs of the rat. Dams were fed control (70 mg Fe/kg), Fe-deficient (5–10 mg Fe/kg), or Fe-loaded (20 g carbonyl Fe/kg) diets, with or without Mn-loaded drinking water (2 g Mn/L), from day 18–19 of pregnancy, and, after weaning the young rats, were continued on the same dietary regimens. Measurements of brain, liver, and kidney Mn and nonheme Fe levels, and the uptake of⁵⁴Mn and⁵⁹Fe from the plasma by these organs and the femurs, were made when the rats were aged 15 and 63 d. Organ nonheme Fe levels were much higher than Mn levels, and in the liver and kidney increased much more with Fe loading than did Mn levels with Mn loading. However, in the brain the increases were greater for Mn. Both Fe depletion and loading led to increased brain Mn concentrations in the 15-d/rats, while Fe loading also had this effect at 63 d. Mn loading did not have significant effects on the nonheme Fe concentrations.⁵⁴Mn, injected as MnCl₂ mixed with serum, was cleared more rapidly from the circulation than was⁵⁹Fe, injected in the form of diferric transferrin. In the 15-d-rats, the uptake of⁵⁴Mn by brain, liver, kidneys, and femurs was increased by Fe loading, but this was not seen in the 63-d rats. Mn supplementation led to increased⁵⁹Fe uptake by the brain, liver, and kidneys of the rats fed the control and Fe-deficient diets, but not in the Fe-loaded rats. It is concluded that Mn and Fe interact during transfer from the plasma to the brain and other organs and that this interaction is synergistic rather than competitive in nature. Hence, excessive intake of Fe plus Mn may accentuate the risk of tissue damage caused by one metal alone, particularly in the brain.