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At least 19 recordsLinked to original sources
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↗
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↗
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↗
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↗
PubMed1988

Toxicity and character of the effect of some zinc compounds.

Investigation of the parameters of toxicity of 8 zinc compounds revealed some differences in the degree of their risk for persons working with them. The following TSELs (tentative safe exposure levels of harmful substances) have been determined: 0.5 mg/m3 for zinc nitrate and hydrogen and dihydrogen zinc phosphates, 2 mg/m3 for zinc carbonate and zinc selenide, as well as MAC (maximum allowable concentration) for zinc sulphide equal to 5 mg/m3. No TSEL have been set for zinc caprylate and zinc stearate, but intratracheal administration of 50 mg caprylate caused 100%, of stearate 50% death of experimental animals due to pulmonary edema. Maximum tolerable doses were 10 and 1 mg, respectively. Zinc nitrate shows an expressed irritative effect on the skin and a highly expressed effect on the conjunctiva. Zinc phosphates, zinc caprylate and zinc stearate are resorbed by the skin. In all cases, working persons must be protected from the effect of the compounds under study because even though the toxicity of a compound may be rather low, highly noxious compounds may develop in the course of the technological process, e.g., in mechanical treatment of zinc selenide and zinc sulphide monocrystals, hydrogen selenide and hydrogen sulphide, respectively, can be isolated.

Administration, Cutaneous↗
PubMed1991

[Working conditions and health status of workers engaged in the production of zinc compounds].

It was established that industrial shops engaged in zinc compounds' processing were characterized by considerable temperature shifts, relative humidity and air motion changes. In drying and packing shops, concentrations of the final product dusts were established at 0.8-2 mg/m3. The major occupational pathology was constituted by skin and upper respiratory tract diseases, including allergic and contact dermatitis, chronic pharyngitis, tonsillitis and rhinitis. Blood tests revealed B-lymphocytes: increases, circulating immune complexes and considerable levels of lymphocytic spontaneous blastotransformations. Erythrocytic acidic hemolysis was markedly changed, which proved disbalances in the system of red blood.

Acetates↗
PubMed1991

Comparative photoactivity of tin and zinc porphyrin inhibitors of heme oxygenase: pronounced photolability of the zinc compounds.

Metalloporphyrin inhibitors of heme oxygenase may also have photosensitizing properties in vivo. To assess photoactivity in serum, the relative ability to mediate photooxidation of tryptophan or other oxidizable targets, presumably by singlet oxygen production, was measured for tin mesoporphyrin, zinc mesoporphyrin, and zinc deuteroporphyrin bisglycol in aqueous solution and when bound to human serum albumin. While tin mesoporphyrin sensitized at the greatest initial rate in aqueous solution, the zinc compounds sensitized at a greater initial rate in detergent micelles or when bound to albumin. There was minimal alteration of the tin mesoporphyrin during the time course of illumination in the Soret or visible absorption regions. The zinc compounds, however, proved to be extremely photolabile and were extensively destroyed by light; the photooxidized forms were found to be ineffective as inhibitors of heme oxygenase.

Animals↗
PubMed1975

[Experimental animal studies on the absorption of zinc from various parts of the small intestine and various zinc compounds].

The absorption of zinc in different parts of the small intestine and from various Zn compounds was studied in situ, using rats. Segments of equal length from the duodenum, jejunum and ileum were ligated. Into these loops, 65Zn-ZnC12 or 65Zn-ZnC12 with an excess of histidine at a molar ratio of 1:250 and 1:2,000 was injected. The uptake of 65Zn was measured in blood, plasma and different organs after 1 h of absorption. The absorption of zinc was significantly greatest from the duodenum, followed by the jejunum and ileum. The jejunum differed only slightly from the ileum in the absorption capacity for zinc. A 250-fold excess of histidine did not alter the Zn absorption in comparison to ZnC12. There were, however, distinct interactions between the site of Zn absorption and the Zn compound at the molar ratio of zinc:histidine of 1:2,000. With this addition of excess histidine, zinc was absorbed just as well from the jejunum as from the duodenum. The 2,000-fold addition of histidine raised the Zn absorption from the jejunum by about 40% in comparison to ZnC12.

Animals↗
PubMed1993

Zinc compounds in urethral catheters. A possible source of toxicity?

The cytotoxicity of latex urinary catheters has been earlier documented. During the manufacturing process tens of chemicals are added to the natural rubber base. Several of the accelerators and other chemicals used have carcinogenic and acute toxic effects. Some of the accelerators are zinc compounds. In the present study, the cytotoxicity and zinc concentration of 68 latex catheter extracts were analysed. The siliconized latex catheters were the most toxic, and a correlation was seen between the IC50 values and the zinc concentration. The good manufacturing practice (GMP) has to some extent resolved the cytotoxicity problem of latex urinary catheters. There is, however, still a need to reformulate the manufacturing process and to find new catheter materials to meet the new EN standards concerning the biological safety of urinary catheters.

Biocompatible Materials↗
PubMedDate not supplied

[Antimicrobial activities of organic zinc compounds].

Taking into account the competitive action of zinc towards other ion essential for pathogenic germs metabolism, the complex erythromycin-zinc, zinc salts of sulfamethoxydiazine, sulfanilamide, sulfacetimide, sulfathiazole as well as the Mannich basis of sulfamethoxydiazine were synthetized. The antimicrobial action towards gram-positive, gram-negative pathogens and fungi was tested by the classic diffusiometric method. An increased antimicrobial action for the Mannich basis of sulfamethoxydiazine and for the zinc salt of sulfamethoxydiazine, alone or in association with metronidazole--chemotherapeutic agent used in the infections with anaerobic organisms was found. A significant antimicrobial action was also found for the complex erythromycin-zinc and zinc salts of sulfacetimide and sulfathiazole.

Anti-Bacterial Agents↗