Studies on biomarkers of copper exposure and toxicity in the marine amphipod Gammarus locusta (Crustacea): I. Induction of metallothionein and lipid peroxidation.

Sublethal exposures of the marine amphipod Gammarus locusta to a concentration range of copper (Cu) in water (4 days' exposure; 3, 5 and 10 micro g Cu l(-1)) or spiked sediments (28 days' exposure; 1, 3 and 6 mg Cu kg(-1) dry weight) were performed, and the resulting bioaccumulation of Cu and effects on putative metallothionein (MT) and lipid peroxidation (LP) were investigated. A time-course exposure study (over 10 days) to a single water-borne concentration of Cu (4 micro g l(-1)) was also carried out. MT and LP were quantified, respectively, by differential pulse polarography and as thiobarbituric acid-reactive malondialdehyde equivalents. The increasing levels of Cu in water and sediment exposures resulted in enhanced uptake of the metal by G. locusta. Synthesis of putative MT occurred in response to exposure to water-borne Cu, the levels being higher (p < 0.05) over the dose range of Cu compared with controls. A positive correlation was observed between putative MT levels and the Cu body-burden concentration (p < 0.001). However, no increase in LP was observed in these animals. In contrast, in the time-course experiment, LP levels increased within 1 day of exposure, subsequently peaking at 4 days (68% greater than control, p < 0.001), before returning to control values by day 6. Higher levels of MT were also observed in this exposure, but at days 6 and 10 (55% and 38%, respectively), paralleling the decrease in LP. No increase in MT levels was recorded with exposure to Cu-contaminated sediments, whereas higher levels of LP were seen in comparison with controls (p < 0.001). Overall, the inverse relationship between putative MT induction and the occurrence of LP indicates that MT may protect against the prooxidant effects of Cu. It is concluded that MT and LP offer potential for application as biomarkers in G. locusta.     

Urinary levels of metallothioneins and metals in subjects from a semiindustrialized area in Tarragona Province of Spain

The monitoring of heavy metals is important if adverse effects on health are to be avoided. In humans, metallothionein (MT) has been used as a biomonitor for the assessment of cadmium (Cd). In the present study, subjects drawn from the population of Tarragona Province (NE Spain) were investigated. Urinary MT, zinc (Zn), and copper (Cu) concentrations, corrected for creatine concentrations, were determined in 625 samples from healthy subjects aged between 10 and 65 yr. Mean values of MT and Cu in females were higher than those in males, with levels of 29.5 (23.8) vs. 22.7 (24.9) μg MT/creatinine (p<0.001) and 4.8 (6.1) vs 3.4 (4.9) μg Cu/g creatinine (p<0.001). No differences between males and females were observed with respect to urinary Zn: 78.0 (66.4) vs 73.0 (85.5) μg/g creatinine, respectively (p=0.332). Significantly higher MT, Zn, and Cu values were observed in the females aged 15–19 yr and, in the age group of 50–54 yr, only in the Zn and Cu values, when compared with those in males. Significant positive correlations of MT vs Zn and Cu as well as correlations of Zn vs Cu levels were observed in both genders. The present findings confirm the proposed role of MT as a biomonitor of mineral status.     

Airborne manganese exposure differentially affects end points of oxidative stress in an age-and sex-dependent manner

Juvenile female and male (young) and 16-mo-old male (old) rats inhaled manganese in the form of manganese sulfate (MnSO₄) at 0, 0.01, 0.1, and 0.5 mg Mn/m³ or manganese phosphate at 0.1 mg Mn/m³ in exposures of 6h/d, 5d/wk for 13 wk. We assessed biochemical end points indicative of oxidative stress in five brain regions: cerebellum, hippocampus, hypothalamus, olfactory bulb, and striatum. Glutamine synthetase (GS) protein levels, metallothionein (MT) and GS mRNA levels, and total glutathione (GSH) levels were determined for all five regions. Although most brain regions in the three groups of animals were unaffected by manganese exposure in terms of GS protein levels, there was significantly increased protein (p<0.05) in the hippocampus and decreased protein in the hypothalamus of young male rats exposed to manganese phosphate as well as in the aged rats exposed to 0.1 mg/m³ MnSO₄. Conversely, GS protein was elevated in the olfactory bulb of females exposed to the high dose of MnSO₄. Statistically significant decreases (p<0.05) in MT and GS mRNA as a result, of manganese exposure were observed in the cerebellum, olfactory bulb, and hippocampus in the young male rats, in the hypothalamus in the young female rats, and in the hippocampus in the senescent males. Total GSH levels significantly (p<0.05) decreased in the olfactory bulb of manganese exposed young male rats and increased in the olfactory bulb of female rats exposed to manganese. Both the aged and young female rats had significantly decreased (p<0.05) GSH in the striatum resulting from manganese inhalation. The old male rats also had depleted GSH levels in the cerebellum and hypothalamus as a result, of the 0.1-mg/m³ manganese phosphate exposure. These results demonstrate that age and sex are variables that must be considered whenassessing the neurotoxicity of manganese.     

Persistent alterations in biomarkers of oxidative stress resulting from combined in Utero and neonatal manganese inhalation

Neonatal female and male rats were exposed to airborne manganese sulfate (MnSO₄) during gestation and postnatal d 1–18. Three weeks post-exposure, rats were killed and we assessed biochemical end points indicative of oxidative stress in five brain regions: cerebellum, hippocampus, hypothalamus, olfactory bulb, and striatum. Glutamine synthetase (GS) protein levels, metallothionein (MT) and GS mRNA levels, and total glutathione (GSH) levels were determined for all five regions. Overall, there was a statistically significant effect of manganese exposure on decreasing brain GS protein levels (p=0.0061), although only the highest dose of manganese (1 mg Mn/m³) caused a significant increase in GS messenger RNA (mRNA) in both the hypothalamus and olfactory bulb of male rats and a significant decrease in GS mRNA in the striatum of female rats. This highest dose of manganese had no effect on MT mRNA in either males or females; however, the lowest dose (0.05 mg Mn/m³) decreased MT mRNA in the hippocampus, hypothalamus, and striatum in males. The median dose (0.5 mg Mn/m³) led to decreased MT mRNA in the hippocampus and hypothalamus of the males and olfactory bulb of the females. Overall, manganese exposure did not affect total GSH levels, a finding that is contrary to those in our previous studies. Only the cerebellum of manganese-exposed young male rats showed a significant reduction (p<0.05) in total GSH levels compared to control levels. These data reveal that alterations in biomarkers of oxidative stress resulting from in utero and neonatal exposures of airborne managanese remain despite 3 wk of recovery; however, it is important to note that the doses of manganese utilized represent levels that are 100-fold to a 1000-fold higher than the inhalation reference concentration set by the US Environmental Protection Agency.     

Effects of Ellagic Acid on Copper,Zinc, and Biochemical Values in Serum and Liver of Experimental Cholestatic Rats

Ellagic acid (EA) is a natural polyphenolic compound. Although, modulator effects of EA on copper (Cu) and zinc (Zn) levels in some liver diseases have been reported in experimental animals, its effects in obstructive jaundice (OJ) has not been clarified. We aimed to evaluate potential effects of EA on Cu and Zn levels in liver and serum of cholestatic rats. Forty Wistar albino rats were equally divided into four groups. First group was used as controls. Second group received EA (60 mg⁻¹ kg⁻¹ day⁻¹) for 8 days. Third was OJ group, and fourth group was OJ plus EA group. After 8 days, blood and liver samples were obtained. Higher serum and liver Cu and lower serum and liver Zn levels were found in OJ group (p < 0.05) compared with other groups. However, these differences reached to significant levels for Cu in serum and for Zn in lever. Higher serum copper levels were decreased, and lower liver Zn levels were increased by EA treatment in cholestatic rats (p < 0.05). Also, higher Cu/Zn ratio in OJ group was decreased by EA treatment both in liver (p < 0.05) and in serum (p < 0.05). Significantly higher serum bilirubin, alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase values were found in OJ and OJ + EA groups compared with the control and EA groups (p < 0.05). In conclusion, result of the current study indicated that ellagic acid has modulator effects on Cu and Zn levels in liver and serum of cholestatic rats.     

Oxidative stress is induced in the rat brain following repeated inhalation exposure to manganese sulfate

Eight-week-old rats inhaled manganese (Mn) in the form of MnSO₄ at 0, 0.03, 0.3, or 3.0 mg Mn/m³ for 6 h/d for 7 d/wk (14 consecutive exposures). Brain manganese concentrations in these animals were reported by Dorman et al. in 2001, noting the following rank order: olfactory bulb>striatum>cerebellum. We assessed biochemical end points indicative of oxidative stress in these three brain regions, as well as the hypothalamus and hippocampus. Glutamine synthetase (GS) protein levels and total glutathione (GSH) levels were determined for all five regions. GS mRNA and metallothionein (MT) mRNA levels were also evaluated for the cerebellum, hypothalamus, and hippocampus. Statistically significant increases (p<0.05) in GS protein were observed in the olfactory bulb upon exposure to the medium and high manganese doses. In the hypothalamus, statistically significant (p<0.05) but more modest increases were also noted in the medium and high manganese dose. Total GSH levels significantly (p<0.05) decreased only in the hypothalamus (high manganese dose), and MT mRNA significantly increased in the hypothalamus (medium manganese dose). No significant changes were noted in any of the measured parameters in the striatum, although manganese concentrations in this region were also increased. These results demonstrate that the olfactory bulb and hypothalamus represent potentially sensitive areas to oxidative stress induced by exceedingly high levels of inhaled manganese sulfate and that other regions, and especially the striatum, are resistant to manganese-induced oxidative stress despite significant accumulation of this metal.     

Levels of lipid peroxidation,nitric oxide,and antioxidant vitamins in plasma of patients with fibromyalgia

The etiology of fibromyalgia is not clearly understood. In recent years, a few studies have investigated the possible role of reactive oxygen species (ROS) in the etiology and pathogenesis of fibromyalgia. The aim of this study was to investigate plasma antioxidant vitamins, lipid peroxidation (LP), and nitric oxide (NO) levels in patients with fibromyalgia and controls. The study was performed on the blood plasma of 30 female patients and 30 age‐matched controls. After a fast of 12 h, blood samples were taken, and plasma samples were obtained for measurement of vitamins A, C, E, and β‐carotene concentrations and levels of LP and NO. Concentrations of vitamins A (p < 0.01) and E (p < 0.001) were significantly lower in patients with fibromyalgia than in controls, and LP levels were significantly (p < 0.05) higher in the plasma of the patients than in controls. Concentrations of vitamin C and β‐carotene and levels of NO did not change significantly. These results provide some evidence for a potential role of LP and fat‐soluble antioxidants in the patients with fibromyalgia. Copyright © 2009 John Wiley & Sons, Ltd.     

Effect of Protein Intake on Bone Mineralization during Weight Loss: A 6‐Month Trial

Objective: The long‐term effect of dietary protein on bone mineralization is not well understood. Research Methods and Procedures: Sixty‐five overweight (body mass index, 25 to 29.9 kg/m²) or obese (≥30 kg/m²) subjects were enrolled in a randomized, placebo‐controlled, 6‐month dietary‐intervention study comparing two controlled ad libitum diets with matched fat contents: high protein (HP) or low protein (LP). Body composition was assessed by DXA. Results: In the HP group, dietary‐protein intake increased from 91.4 g/d to a 6‐month intervention mean of 107.8 g/d (p < 0.05) and decreased in the LP group from 91.1 g/d to 70.4 g/d (p < 0.05). Total weight loss after 6 months was 8.9 kg in the HP group, 5.1 kg in the LP group, and none in the control group. After 6 months, bone mineral content (BMC) had declined by 111 ± 13 g (4%) in the HP group and by 85 ± 13 g (3%) in the LP group (not significant). Loss of BMC was more positively correlated with loss of body fat mass (r = 0.83; p < 0.0001) than with loss of body weight. Six‐month BMC loss, adjusted for differences in fat loss, was greater in the LP group than in the HP group [difference in LP vs. HP, 44.8 g (95% confidence interval, 16 to 73.8 g); p < 0.05]. Independent of change in body weight and composition during the intervention, highprotein intake was associated with a diminished loss of BMC (p < 0.01). Discussion: Body‐fat loss was the major determinant of loss of BMC, and we found no adverse effects of 6 months of high‐protein intake on BMC.     

Metallothionein induction related to hepatic structural perturbations and antioxidative defences in roach (Rutilus rutilus) exposed to the fungicide procymidone

A variety of stresses, hormones, glucocorticoids and cytokines are known to induce metallothioneins (MTs) in animals. The aim of this study was to investigate the effects of chemical stress induced by the dicarboximide fungicide procymidone on hepatic structure, MT content and antioxidative defences (catalase and glutathione reductase activities and glutathione content) in the common fish Rutilus rutilus. Catalase and glutathione reductase activities remained stable throughout the experiment. Four days of exposure to 0.2 or 0.4 mg l^?1 of procymidone induced an obvious increase in liver MT content, perturbation of metal MT contents, and an increase in hepatic glutathione content. After 14 days' exposure, obvious and large structural alterations of the hepatic parenchyma occurred simultaneously with a decrease in MT and glutathione content. These events were interpreted as degeneration of the liver. Fish exposed for 14 days to procymidone and then placed for 14 days in clean water showed nearly complete decontamination of the liver, but MT concentrations remained high. The toxicological significance of these events is discussed.     

Essential trace elements selenium, zinc, copper, and iron concentrations and their related acute-phase proteins in patients with vivax malaria

The aim of the present study is to evaluate the status of plasma essential trace elements selenium (Se), zinc (Zn), copper (Cu), and iron (Fe) concentrations and their related acute-phase proteins, ceruloplasmin (Cp), ferritin, transferrin (Tf), and albumin levels in patients with vivax malaria. Plasma Cu and Zn concentrations were determined by atomic absorption spectrometry (AAS). Se concentrations were determined by graphite furnace AAS. Fe, Cp, Tf, and albumin levels were determined by colorimetric methods. Plasma Se, Fe, and albumin levels were found to be significantly lower (p<0.01, p<0.001, and p<0.05, respectively) and Cu, Cp, and ferritin levels and Cu/Zn ratios were significantly higher (p<0.001, p<0.001, p<0.001, and p<0.05, respectively) in patients when compared with those of healthy subjects. Plasma, Tf, and Zn levels were not found to be significantly different (p>0.05) in patients and controls. There were positive important correlations between Cu and Cp (r=0.908, p<0.001), Zn and albumin (r=0.633, p<0.001), and negative correlations between Fe and ferritin content (r=−0.521, p<0.05) and Fe and Tf (r=−0.616, p<0.01) in the patients group. Our findings demonstrated that plasma essential trace elements Se, Cu, and Fe change, but these changes might be dependent on acute-phase proteins, which were regulated as a part of defense strategies of the organism, induced by hormonelike substances.     

Serum and tissue levels of six trace elements and copper/zinc ratio in patients with cervical cancer and uterine myoma

The aim of this study is to investigate the relationship between trace elements and the incidence of cervical cancer. Tissue and serum levels of six elements (Cu, Zn, Fe, Mn, Ca, and Se) and the Cu/Zn ratio in 40 cases of patients with cervical cancer, 30 cases of uterine myoma, and 50 healthy subjects were measured by atomic absorption spectrophotometry; the selenium content was determined by atomic fluorescence spectrometry. The results showed that the tissue contents of Zn, Se, and Ca were significantly lower and the Cu and Fe concentrations and Cu/Zn ratio were significantly higher in cervical cancer tissue than that for paired nonlesion tissue (p<0.02 and p<0.001, respectively). The serum levels of Zn, Se, Ca, and Fe were lower and Cu and Mn levels and Cu/Zn ratio were higher in patients with cervical cancer than in healthy subjects (p<0.01 and p<0.001, respectively) and in the uterine myoma group compared with healthy subjects (p< 0.05–0.001). There are no significant differences in the contents of six elements and the Cu/Zn ratio between uterine myoma tissue and paired nonlesion tissue. The results showed also that the Fe level and Cu/Zn ratio were significantly higher and the Zn and Se levels were significantly lower in cervical cancer tissue than in uterine myoma tissue (p<0.01 and p<0.001, respectively). The serum Cu level and Cu/Zn ratio were significantly higher in the cervical cancer group than the uterine myoma group (p<0.01). Data were also analyzed using multivarate logistic regression. After adjustment for age, occupation, life habit, and other covariates for the development of cervical cancer, the odds ratios were 22.64 (95% confidence interval [CI]: 5.64–90.88, p=0.001) for Cu, 0.11 (95% CI: 0.034–0.373; p=0.005) for Zn, and 0.60 (95% CI: 0.36–0.99, p=0.01) for Se. Thus, the serum and tissue levels of Cu increase and the deficiency of Zn and Se may be risk factors for the development of cervical cancer.     

Alterations of oxidative stress biomarkers due to in utero and neonatal exposures of airborne manganese

Neonatal rats were exposed to airborne manganese sulfate (MnSO₄) (0, 0.05, 0.5, or 1.0 mg Mn/m³) during gestation (d 0–19) and postnatal days (PNDs) 1–18. On PND19, rats were killed, and we assessed biochemical end points indicative of oxidative stress in five brain regions: cerebellum, hippocampus, hypothalamus, olfactory bulb, and striatum. Glutamine synthetase (GS) and tyrosine hydroxylase (TH) protein levels, metallothionein (MT), TH and GS mRNA levels, and reduced and oxidized glutathione (GSH and GSSG, respectively) levels were determined for all five regions. Mn exposure (all three doses) significantly (p=0.0021) decreased GS protein levels in the cerebellum, and GS mRNA levels were significantly (p=0.0008) decreased in the striatum. Both the median and high dose of Mn significantly (p=0.0114) decreased MT mRNA in the striatum. Mn exposure had no effect on TH protein levels, but it significantly lowered TH mRNA levels in the olfactory bulb (p=0.0402) and in the striatum (p=0.0493). Mn eposure significantly lowered GSH levels at the median dose in the olfactory bulb (p=0.032) and at the median and high dose in the striatum (p=0.0346). Significantly elevated (p=0.0247) GSSG, which can be indicative of oxidative stress, was observed in the cerebellum of pups exposed to the high dose of Mn. These data reveal that alterations of oxidative stress biomarkers resulting from in utero and neonatal exposures of airborne Mn exist. Coupled with our previous study in which similarly exposed rats were allowed to recover from Mn exposure for 3 wk, it appears that many of these changes are reversible. It is important to note that the doses of Mn utilized represent levels that are a hundred- to a thousand-fold higher than the inhalation reference concentration set by the United States Environmental Protection Agency.     

Spatiotemporal regulation of galectin-1-induced T-cell death in lamina propria from Crohn’s disease and ulcerative colitis patients

Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is characterized by chronic, relapsing intestinal inflammation. Galectin-1 (Gal-1) is an endogenous lectin with key pro-resolving roles, including induction of T-cell apoptosis and secretion of immunosuppressive cytokines. Despite considerable progress, the relevance of Gal-1-induced T-cell death in inflamed tissue from human IBD patients has not been ascertained. Intestinal biopsies and surgical specimens from control patients (n?=?52) and patients with active or inactive IBD (n?=?97) were studied. Gal-1 expression was studied by RT-qPCR, immunoblotting, ELISA and immunohistochemistry. Gal-1-specific ligands and Gal-1-induced apoptosis of lamina propria (LP) T-cells were determined by TUNEL and flow cytometry. We found a transient expression of asialo core 1-O-glycans in LP T-cells from inflamed areas (p?<?0.05) as revealed by flow cytometry using peanut agglutinin (PNA) binding and assessing dysregulation of the core-2 β 1-6-N-acetylglucosaminyltransferase 1 (C2GNT1), an enzyme responsible for elongation of core 2 O-glycans. Consequently, Gal-1 binding was attenuated in CD3⁺CD4⁺ and CD3⁺CD8⁺ LP T-cells isolated from inflamed sites (p?<?0.05). Incubation with recombinant Gal-1 induced apoptosis of LP CD3⁺ T-cells isolated from control subjects and non-inflamed areas of IBD patients (p?<?0.05), but not from inflamed areas. In conclusion, our findings showed that transient regulation of the O-glycan profile during inflammation modulates Gal-1 binding and LP T-cell survival in IBD patients.

     

Effects of acute manganese chloride exposure on lipid peroxidation and alteration of trace metals in rat brain

Although manganese (Mn) is an essential element, exposure to excessive levels of Mn and its accumulation in the brain can cause neurotoxicity and extrapyramidal syndrome. We have investigated the differences in the accumulated levels of Mn, the degree of lipid peroxidation, and its effects on the levels of trace elements (Fe, Cu, and Zn) in various regions in the brain of rats having undergone acute Mn exposure. The rats in the dose—effect group were injected intraperitoneally (ip) with MnCl₂ (25, 50, or 100 mg MnCl₂/kg) once a day for 24 h. The Mn significantly accumulated (p<0.05) in the frontal cortex, corpus callosum, hippocampus, striatum, hypothalamus medulla, cerebellum, and spinal cord in each case. The rats in the timecourse group were ip injected with MnCl₂ (50 mg MnCl₂/kg) and then monitored 12, 24, 48, and 72 h after exposure. The Mn accumulated in the frontal cortex, corpus callosum, hippocampus, striatum hypothalamus, medulla, cerebellum, and spinal cord after these periods of time, In both the dose—effect and time-course studies, we observed that the concentration of malondialdehyde, an end product of lipid peroxidation, increased significantly in the frontal cortex, hippocampus, striatum, hypothalamus, medulla, and cerebellum. However, no relationship between the concentrations of Mn in the brain and the extent of lipid peroxidation was observed. In addition, we found that there was a significant increase (p<0.05) in the level of Fe in the hippocampus, striatum, hypothalamus, medulla, and cerebellum, but the Cu and Zn levels had not changed significantly. These findings indicated that Mn induces an increase in the iron level, which provides direct evidence for Fe-mediated lipid peroxidation in the rats' brains; these phenomena might play important roles in the mechanisms of Mn-induced neurotoxicology.     

Relationship among levels of leptin and zinc,copper, and zinc/copper ratio in plasma of patients with essential hypertension and healthy normotensive subjects

Obesity is among the main contributing factors in the etiology of essential hypertension (EHT). Leptin, the product of the ob gene, is expressed mainly in adipose tissue. We examined the relationship between two trace elements, zinc (Zn) and copper (Cu), and leptin in patients with EHT (n=35) and normotensive (NT) controls (n=50) because leptin as well as Zn and Cu were reported to be associated with the pathophysiology of EHT. Plasma leptin levels were determined with a commercial enzyme-linked immunosorbent assay (ELISA) kit. Atomic absorption spectrophotometry was utilized to determine plasma Zn and Cu levels. There was a negative correlation between leptin and Zn, and the Zn/Cu ratio (r=−0.359, p<0.05; r=0.361, p<0.05, respectively) in pooled subjects. When subjects were divided based on the presence or absence of hypertension, there was a negative correlation between leptin and Zn (r=−0.375, p<0.05) as well as leptin and Zn/Cu ratio (r=−0.398, p<0.05) in NT subjects. Similar trends were observed when leptin/BMI (body mass index) levels were utilized. There was no significant correlations between levels of Cu and leptin or leptin/BMI. In conclusion, in addition to high leptin levels, Zn and the Zn/Cu ratio were lower in patients with EHT compared to NT controls.     

Copper kinetics and hepatic metallothionein levels in the frog Rana ridibunda, after exposure to CuCl2

Adult female frogs Rana ridibunda were exposed to 50 and 100 ppm of Cu (as CuCl₂) dissolved in water for 5, 15 and 30 days. We measured the Cu content in the liver, kidneys, ventral skin, and large intestine. Hepatic metallothionein (MT) was also measured and we identified by elution the type of proteins bound to copper. Gross morphological characteristics of the frogs were not affected by Cu accumulation. Cu uptake took place first across the skin, then accumulated first in the large intestine, and then in the liver which was continuously accumulating Cu at all exposure concentrations and times. The highest concentration of the metal was recorded in the kidneys at 30 days and 100 ppm exposure. It appears that the kidneys act as the secondary route of Cu detoxification, probably after a Cu overload of liver. The concentration of hepatic MT increased with the increase of Cu concentration in liver at the 5^th and 15^th day of exposure but we observed a decrease by the end of the experiment. Cu was observed in the MT-fraction, and in the high-molecular weight protein fraction.     

Selected trace elements and esterase activity of carbonic anhydrase levels in lambs with pneumonia

The levels of, zinc, copper, Fe, Zn, Cu, Mn, Mg, K, Na, and Cl and the activity of carbonic anhydrase were determined in lambs with pneumonia. A significant decrease of p<0.01 level in Zn concentration, in Cu level (p<0.001) and significant increases in K and Na levels (p<0.05) and of the Cu/Zn ratio (p<0.001) were observed in the study group. The carbonic anhydrase activity was decreased in the study group, but the decrease was not statistically significant (p>0.05). Also, nonsignificant decreases of Fe, Mg, and Cl and increase of the Mn concentration were also observed in the lambs with pneumonia (p>0.05). Our results suggest that the significant element changes reported here and the Cu/Zn ratio, but not the activity of carbonic anhydrase, can be used as indicators of pneumococcal infection.     

Effect of long-term swimming exercise on zinc,magnesium, and copper distribution in aged rats

Trace element content of different tissues might be altered by both age and exercise training. We aimed to determine the effects of a 1-yr swimming protocol (60 min/d, 5 day/wk) on tissue levels and the distribution of zinc (Zn), magnesium (Mg), and copper (Cu) in aging rats. Three groups were formed: sedentary and trained old groups and a young control group. Tissue Zn, Mg, and Cu concentrations were measured in the kidney, heart, liver, lungs, and gastrocnemius and soleus muscles. Kidney zinc concentration significantly decreased in the sedentary old group compared to the young control group (p<0.01) and was significantly higher in the trained old group compared to the sedentary old group (p<0.01), whereas Zn levels in the soleus muscle significantly increased in the sedentary old group in comparison to young controls (p<0.05). Tissue Mg concentrations remained unchanged. The sedentary old group exhibited a significant decrease in kidney Cu concentration compared to the young control group (p<0.01). Although kidney Cu levels also decreased in trained old rats in comparison to young controls (p<0.05), they were significantly higher than in sedentary old rats (p<0.01). The decrease in kidney Zn and Cu content as a result of aging was partly prevented by long-term swimming exercise.     

Alterations in plasma essential trace elements selenium, manganese, zinc, copper, and iron concentrations and the possible role of these elements on oxidative status in patients with childhood asthma

The aim of the present study is to evaluate the status of plasma essential trace element selenium (Se), manganese (Mn), copper (Cu), zinc (Zn), and iron (Fe) concentrations and the effect of these elements on oxidative status in patients with childhood asthma. Plasma Se, Mn, Cu, and Zn concentrations were determined by atomic absorption spectrophotometry (AAS) and Fe concentrations, malondialdehyde (MDA), and total antioxidant capacity (TAC) were determined by the colorimetric method. The plasma MDA/TAC ratio was calculated as an index of oxidative status. Plasma albumin levels were measured to determine nutritional status. Plasma Fe concentrations, MDA levels and the MDA/TAC ratio were significantly higher (p<0.001, p<0.001, and p<0.01, respectively) and Se and Mn concentrations and TAC were lower (p<0.01, p<0.05, and p<0.01, respectively) in patients when compared to the healthy subjects. Plasma Zn, Cu, and albumin levels were not found to be significantly different in patients and controls (p>0.05). There were positive relationships between plasma MDA and Fe (r=0.545, p<0.001) and TAC and Se (r=0.485, p<0.021), and a negative correlation between TAC and MDA values (r= −0.337, p<0.031) in patients with childhood asthma. However, there was no correlation between these trace elements and albumin content in patient groups. These observations suggest that increased Fe and decreased Se concentrations in patients with childhood asthma may be responsible for the oxidant/antioxidant imbalance.     

Copper-silicon interaction studies in young, rapidly growing turkeys fed semipurified starter diets

A 3 × 3 factorial experiment was conducted to study the interactions between Cu and Si in growing turkeys fed a basal dextrosecasein semipurified diet supplemented at 0, 270, and 540 ppm Si, and 2, 8, and 75 ppm Cu levels of inclusion. There were no significant (p>0.05) Cu, Si, or Cu-Si interaction effects on turkey growth. However, there were significant (p<0.05) Si effects on hemoglobin concentrations, and Cu−Si interaction effects on hematocrit and plasma Mg levels (p<0.01). Plasma Ca, P, Zn, Cu, total cholesterol, and serum alkaline phosphatase activity were not affected (p>0.05) by Cu, Si, or Cu−Si interaction. Heart and liver weights were affected (p<0.05) by the Cu-Si interaction. In general, a 8-ppm Cu supplemental level prevented cardiac hypertrophy only in the presence of 270 or 540 ppm Si inclusion in the diets. There were significant (p<0.05) Cu effects on liver Cu and Mn and heart Zn concentrations, Si effects on liver Mn levels, and Cu-Si interaction on liver Zn concentrations. Within the 0- and 270-ppm Si groups, Cu-deficient turkeys (2 ppm Cu) had higher liver Zn levels but not within the 540-ppm Si group. The Cu-Si interaction did not affect (p>0.05) concentrations of Cu in the heart and liver tissues. It is postulated that the Cu-Si interactions demonstrated in this study could have profound implications on the cardiovascular and skeletal health of birds.