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A supplementation trial starting with 224 postmenopausal women provided with adequate vitamin D and Ca was conducted to determine whether increased Cu and Zn intakes would reduce the risk for bone loss. Healthy women aged 51-80 years were recruited for a double-blind, placebo-controlled study. Women with similar femoral neck T scores and BMI were randomly assigned to two groups of 112 each that were supplemented daily for 2 years with 600 mg Ca plus maize starch placebo or 600 mg Ca plus 2 mg Cu and 12 mg Zn. Whole-body bone mineral contents, densities and T scores were determined biannually by dual-energy X-ray absorptiometry, and 5 d food diaries were obtained annually. Repeated-measures ANCOVA showed that bone mineral contents, densities and T scores decreased from baseline values to year 2. A priori contrasts between baseline and year 2 indicated that the greatest decreases occurred with Cu and Zn supplementation. Based on 5 d food diaries, the negative effect was caused by Zn and mainly occurred with Zn intakes ≥ 8·0 mg/d. With Zn intakes < 8·0 mg/d, Zn supplementation apparently prevented a significant decrease in whole-body bone densities and T scores. Food diaries also indicated that Mg intakes < 237 mg/d, Cu intakes < 0·9 mg/d and Zn intakes < 8·0 mg/d are associated with poorer bone health. The findings indicate that Zn supplementation may be beneficial to bone health in postmenopausal women with usual Zn intakes < 8·0 mg/d but not in women consuming adequate amounts of Zn.

Objective: High-fat and marginally copper-deficient diets impair heart function, leading to cardiac hypertrophy, increased lipid droplet volume, and compromised contractile function, resembling lipotoxic cardiac dysfunction. However, the combined effect of the two on cardiac function is unknown. This study was designed to examine the interaction between high-fat and marginally copper-deficient diets on cardiomyocyte contractile function., Research Methods and Procedures: Weanling male rats were fed diets incorporating a low- or high-fat diet (10% or 45% of kcal from fat, respectively) with adequate (6 mg/kg) or marginally deficient (1.5 mg/kg) copper content for 12 weeks. Contractile function was determined with an IonOptix system including peak shortening (PS), time-to-PS, time-to-90% relengthening, maximal velocity of shortening/relengthening, and intracellular Ca(2+) ([Ca(2+)](I)) rise and decay., Results: Neither dietary treatment affected blood pressure or glucose levels, although the high-fat diet elicited obesity and glucose intolerance. Both diets depressed PS, maximal velocity of shortening/relengthening, and intracellular Ca(2+) ([Ca(2+)](I)) rise and prolonged time-to-90% relengthening and Ca(2+) decay without an additive effect between the two. Ca(2+) sensitivity, apoptosis, lipid peroxidation, nitrosative damage, tissue ceramide, and triglyceride levels were unaffected by either diet or in combination. Phospholamban (PLB) but not sarco(endo)plasmic reticulum Ca(2+)-ATPase was increased by both diets. Endothelial NO synthase was depressed with concurrent treatments. The electron transport chain was unaffected, although mitochondrial aconitase activity was inhibited by the high-fat diet., Discussion: These data suggest that high-fat and marginally copper deficient diets impaired cardiomyocyte contractile function and [Ca(2+)](i) homeostasis, possibly through a similar mechanism, without obvious lipotoxicity, nitrosative damage, and apoptosis.

Sensitivity of the assay for Cu,Zn superoxide dismutase 3 (SOD3), the predominant form of SOD in serum, can be increased, and interferences caused by low-molecular-weight substances in the serum can be reduced by conducting the assay at pH 10 with xanthine/xanthine oxidase and acetylated cytochrome c (cyt c) as superoxide generator and detector, respectively. Serum SOD3 activity was assayed under these conditions in an experiment where weanling, male rats were fed diets for 6 weeks containing 3, 5 and 15 mg Zn/kg with dietary Cu set at 0.3, 1.5 and 5 mg Cu/kg at each level of dietary Zn. Serum SOD3 responded to changes in dietary Cu but not to changes in dietary Zn. A second experiment compared serum SOD3 activity to traditional indices of Cu status in weanling, male and female rats after they were fed diets containing, nominally, 0, 1, 1.5, 2, 2.5, 3 and 6 mg Cu/kg for 6 weeks. Serum SOD3 activity was significantly lower (P < .05) in male rats fed diets containing 0 and 1 mg Cu/kg and female rats fed diet containing 0 mg Cu/kg compared with rats fed diet containing 6 mg Cu/kg. These changes were similar to changes in liver Cu concentrations, liver cyt c oxidase (CCO) activity and plasma ceruloplasmin in males and females. Serum SOD3 activity was also strongly, positively correlated with liver Cu concentrations over the entire range of dietary Cu concentrations (R(2) = .942 in males, R(2) = .884 in females, P < .0001). Plots of serum SOD3 activity, liver Cu concentration, liver CCO activity and ceruloplasmin as functions of kidney Cu concentration all had two linear segments that intersected at similar kidney Cu concentrations (18-22 microg/g dry kidney in males, 15-17 microg/g dry kidney in females). These findings indicate that serum SOD3 activity is a sensitive index of Cu status.

The mechanism for reduced Fe absorption in Cu deficiency is unknown, but may involve the intestinal Cu-dependent ferroxidase, Hephaestin (Hp). A 2 x 2 factorial experiment was designed to include Cu-deficient (CuD) and Cu-adequate (CuA) male and female rats. Weanling rats of both sexes were randomly divided into 2 groups each and fed an AIN-93G diet with low (<0.3 mg/kg; CuD) or adequate Cu (5.0 mg/kg; CuA). After 19 d, rats were fed 1.0 g each of their respective diets labeled with (59)Fe. Retained (59)Fe was monitored by whole-body counting for 12 d. Then, rats were killed for (59)Fe and Fe measurements in blood and various organs. Duodenal enterocytes were isolated for Western blot analysis of Hp. Signs of Cu and Fe deficiency were evident in both sexes. CuD male rats absorbed 60% as much Fe as CuA male rats (P < 0.001), whereas CuD female rats absorbed 70% (P < 0.001) as much as CuA females, with no difference between the sexes. Hp protein in enterocytes of CuD rats of both sexes was only 35% of that in CuA rats. The biological half-life of (59)Fe in CuD rats was only 50% (P < 0.001) of that in CuA rats, suggesting that Fe turnover was faster in CuD rats than CuA rats. Serum, spleen, and kidney Fe were lower (P < 0.001) in CuD rats than in CuA rats. Duodenal mucosa and liver Fe were higher (P < 0.01) in CuD male rats than CuA rats. Duodenal Fe but not liver Fe was higher in CuD female rats than CuA rats. Liver Fe was much higher (<0.001) overall in females than males. The data suggest that Cu deficiency reduces Fe absorption in rats through reduced expression of duodenal Hp protein.

Dietary nutrient interactions are important factors to consider in the study of nutrient status and requirements. Here, the effects of dietary interactions among copper (Cu), iron (Fe), manganese (Mn) and sulfur amino acids (SAA) on blood cell characteristics and enzyme activities were observed. Male rats (n = 8) were used in a 2 x 2 x 2 x 2 factorial design and fed an AIN-93G-based diet containing dietary Cu (<1 and 5 mg/kg), Fe (10 and 35 mg/kg), Mn (10 and 50 mg/kg) and either L-cystine (LCys) or DL-methionine (DLMet). Blood was analyzed by automated hematology cell counting and by flow cytometry. Severe Cu deficiency was verified by reductions in the activities of serum ceruloplasmin (1% of control), RBC superoxide dismutase (SOD1) (14% of control), liver cytochrome c oxidase activity (25% of control) and serum extracellular SOD (SOD3) activity (20% of controls). Because Cu is required for Fe utilization, many physiologic responses that require Fe were affected by both deficiencies, including lowered blood hemoglobin (Hgb), lower RBC volume and Hgb concentration, and an increased number of reticulocytes. Cu and Fe deficiencies together worsened some conditions, i.e., lower Hgb, lower RBC Hgb, increased RBC distribution width, increased number of reticulocytes and nucleated RBC, and a higher platelet count. Increasing dietary Mn had little effect on most variables, except to reduce serum Cu when dietary Cu was adequate but not when it was low, and to reduce RBC SOD1 activity when dietary Fe was low but not when it was adequate. Hgb concentrations were higher (P < 0.002) in Cu-deficient rats fed LCys than in those fed DLMet. There was no effect in Cu-adequate rats. Hgb was higher (P < 0.004) in Fe-adequate rats fed LCys than in those fed DLMet, with no effect in Fe-deficient rats. Although the anemia of Cu deficiency in AIN-93G-fed rats was not as pronounced as that reported in rats fed the AIN-76A-based diet, other manifestations of the deficiency were prominent.

This study examined the effects of graded intakes of zinc (Zn) and copper (Cu) on serum insulin-like growth-factor-I (IGF-I) concentration and bone quality in growing rats. Using a 3 x 4 factorial design, weanling male Sprague-Dawley rats were randomly assigned to 12 groups (n = 7 per group) and were fed one of nine modified AIN-93G basal diets with varying amounts of Cu (0.3, 3 and 10 micro g/g) and Zn (5, 15 and 45 micro g/g) for 6 wk. A group of rats was pair-fed to each low Zn group. Although dietary Zn mainly influenced body weights (P < 0.0001), dietary Cu was the main determinant of most of the variables related to bone quality. Low Cu intake reduced serum IGF-I and femur breaking force and ultimate stress (by 27, 14 and 7%, respectively; P < 0.05) and increased bone IGF-I concentration (by 62%; P < 0.0001). Low Cu intake also increased femur nitrogen, hydroxyproline, hexosamine and calcium (Ca) concentrations of long bones (P < 0.05). Lumbar vertebrae dry weight and density were the lowest in the rats fed the low Cu diets (P < 0.001) and were higher in the rats fed high amounts of both Cu and Zn (P < 0.01). In summary, growing rats fed low and marginal Cu had lower serum IGF-I than those fed high dietary Cu. Bone strength was also reduced with low dietary Cu, despite compensatory changes in the bone matrix. In the presence of graded intakes of Cu, the effects of low dietary Zn were more pronounced on the spinal bones than the long bones.

Heat acclimation (HA) reportedly conveys conservation in sweat micromineral concentrations when sampled from arm sweat, but time course is unknown. The observation that comprehensive cleaning of the skin surface negates sweat micromineral reductions during prolonged sweating raises the question of whether the reported HA effect is real or artifact of surface contamination. Purpose: To measure sweat mineral concentrations serially during HA and determine if surface contamination plays a role in the reported mineral reductions. Methods: Calcium (Ca), copper (Cu), magnesium (Mg), and zinc (Zn) were measured in sweat obtained from 17 male volunteers using an arm bag on Day 1, 5, and 10 of a HA protocol. To study the role of contamination, sweat was simultaneously (n = 10 subjects) sampled twice daily from a cleaned site (WASH) and unclean site (NO WASH) on the scapular surface. Results: Sweat Ca, Cu, and Mg from Arm Bag trended progressively downward from Day 1 to Day 10 of HA (p = .10–0.25). Micromineral concentrations from the WASH site did not change between Day 1, 5, or 10 (Ca = 0.30 ± 0.12 mmol/L, Cu 0.41 ± 0.53 μmol/L; Zn 1.11 ± 0.80 μmol/L). Surface contamination can confound sweat mineral estimates, as sweat Ca and Cu from NO WASH site were initially higher than WASH (p < .05) but became similar to WASH when sampled serially. Conclusion: Heat acclimation does not confer reductions in sweat Ca, Cu, Mg, or Zn. When the skin surface is not cleaned, mineral residue inflates initial sweat mineral concentrations. Earlier reports of micromineral reductions during HA may have been confounded by interday cleaning variability. [ABSTRACT FROM AUTHOR]

Context: Uncertainty exists regarding the effect of sustained sweating on sweat mineral-element composition. Purpose: To determine the effect of multiple hours of exercise-heat stress on sweat mineral concentrations. Methods: Seven heatacclimated subjects (6 males, 1 female) completed 5x 60 min of treadmill exercise (1.56 m/s, 2% grade) with 20 min rest between exercise periods in 2 weather conditions (27 °C, 40% relative humidity, 1 m/s and 35 °C, 30%, 1 m/s). Sweat was collected from a sweat-collection pouch attached to the upper back during exercise bouts 1, 3, and 5. Mineral elements were determined by using inductively coupled plasma-emission spectrography. Results: At 27 °C, sweat sodium (863 [563] µg/mL; mean [SD]), potassium (222 [48] µg/mL), calcium (16 [7]) µg/mL), magnesium (1265 [566] ng/mL), and copper (80 [56] ng/mL) remained similar to baseline over 7 h of exercise-heat stress, whereas sweat zinc declined 42-45% after the initial hour of exercise-heat stress (Ex1 = 655 [362], Ex3 = 382 [168], Ex5 = 355 [288] µg/mL, P < 0.05). Similar outcomes were observed for sweat zinc at 35 °C when sweat rates were higher. Sweat rate had no effect on sweat trace-element composition. Conclusions: Sweat sodium, potassium, and calcium losses during multiple hours of sustained sweating can be predicted from initial sweat composition. Estimates of sweat zinc losses, however, will be overestimated if sweat zinc conservation is not accounted for in sweat zinc-loss estimates. [ABSTRACT FROM AUTHOR]

Several sweat mineral element concentrations decline with serial sampling. Possible causes include reduced dermal mineral concentrations or flushing of surface contamination. The purpose of this study was to simultaneously sample mineral concentrations in transdermal fluid (TDF), sweat, and serum during extended exercise-heat stress to determine if these compartments show the same serial changes during repeat sampling. Sixteen heat-acclimated individuals walked on a treadmill (1.56 m/s, 3.0% grade) in a 35°C, 20% relative humidity (RH), 1 m/s wind environment 50 min each hour for 3 h. Mineral concentrations of Ca, Cu, Fe, K, Mg, Na, and Zn were measured each hour from serum, sweat from upper back (sweat pouch) and arm (bag), and TDF from the upper back. Sites were meticulously cleaned to minimize surface contamination. Mineral concentrations were determined by spectrometry. TDF remained stable over time, with exception of a modest increase in TDF [Fe] (15%) and decrease in TDF [Zn] (-18%). Likewise, serum and pouch sweat samples were stable over time. In contrast, the initial arm bag sweat mineral concentrations were greater than those in the sweat pouch, and [Ca], [Cu], [Mg], and [Zn] declined 26-76% from initial to the subsequent samples, becoming similar to sweat pouch. Nominal TDF mineral shifts do not affect sweat mineral concentrations. Arm bag sweat mineral concentrations are initially elevated due to skin surface contaminants that are not removed despite meticulous cleaning (e.g., under fingernails, on arm hair), then decrease with extended sweating and approach those measured from the scapular region. [ABSTRACT FROM AUTHOR]

The article presents the study which sought to examine the impact of 10 days of exercise-heat acclimation on sweat mineral concentrations. Researchers recruited eight male subjects who walked on a treadmill at 3.5 miles per hour (mph), 4% grade for 100 continuous minutes or until rectal temperature reached 39.5°C on 10 consecutive days in an environmental chamber set at 45°C. Results of the study showed that heat acclimation had induced significantly lower sweat concentrations and estimated whole-body sweat losses for calcium, copper and magnesium.