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PubMedDate not supplied

A novel zinc compound (zinc monocysteine) enhances the antioxidant capacity of human retinal pigment epithelial cells.

PURPOSE: The aim of this study was to document the effect of a novel zinc amino acid combination on the concentrations of important antioxidants in cultured human retinal pigment epithelial (hRPE) cells. METHODS: Primary confluent hRPE cells were treated with 30 microM of zinc acetate, zinc chloride, zinc cysteine, and zinc sulfate. The antioxidants catalase, glutathione, glutathione peroxidase, and metallothionein were measured. MTT assays were performed to determine the relative protection of the zinc compounds from the cytotoxic effects of H202 and t-butyl hydroperoxide. RESULTS: Catalase and glutathione peroxidase activities were increased by the zinc formulations compared with the untreated control. Glutathione and metallothionein content were also increased. The greatest increases occurred with zinc conjugated to the amino acid cysteine. The MTT assays showed that zinc monocysteine protected cultured RPE cells from the toxicity of H2O2 and t-butyl hydroperoxide. CONCLUSIONS: Our results demonstrate that zinc treatment of RPE cells increases antioxidants and protects cultured RPE cells from the cytotoxic effects of H2O2 and t-butyl hydroperoxide. The results show that zinc conjugated to cysteine offers greater benefits than either zinc salts or cysteine alone.

Antioxidants↗
PubMed1989

[Toxic-dynamics of lead compound and zinc compound in the evaluation of experimental animal behavior].

The aim of the studies was to determine the effect of lead and zinc compound on the mice behaviour. The animals were given intraperitoneally the solution of lead acetate and zinc chloride for 30 days. The mice were subjected to the tests determining their effects on the coordination of movements, the spontaneous motility, the cognitive motility and the motility in the straight rod test as well as on the body temperature. Due to the prolonged exposition to the action of lead and zinc compounds the inhibiting effect of those substances in the central nervous system in the maximal doses was proved while in the minimal doses the antagonistic action of zinc compound was observed. The nerve conduction disorders in the peripheral and central nervous system after the administration of the maximal doses of lead compound may be due to the inhibiting effect of this compound while the lack of this effect in the minimal doses probably results from the antagonistic action of zinc compound.

Animals↗
PubMed1989

[Behavioral effects in mice exposed to the prolonged action of cadmium compound and zinc compound].

The aim of the present paper was to determine the effect of cadmium and zinc on the central nervous system in the experimental animals. The animals were given intraperitoneally the solution of cadmium and zinc chloride for 30 days. The behaviour of the mice was being observed in the test of the coordination of movements, the cognitive activity, the spontaneous motility, the motility in the straight rod test and the effect of the examined compounds on the temperature of the animal body was examined. Together with the dose and exposure time increase the cumulative action of cadmium compound was showed, resulting in the inhibiting effect on the central nervous system. The competitive action of zinc compound in relation to the toxic action of cadmium compound was revealed after the administration of the minimal doses.

Animals↗
PubMed1999

Preventive effect of zinc compounds, polaprezinc and zinc acetate against the onset of hepatitis in Long-Evans Cinnamon rat.

It is known that Long-Evans Cinnamon (LEC) rats are characterized by the fulminant hepatitis occurring as a result of an abnormal hepatic deposition of Cu due to the lack of the Cu-transporter p-type ATPase. To prevent the hepatitis, two Zn compounds, Zn acetate and polaprezinc were given orally to LEC rats aged 30 days. At 100 days after birth, the control group composed of LEC rats fed a basal diet (Cu, 17 ppm; Zn, 50 ppm; Fe, 150 ppm) exhibited slight jaundice and showed high activities of serum enzymes related to hepatic function. The groups fed the diet fortified (1000 ppm as Zn) with Zn acetate or polaprezinc did not have jaundice. The hepatic Cu concentrations were 174 +/- 34 micrograms/g and 156 +/- 23 micrograms/g in the polaplezinc group and Zn acetate group, respectively. The control group showed 267 +/- 17 micrograms Cu/g and 298 +/- 62 micrograms Fe/g in the liver. The Fe concentration was about 1.7 times the concentration in the two Zn groups. Hepatic free Cu and Fe concentrations were 2.6 +/- 0.3 and 21.4 +/- 5.8 micrograms/g, 1.7 +/- 0.7 and 6.8 +/- 1.1 micrograms/g, and 1.3 +/- 0.1 and 6.2 +/- 0.8 micrograms/g in the control, polaprezinc and zinc acetate groups, respectively. Intestinal metallothionein (MT) concentrations were not increased significantly by the Zn diets. The two Zn compounds inhibit Cu absorption from the intestinal tract, resulting in a decrease of hepatic Cu deposition. The new Zn compound as well as Zn acetate is categorized as a therapeutic drug for Cu poisoning, including Wilson's disease.

Animals↗
PubMed1990

A new zinc compound, beta-alanyl-L-histidinato zinc, stimulates bone growth in weanling rats.

The effect of a new zinc compound. beta-alanyl-L-histidinato zinc (AHZ), on bone metabolism in weanling rats was investigated. Rats were orally administered AHZ (0.5-2.5 mg/100 g body weight) for 3 days, and 24h later they were killed. Administration of AHZ (1.0 and 2.5 mg/100 g) caused a significant increase of zinc content in the femoral diaphysis and a corresponding elevation of calcium content, alkaline phosphatase activity, and DNA content. A dose of 0.5 mg/100g AHZ did not produce an appreciable increase in bone components. When zinc sulfate (0.55 mg Zn/100g) was orally administered in rats for 3 days, the bone zinc content, calcium content, and alkaline phosphatase activity were raised significantly, but bone DNA content was not appreciably affected. Thus, the stimulation of AHZ (2.5 mg/100g), which corresponds to 0.55 mg Zn/100g, on bone metabolism was more intensive than that of zinc sulfate. These results suggest that AHZ can stimulate bone growth in weanling rats, and that the compound has a greater effect in comparison with zinc sulfate.

Alkaline Phosphatase↗
PubMed1990

Effect of the new zinc compound beta-alanyl-L-histidinato zinc on bone metabolism in elderly rats.

The effect of a new zinc compound beta-alanyl-L-histidinato zinc (AHZ) on bone metabolism was investigated in aged rats (30 weeks old). AHZ (1.0, 2.5 and 7.5 mg/100 g body weight) was orally administered to rats 3 times at 24-hour intervals, and the rats were bled 24 h after the last administration. The administration of AHZ (7.5 mg/100 g) did not cause an appreciable alteration of calcium and inorganic phosphorus concentrations in the serum, and zinc, calcium and deoxyribonucleic acid contents in the femoral diaphysis were significantly increased by the administration of AHZ (7.5 mg/100 g). The bone alkaline phosphatase activity was significantly increased by doses of 1.0-7.5 mg AHZ/100 g. These results suggest that AHZ has a stimulatory effect on bone formation and calcification in aged rats.

Administration, Oral↗
PubMed2000

Comparison of chromosome damage induced by three zinc compounds using human leukocyte culture.

The degree of chromosome damage induced by three compounds of zinc (zinc chloride, zinc sulfate, zinc acetate) was compared in human leucocytes in vitro. Three concentrations of each salt, 3.0 x 10(-5)M, 3.0 x 10(-4)M, and 1.5 x 10(-3)M, were added to leukocyte cultures. The cells were harvested after 48 and 72 h and chromosome spreads were prepared following a colchicine-hypotonic-fixation-air drying-Giemsa staining schedule. The end point screened was chromosome aberrations. All three salts were lethal at the highest concentration. The degree of chromosome damage was directly proportional to the concentrations used for zinc sulfate and zinc acetate but not for zinc chloride.

Adult↗
PubMed1993

[Neuroactive complexed zinc compounds from bovine brain].

The fraction obtained from acidic extract of bovine brain homogenate after several steps of chromatographic purification provokes spontaneous aggressive encounters in rats upon intracerebroventricular injection. The simultaneous long-term raising of electric shock-induced aggression with the suppressing of muricidal and intraspecies aggressive behaviour has been observed. Intravenous and intraperitoneal injections of this fraction induce no behavioural changes in rats. It has been determined that the fraction consists of complex compounds of zinc with various aliphatic amines. A similar or higher behavioural activity has been discovered in series of synthetic complexes of zinc with different ligands, that are suggested for use in modelling any nervous and psychiatric disorders connected with an increased aggression level.

Aggression↗
PubMed2005

X-ray absorption fine structure analysis of the local environment of zinc in dentine treated with zinc compounds.

It has been reported that zinc oxide (ZnO) inhibits dentine demineralization. By using the X-ray absorption fine structure (XAFS) technique, our aims in this study were to provide information about the local environment of zinc atoms in dentine that had been treated with zinc compounds. We measured the Zn K-edge X-ray absorption near-edge structure (XANES) and the extended X-ray absorption fine structure (EXAFS) of dentine specimens treated with zinc chloride or ZnO. In XAFS analyses, the spectra of dentine specimens treated with ZnO (D-ZO) or with zinc chloride (D-ZC) were similar and obviously different from the reference ZnO spectrum. This suggests that most of the zinc atoms detected in D-ZO are not derived from particles of ZnO. The spectra of D-ZO and D-ZC were similar to the spectrum of the synthetic, zinc-containing hydroxyapatite, but were not similar to that of zinc in ZnCl2-treated collagen. The results of this study suggest that most of the zinc atoms detected were attached to hydroxyapatite and not to collagen.

Animals↗
PubMed1991

Interspecies variations in response to topical application of selected zinc compounds.

The dermal irritancy of six zinc compounds was examined in three animal models. In open patch tests involving five daily applications, zinc chloride (1% aqueous solution) was severely irritant in rabbit, guinea-pig and mouse tests, inducing epidermal hyperplasia and ulceration; aqueous zinc acetate (20%) was slightly less irritant. Zinc oxide (20% suspension dilute Tween 80), zinc sulphate (1% aqueous solution) and zinc pyrithione (20% suspension) were not overtly irritant, but induced a marginal epidermal hyperplasia and increased hair growth. Zinc undecylenate (20% suspension) was not irritant. Epidermal irritancy in these studies is related to the interaction of zinc ion with epidermal keratin. The compounds studied were not consistently bacteriostatic in the three species tested.

Administration, Topical↗
PubMed1996

Zinc compounds inhibit osteoclast-like cell formation at the earlier stage of rat marrow culture but not osteoclast function.

The effect of zinc compounds on osteoclast-like cell formation in rat marrow culture in vitro was investigated. The bone marrow cells were cultured for 7 days in alpha-minimal essential medium containing a well-known bone resorbing hormone (1, 25-dihydroxyvitamin D3 and parathyroid hormone [1-34]). Osteoclast-like cell formation was estimated by staining for tartrate-resistant acid phosphatase (TRACP), a marker enzyme of osteoclasts. The presence of 1, 25-dihydroxyvitamin D3 (10(-8) M) or parathyroid hormone (PTH; 10(-8) M) induced a remarkable increase in osteoclast-like multinucleated cells (MNC). These increases were clearly inhibited by the presence of zinc sulfate or zinc-chelating dipeptide (beta-alanyl-L-histidinato zinc; AHZ) in the concentration range of 10(-7) to 10(-5) M. The inhibitory effect was seen at the earlier stage of osteoclast-like MNC formation. However, zinc compounds (10(-6) M) did not have an effect on PTH (10(-8) M)-induced osteoclast-like cell formation in the presence of EGTA (5 x 10(-4) M), dibucaine (10(-5) M) or staurosporine (10(-9) M). Moreover, when osteoclasts isolated from rat femoral-diaphyseal tissues were cultured for 24 h in the presence of zinc compounds (10(-7) to 10(-5) M), the compounds did not have an effect on cell numbers or lysosomal enzymes activity (acid phosphatase and beta-glucuronidase) in the cells. The present study clearly demonstrates that zinc compounds inhibit osteoclast-like cell formation at the earlier stage with differentiation of marrow cells.

Acid Phosphatase↗
PubMed1994

Inhibitory effect of zinc compounds on osteoclast-like cell formation in mouse marrow cultures.

The effect of zinc compounds on osteoclast-like cell formation in mouse marrow culture in vitro was investigated. The bone marrow cells were cultured for 7 days in alpha-minimal essential medium containing a well-known bone resorbing agent [1,25-dihydroxyvitamin D3, parathyroid hormone (1-34), interleukin-1 alpha or prostaglandin E2]. Osteoclast-like cell formation was estimated by staining for tartrate-resistant acid phosphatase (TRACP), a marker enzyme of osteoclasts. The presence of 1,25-dihydroxyvitamin D3 (10(-8) M), parathyroid hormone (10(-8) M), interleukin-1 alpha (50 U/mL) or prostaglandin E2 (10(-6) M) induced a remarkable increase in osteoclast-like multinucleated cells. These increases were inhibited by the presence of zinc sulfate or zinc-chelating dipeptide (beta-alanyl-L-histidinato zinc; AHZ) in the concentration range of 10(-8) to 10(-5) M. The inhibitory effect of AHZ (10(-8) and 10(-7) M) was more intensive than that of zinc sulfate. Furthermore, the presence of Ni2+, Cu2+, Mn2+ or Co2+ (10(-7) and 10(-6) M) did not have an effect on parathyroid hormone (10(-8) M)-induced osteoclast-like cell formation. The present study clearly demonstrates that zinc compounds have a potent inhibitory effect on osteoclast-like cell formation in mouse marrow culture.

Acid Phosphatase↗
PubMed1991

Stability of steroid ointments diluted with Compound Zinc Paste B.P.

The chemical stability of a range of corticosteroid ointments diluted with Compound Zinc Paste B.P. was studied by high-performance liquid chromatography (HPLC). Betamethasone dipropionate degraded by first-order kinetics at both 25 degrees C and 32 degrees C. At 25 degrees C the mean first-order reaction rate constant was 9.58 x 10(-3)/day, with a t90 (time to reach 90% of the original concentration) of 11.0 days. At 32 degrees C the mean first-order reaction rate constant was 2.42 x 10(-2)/day, with a t90 of 4.4 days. Of the other steroids studied, Fluocinolone acetonide was the least stable, with 33.8% remaining after a 7-day storage period at 25 degrees C. Betamethasone-17-valerate and fluocinonide were of intermediate stability between betamethasone dipropionate and fluocinolone acetonide. None of the steroid ointments studied had adequate stability in Compound Zinc Paste B.P. to allow extemporaneous dilution with this base.

Adrenal Cortex Hormones↗
PubMed1989

Zinc compounds as therapeutic agents in peptic ulcer.

Zinc acexamate (ZAC) is the first zinc compound developed and marketed for use in the therapy of peptic ulcer. ZAC is active in several ulcer experimental models. This action is secondary to an effect on both aggressive and defensive mucosal factors. ZAC reduces acid and peptic secretion, increases mucus secretion, protects mucosa from disruption by aspirin and reverses the reduction of blood flow caused by noradrenaline. Clinically, ZAC has proven to be a useful drug in the healing of peptic ulcer. Reduction of inflammatory associated processes of peptic ulcer, which has not been seen with H2-blockers, suggests that ZAC may be highly effective in preventing ulcer relapse. These properties, together with its good safety profile, indicate that ZAC would be an interesting option in the treatment of peptic ulcer.

Humans↗
PubMed1985

[Mechanism of the antihypoxic action of zinc compounds].

It was established in experimental normobaric and hypobaric hypoxia and hemic hypoxia induced by carbon monoxide poisoning that zinc compounds administered in a dose of 0.15 mA/kg have a marked prophylactic protective effect. The mechanism of action of zinc compounds consists in changes of oxygen transport blood function. It was shown that interaction of the hemoglobin molecule with zinc ion brings about an increase in Hb affinity for O2 (the left drive of the oxyhemoglobin dissociation curve), a reduction in cooperative interaction of hemoglobin subunits, and a relative decrease in hemoglobin affinity for carbon monoxide. The leading defence mechanism against hypoxic hypoxia is the left drive, the mechanism of defence against carbon monoxide protection consists in the lowering of the "hem-hem" cooperation and of the relative hemoglobin affinity for carbon monoxide.

Acute Disease↗
PubMed2005

The European Union risk assessment on zinc and zinc compounds: the process and the facts.

A risk assessment on zinc and zinc compouns was carried out withn the framework of Council Regulation 793/93/EEC on Existing Chemicals. This risk assessment basically followed the European Union (EU) technical guidance documents (TGDs). These TGDs are built on the current knowledge on quantitative risk assessments, mainly for organic chemicals. This article describes the tailor-made approach for the zinc risk assessment. This work lasted almost a decade and involved the contributions of all EU member states and industry, who discussed the risk assessment during technical meetings. The risk assessment is initially based on scientific findings but is interrelated with pragmatic considerations. It follows a comprehensive approach, covering both environmental and human health. In the environmental part, new methodologies were developed to deal with the natural background of zinc, essentiality, speciation, and the use of species sensitivity distributions. The major results and the process of drawing conclusions of the risk assessment are outlined: potential environmental risks of zinc and zinc compounds may occur at local and regional scales in surfacewater, sediment, and soil. No potential health risks were identified for consumers and man indirectly exposed via the environment. For workers, potential health risks were identified only for zinc oxide and zinc chloride.

Animals↗