Linda Strause

The effect of deficiencies of manganese and copper on osteoinduction and on resorption of bone particles in rats

SummarySubcutaneous implantation of devitalized demineralized bone powders (DBP) and mineral-containing bone particles (BP) into rats raised on either a control (C), low manganese and low copper (L), or manganese-deplete (D) diet, allowed the separate evaluation of bone formation and of bone resorption, respectively. DBP failed to induce chondrogenesis or osteogenesis in D rats. Cartilage formation was delayed in the L rats compared to C rats. There was significantly less resorption of BP by L and D rats than C rats. These results show multiple cellular effects of long-term manganese (Mn) and copper (Cu) deficiencies on bone metabolism including decreased osteogenesis and a decrease in osteoclast activity.

Effects of exercise on iron metabolism in rats

Abstract The effect of exercise on the uptake, redistribution, and excretion of iron was studied in normal iron-sufficient rats. Rats were run to exhaustion in a “sprint” protocol seven times over a twentyone day period. Exercised rats did not differ significantly from sedentary rats in hemoglobin concentrations or in body or organ weights. Exercised rats absorbed more iron than sedentary rats in radioiron tracer studies. Radioiron accumulated mainly in heart, liver, and spleen. Strikingly, tracer iron accumulated significantly in hearts of exercised rats. Exercised rats had less total iron in liver and spleen than sedentary rats. Myoglobin concentrations in heart and soleus muscles were significantly higher in rats after the exercise regimen and decreased following fourteen days of rest. Brief, strenuous exercise appears to signal increased absorption of iron and to stimulate the redistribution of storage iron. This mobilization of iron during exercise may be directed towards the enhancement of oxygen-accepting ability in muscles at work.

Transitory hematologic effects of moderate exercise are not influenced by iron supplementation

SummaryA young womens exercise/fitness class tested the idea that administration of supplemental iron would prevent “sports anemia” that may develop during exercise and training and improve iron status of exercising females of menstrual age. Fifteen women (aged 18–37) were selected for each of three treatment groups: (1) no supplemental iron; (2) 9 mg·d−1 of Fe; and (3) 18 mg·d−1 of Fe (1 US Recommended Daily Allowance). Women exercised at approximately 85% of maximal heartrate for progressively increasing lengths of time in a jogging program and worked up to 45 min of exercise 4 d·week−1 for 8 weeks. Hematologic analysis was performed in weeks 1, 5, and 8. A significant decline in hemoglobin (Hb) concentration and hematocrit (Hct) was observed at week 5 when all data were examined without regard for iron intake; these red cell indices returned to pre-exercise levels by week 8. Reduction of mean cell hemoglobin concentration (MCHC) indicated that the midpoint decline was not caused by simple hemodilution during exercise. Serum ferritin (SF) concentration changed in parallel with Hb and Hct. Although the midpoint decline in SF was not statistically significant, it ruled out the possibility that turnover of red cell iron was directed to storage. Lowered MCHC and SF suggested lower availability of iron during the synthesis of a new generation of red cells. Few iron treatment effects of magnitude were observed. Iron did not prevent the midpoint decline in Hb concentration. Iron intake did not affect SF, serum iron, transferrin saturation, or final Hb, and Hct. Dietary iron availability thus does not appear to play a role in the phenomenon of “sports anemia”. Temporary alteration of priorities for iron needs during exercise, perhaps for muscle myoglobin, may be responsible for this transitory “anemia”.

Mitochondrial NADH dehydrogenase in iron‐deficient and iron‐repleted rat muscle: an EPR and work performance study

Summary. Iron may affect both respiratory O2 transport and mitochondrial electron transport in the performance of muscle work. This study was designed to elucidate the molecular defect iron‐deficient work performance by identifying heretofore unmeasurable mitochondrial enzymes that are diminished by iron deficiency and may be restored by iron repletion. Female rats were made iron‐deficienty by dietary control and were repleted by oral iron. Iron deficiency reduced physical work capacity (treadmill running time), haemoglobin (Hb), and mitochondrial ironsulphur (Fe‐S) centres in heart and skeletal muscles; mitochondrial number was unaffected. Oral iron supplementation restored work capacity and Hb within 4 d to normal or near‐normal levels, but in general Fe‐S centrres of mitochondria due to NADH dehydrogenase remained at iron‐deficient levels. Subnormal concentrations of mitochondrial iron‐dependent NADH dehydrogenase in muscle are not by themselves rate‐limiting in work performance.

Neuro-pharmacological studies on firefly light organs during metamorphosis

Abstract Luminescences in response to electrical stimulation and pharmacological treatment were characterized during progressive degeneration of the larval light organ and differentiation of the adult light organ during metamorphosis. It was found that: (1) neural control of the larval light organ persists during pupation, (2) the differentiating adult light organ, while frequently luminescing, is not directly or neurally excitable until eclosion (3), a gradual loss of postsynaptic receptor chemical responsiveness occurs in parallel with declining neural excitability of the larval light organ, (4) postsynaptic chemical sensitivity of the adult light organ appears prior to establishment of neural control, (5) both larval and adult light organs spontaneously luminesce in the absence of neural control, and (6) synapses between nerve terminals and photocytes of the larval light organ are present throughout pupation.

Immunodeficiency and lymphocyte ecto-5′-nucleotidase activity in the elderly: A comparison of the effect of a trace mineral supplement (1 USRDA) with high zinc (6.7 X USRDA)

Abstract The effect of administering a total mineral supplement (TMS) or 100 mg of elemental zinc alone on immune function was studies in 17 normal subjects, aged 66–85. Subjects were given either TMS containing 1 USRDA of zinc, copper, iron, and manganese or 100 mg of elemental zinc alone as zinc sulfate (ZnSO 4 ). Administration of either supplement led to a slight increase in peripheral blood lymphocytes and improved maturation of B-lymphocytes to antibody-producing cells in culture of peripherla blood mononuclear cells. Ecto-5′-nucleotidase, a zinc obligate enzyme of lymphocyte cell membranes, increased when TMS was administered daily but failed to increase when ZnSO 4 was administered. Serum zinc levels increased in all subjects receiving the ZnSO 4 . Only those subjects with low initial serum zinc levels had higher serum zinc levels after 3 months on the TMS. These studies indicate that dietary supplementation with a TMS (1 USRDA) can improve certain in vitro parameters of immune competence in the aged, avoiding the deleterious effects possible with excessive intake.

Failure of dietary zinc supplementation to improve the antibody response to influenza vaccine

Abstract The effect of administering zinc gluconate on the immune response of elderly subjects to influenza vaccine was studied. Sixty health men and women aged 64 to 90 years (mean=74) were randomly assigned to two groups and asked to discontinue all mineral and vitamin supplements for a period of one month. Members of each group were then started on either 50 mg of elemental zinc as zinc gluconate or an identical appearing and tasting placebo in a double blinded manner for one month. Blood samples were then obtained to determine serum zinc and copper levels, and antibody titers to A/Philippines, A/Chile, B/USSR, B/Ann Arbor strains of influenza virus. All individuals were then immunized using trivalent influenza vaccine (Fluogen, Park-Davis), and continued on either zinc or placebo for one month. A second blood sample was then obtained and similarly analyzed. Serum zinc levels increased in both groups, however in the group receiving zinc gluconate supplementation there was a 5.8-fold greater increase than in the control group (p

The oral assimilation of radiomanganese by the mouse

The metabolism of orally administered radiomanganese was studied in mice. Assimilation of absorbed manganese (Mn) was determined using whole body counting techniques. When54MnCl2 was administered, 2.7% of the dose was retained after 10 d compared with 1.2% from the54Mn-nitrilotriacetate (NTA) complex. However, this difference was accounted for by the rapid and persistent adsorption of the Mn onto the teeth of the lower jaw when fed as the ionic salt at pH 2.0 compared with the NTA-chelate fed at pH 9.0. Once corrected for the amount adsorbed onto the teeth, the biodistribution and relative specific activity of the assimilated radiomanganese into a variety of tissues were similar for both forms of the metal.