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PubMed1997

[The serum zinc level in patients with tinnitus and the effect of zinc treatment].

We measured the serum zinc level in patients with tinnitus and evaluated the effectiveness of zinc in the treatment of tinnitus. Blood zinc levels were measured in 121 patients with tinnitus. All patients were examined between 1995 and 1997 at the outpatient clinic of otorhinolaryngology St. Marianna University Toyoko Hospital. Forty-seven patients who had received any drug such as a calcium channel blocker and others or had been affected by any diseases were excluded and therefore 74 patients consisting of 46 females (62%) and 28 males (38%) were investigated. Twenty two healthy volunteers served as a control group. The mean age and standard deviations for the tinnitus group and the control group were 47.8 +/- 17.1 and 31.4 +/- 8.2 years, respectively. There was a significant decrease (p < 0.0001) in serum zinc levels in patients with tinnitus compared with the control group. Because there was a significant difference (p < 0.0001) in age distribution between tinnitus and control groups, patients were selected by their age in order to neglect the effect of aging. In this situation, a significant difference (p < 0.01) was noted between the tinnitus group and control group. Low blood zinc level was defined by using the mean and standard deviation for the control group (mean-1 S.D.). We treated patients with low blood zinc levels. A total dose of 34-68 mg of Zn++ was administered daily for over 2 weeks. The degree of tinnitus was expressed on a numeric scale from 0 to 10 before and after treatment. Blood zinc levels were significantly elevated (p < 0.05) after treatment. We found a significant decrease (p < 0.01) in the numeric scale. These findings suggest that zinc is useful in at least some patients suffering from tinnitus. It is possible to classify patients with tinnitus by measuring serum zinc level and this leads to improvement of the overall treatment effect.

Adolescent↗
PubMed1999

[Serum levels of zinc, copper and selenium in patients with Wilson's disease treated with zinc].

Zinc administered on a long-term basis in excess to patients with Wilson a disease blocks in a significant way copper absorption from the gut, prevents its accumulation and toxic action in the organism. The authors investigated the effect of its long-term administration on the plasma concentration of copper, zinc, and selenium, on the superoxide dismutase activity in red blood cells and glutathione peroxidase activity in whole blood. In seven patients with Wilson a disease treated with zinc sulphate, 136 mg of elemental zinc for 1.5 years (18 months), the authors assessed the plasma concentration of zinc, copper, selenium and ceruloplasmin, the activity of superoxide dismutase in red blood cells, the activity of glutathione peroxidase in whole blood and the urinary excretion of zinc and copper in 24 hours. Envisaged findings with regard to the diagnosis of the investigated patients and their treatment: elevated plasma zinc concentration and increased urinary excretion, reduced copper and ceruloplasmin plasma concentration and increased urinary copper excretion. The authors recorded also a significantly elevated selenium plasma concentration and a significantly higher concentration of superoxide dismutase in red blood cells (p < 0.05). The increase of the glutathione peroxidase activity in whole blood in the investigated patients was not significant (p < 0.05). Changes in the values of the investigated parameters in patients with Wilson s disease treated on a long-term basis with zinc indicate the possible mutual interaction of zinc with other trace elements with an impact on the activity of the corresponding metalloenzymes, i.e. in the sphere in antioxidant systems.

Adolescent↗
PubMed1991

Moderate zinc deficiency in rhesus monkeys. An intrinsic defect of neutrophil chemotaxis corrected by zinc repletion.

Experimental animals fed zinc-deficient diets are well known for susceptibility to infections and impaired mitogen response and Ig production. However, the levels of zinc deficiency used have generally been severe, not comparable to human populations, and have not addressed neutrophil function. To address this issue we have studied the effect in rhesus monkeys of a well defined moderately zinc-deficient (MZ) diet on polymorphonuclear leukocyte (PMN) function. Female adult rhesus monkeys were fed either a control (100 micrograms Zn/g) or MZ (2 micrograms Zn/g) diet for 9 mo with quantitation of PMN chemotaxis, and phagocytosis of opsonized yeast. In addition, membrane potential and secretion responses (changes in 90 degrees light scatter) and changes in PMN shape (forward light scatter shifts) were also measured. When compared to the PMN of animals fed control diets, there was a significant reduction in chemotaxis to FMLP of MZ-fed monkey PMN. Although shape change, cell membrane depolarization, as well as phagocytosis were not significantly different among the two groups, the PMN of MZ animals had significantly lower relative loss of orthogonal light scatter (degranulation) due primarily to a lower resting orthogonal light scatter and also a smaller loss when stimulated with FMLP. In vitro addition of zinc to the cells (25 microM) did not improve chemotaxis, and in fact, was inhibitory for most control and zinc-deficient cells. However, after 2 wk of dietary zinc repletion (100 micrograms Zn/g), chemotaxis in the low zinc group was higher and comparable to the control response. These data indicate that zinc deficiency is associated with an intrinsic PMN defect that specifically affects chemotaxis and is corrected with dietary zinc repletion.

Animals↗
PubMed1988

Diagnostic value of zinc concentrations in serum, leucocytes and hair of dogs with zinc-responsive dermatosis.

The concentrations of zinc in serum, leucocytes and hair of normal dogs, dogs with zinc-responsive dermatosis and dogs with dermatitis not associated with zinc deficiency was determined. The mean concentration of zinc in serum and hair of dogs with zinc-responsive dermatosis was significantly lower than in other dogs but the range of zinc concentrations overlapped that of the other dogs. The mean leucocyte zinc concentration was similar for each group of dogs. It is concluded that low zinc concentrations in serum and hair have only a corroborative value in the diagnosis of zinc-responsive dermatosis in dogs.

Animals↗
PubMed1987

Zinc status and dark adaptation in patients subjected to total gastrectomy: effect of zinc supplementation.

Totally gastrectomized patients could be regarded at risk for development of nutritional deficiencies including trace elements. Sensitive indices for early detection of these deficiencies are lacking. In order to evaluate the nutritional status of trace elements in patients previously subjected to a total gastrectomy we studied the zinc status in 10 patients by determining serum zinc, urinary zinc excretion and also, by a simplified dark adaptation test, the effect on these parameters of 4 weeks of zinc supplementation. The serum zinc level but not the 24-h urinary zinc excretion was lower in gastrectomized patients compared to age-matched controls. A slower dark adaptation was observed in the former patients when measured in the non-fasting state but not when fasted. Dark adaptation was slower in the patients as well as the age-matched controls compared to younger healthy subjects. Zinc supplementation increased the serum zinc levels and the urinary zinc excretion in the gastrectomized patients but had no effect on dark adaptation.

Aged↗
PubMed1987

Plasma and leucocyte zinc concentrations and their response to zinc supplementation in an elderly population.

Plasma, mononuclear cell and granulocyte zinc were assessed in a group of 15 institutionalised elderly female patients, and the effect of different levels of zinc supplements (50, 100, 150 mg elemental zinc/day) on these parameters was measured. Plasma but not cellular zinc was lower in the elderly compared with a young control group, but a diminished serum albumin may explain the plasma results. Plasma zinc increased with supplementation, but only when the daily intake was 100 or 150 mg/day; the greatest response was with the higher dose. Mononuclear cell zinc did not respond to zinc supplements. There was a decrease in granulocyte zinc at all levels of zinc supplements, the greatest decrease being found with the highest dose (150 mg/day). The decrease in granulocyte zinc at high intakes may have implications in phagocytosis and chemotaxis.

Aged↗
PubMed1985

Reduced serum zinc levels and oral zinc supplementation in geriatric patients.

Serum Zinc levels have been measured in 15 male and 64 female patients admitted to geriatric wards from home or other hospital wards. There was no significant difference between the zinc levels in the two sexes. The zinc concentrations were significantly lower in the geriatric patients than in adult patients whose serum zinc levels were measured by the same method. Levels for serum zinc did not differ significantly between the patients who had previously been receiving hospital diets in other hospital wards, and the patients admitted directly from home who had been receiving less nutritious domestic diets. Oral supplementation with zinc salts resulted in a variable response in serum zinc. It is concluded that the low serum zinc concentrations found in geriatric patients are attributable to abnormal cell metabolisms in individual patients rather than to deficient dietary intake of zinc.

Administration, Oral↗
PubMed1979

Serum zinc before and after cholecystectomy in zinc-treated patients.

Nine female patients were given zinc sulphate (Solvezinc) 220 mg three times daily for 4 weeks prior to cholecystectomy. Mean serum zinc before zinc treatment was 17 +/- 0.8 mumol/l and rose 25 +/- 1.6 mumol/l after zinc treatment. 6 hours postoperatively serum zinc was 13 +/- 1.4 mumol/l. Thereafter it gradually increased to 20 +/- 0.7 mumol/l by the third postoperative day. The present investigation thus shows that pretreatment with zinc increases the serum zinc level but does not prevent the drop in serum zinc in connection with cholecystectomy. However, with the pretreatment serum zinc never falls below the normal range.

Administration, Oral↗
PubMed1994

Treatment of Wilson's disease with zinc. XIII: Therapy with zinc in presymptomatic patients from the time of diagnosis.

The siblings of patients with newly diagnosed Wilson's disease are each at 25% risk of also having this autosomal recessive disease. Screening these siblings allows their detection and institution of prophylactic therapy before they become clinically ill. Herein we report the successful treatment of 13 presymptomatic patients with zinc acetate. These patients who received zinc have been followed for 3 to 9 years. In well-complying patients, 24-hour urine copper and non-ceruloplasmin plasma copper levels have decreased over years of follow-up, consistent with the elimination of the excess easily mobilized copper (the potentially toxic copper) of the body. Effect of therapy and compliance are easily monitored by following 24-hour urine zinc and copper levels. The urine copper level is a good reflection of the body's excess load of easily mobilizable copper. It will increase if control is not adequate. A decrease in urine zinc is an early signal that the patient's compliance is not optimal. The levels of hepatic copper in response to several years of zinc therapy may remain the same, go down, or go up temporarily. This is a reflection of zinc induction of hepatic metallothionein, which sequesters copper in a non-toxic pool. Hepatic copper levels should not be used to manage therapy. Liver function is well preserved by zinc therapy, and no zinc toxicity occurred in these 13 patients. No patient developed symptoms related to Wilson's disease. We conclude that zinc acetate is a fully effective and non-toxic therapy for the prophylactic treatment of the presymptomatic Wilson's disease patient.

Adolescent↗
PubMed1978

Acne treatment with oral zinc and vitamin A: effects on the serum levels of zinc and retinol binding protein (RBP).

The serum levels of zinc, vitamin A and retinol binding protein (RBP) were studied in 75 acne patients before and during oral treatment with zinc, vitamin A or placebo. In the zinc-treated patients an increase in the mean serum zinc level was seen after 2 weeks, when also the first clinical improvement occurred. After 4 weeks the zinc level had increased by about 30% and no further significant increase was observed during 3 months of treatment. In 33 healthy subjects there was an increase of 14% after 4 weeks of zinc therapy. Vitamin A and placebo induced no significant changes in the serum zinc status. Prior to therapy the serum levels of vitamin A and RBP were lower in the acne patients than in the controls. Zinc + vitamin A treatment raised the serum RBP value to normal after 4 weeks. In patients given vitamin A alone, a probable increase in RBP was achieved. Zinc and placebo treatment did not change the serum level of RBP.

Acne Vulgaris↗
PubMed1980

[Study on the setting reaction of the zinc phosphate dental cement (2). The setting reaction of cement substituted magnesia clinker for zinc oxide (author's transl)].

In previous paper it has been reported by author that setting of the zinc phosphate cement is due to precipitation of amorphous aluminium phosphate rather than zinc phosphate. If such the setting reaction on the zinc phosphate cement is right, there is no necessity that cement powder is zinc oxide clinker. In this paper magnesia clinker is substituted for zinc oxide, and the reaction products of set cement are examined by the same methods as having shown in previous paper. When commercial cement liquid is used for mixing with magnesia clinker, the reaction products become amorphous for effects of Al3+ in liquid. These are the same amorphous reaction products as precipitating in set zinc phosphate cement. From result in previous and this paper, it has been made sure that setting reaction of zinc phosphate cement is due to precipitation of amorphous aluminium and zinc (in liquid) phosphate.

Aluminum↗
PubMed2001

Carboxy ester hydrolysis promoted by a zinc(II) 2-[bis(2-aminomethyl)amino]ethanol complex: a new model for indirect activation on the serine nucleophile by zinc(II) in zinc enzymes.

A complexation study on the new Zn(II) complexes of asymmetric tripodal ligand 2-[bis(2-aminoethyl)amino]ethanol (L) has revealed that the alcoholic OH group of complex ZnL exhibits remarkable acidity with a very low pK(a) value of 7.7 at 25 degrees C. Both the monomeric complex [ZnH(-0.25)L(H(2)O)](ClO(4))(1.75) (I) and the dimeric alkoxide-coordinating complex [Zn(2)(H(-1)L)(2)](ClO(4))(2) (II) were synthesized, and their structures were determined by X-ray diffraction. The Zn(II)-bound alkoxide, as the reactive nucleophile toward the hydrolysis of esters, has shown a second-order rate constant of 0.13 +/- 0.01 M(-1) s(-1) in 10% (v/v) CH(3)CN at 25 degrees C in 4-nitrophenyl acetate (NA) hydrolysis, which is almost the same as the corresponding value for the very reactive alcohol-dependent [12]aneN(3)-Zn complex. Present work shows for the first time that Zn(II) complexes of the asymmetric tripodal polyamine bearing an ethoxyl pod can also serve as good models of Zn(II)-containing enzymes.

Chelating Agents↗
PubMed2002

Zinc transformations in acidic soil and zinc efficiency on maize by adding six organic zinc complexes.

Experiments under laboratory and greenhouse conditions were conducted to study the response of maize (Zea mays L.) to Zn fertilizer applications (Zn-phenolate, Zn-EDDHA, Zn-EDTA, Zn-lignosulfonate, Zn-polyflavonoid, and Zn-heptagluconate) in an Aquic Haploxeralf soil. The application of Zn complexes significantly increased Zn uptake by the plant compared with that in the control soil. The highest enhancements were obtained in soil treated with Zn-EDTA, Zn-lignosulfonate, and Zn-EDDHA. The highest percentages of Zn taken up by the plants occurred when 20 mg x kg(-1) Zn was applied as Zn-EDTA fertilizer and 10 mg x kg(-1) as Zn-lignosulfonate fertilizer. In the greenhouse experiment, Zn speciation in soil after harvesting showed that almost all Zn was found in the residual fraction followed by metal in the water-soluble plus exchangeable fraction and metal bound to organic matter. The most effective fertilizers maintaining Zn in the most labile fractions were Zn-phenolate, Zn-EDTA, and Zn-lignosulfonate. Conversely, in the incubation experiment, only a small percentage of Zn was found in the water-soluble plus exchangeable fraction and no differences in the Zn distribution were observed between the different fertilizer treatments. The micronutrient content in maize was positively correlated with the water-soluble plus exchangeable Zn as well as with the available Zn determined by the diethylenetriaminepentaacetic acid and Mehlich-3 methods, in the greenhouse experiment. Results of this study showed that the incubation experiment in acidic soil is not a suitable tool to establish the different effectiveness of Zn chelates in plants.

Chelating Agents↗
PubMed1983

Zinc toxicity, zinc deficiency and zinc-copper interrelationship in Eimeria acervulina-infected chicks.

Three experiments were conducted with young chicks to investigate the effect of duodenal coccidiosis caused by Eimeria acervulina infection on Zn toxicity, Zn deficiency and the interrelationship between Zn and Cu. The coccidial infection depressed both rate and efficiency of weight gain. Dietary Zn addition at 2000 mg/kg depressed performance only slightly, but the 4000 mg/kg reduced both gain and gain/feed markedly. The coccidial infection appeared to have an ameliorative effect on Zn toxicity as assessed by performance and by hematological parameters. Excess Zn (2000 and 4000 mg/kg) dramatically increased liver, pancreas and bone Zn levels. The coccidial infection, however, decreased tissue Zn levels. Copper toxicity caused by feeding 500 mg Cu per kilogram diet was exacerbated by E. acervulina infection. A Zn-Cu antagonism was observed in both control and in coccidiosis-infected chicks. Excess dietary Zn decreased tissue Cu deposition, but excess Cu did not affect tissue Zn deposition. Copper partially ameliorated Zn toxicity symptoms. The efficacy of Cu in overcoming the Zn-induced depressed hematological parameters, however, was enhanced slightly by coccidiosis. E. acervulina infection did not affect the chick's Zn requirement. Growth data were more reliable as indicators of the Zn requirement than were blood or bone parameters.

Animals↗