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PubMed2001

The influence of zinc on caspase-3 and DNA breakdown in cultured human retinal pigment epithelial cells.

OBJECTIVES: To investigate the role of extracellular zinc on the death process of cultured human retinal pigment epithelial (RPE) cells. METHODS: Confluent cells on borosilicate glass coverslips were treated with substances in serum-free growth medium for various times and were analyzed for death by means of changes in morphologic features, numbers of attached cells, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) procedure. Some cultures were also exposed to experimental ischemia (defined as a lack of oxygen, glucose, and serum). Electrophoresis and Western blotting and enzyme assays were used to investigate changes in expression of the protease enzyme, caspase-3. RESULTS: Experimental ischemia caused death of RPE cells. Zinc sulfate had no effect on these cells at low concentrations (100 pmol/L to 10 nmol/L), but protected them at higher concentrations (< or = 10 micromol/L) and appeared to exacerbate cell death at still greater concentrations. Moreover, zinc compounds (>10 micromol/L) also induced death of cells in control cultures that could be blocked by zinc chelators and partially by the caspase-3 inhibitor, DEVD-FMK. Zinc also increased the amount of the active form of caspase-3 in RPE cells. CONCLUSIONS: Zinc salts protect RPE cells from experimental ischemia-induced death at low concentrations (100 pmol/L-10 nmol/L). However, at higher concentrations, zinc causes cell death and alters the cellular level of caspase-3. These observations are consistent with the death process being apoptosis. CLINICAL RELEVANCE: Zinc supplements are taken by many individuals. Low doses of zinc can protect RPE cells against ischemic-type insults as may occur in certain ocular complaints. Furthermore, high concentrations of zinc can damage RPE cells. Because zinc ions are known to be taken up by RPE cells from the choroidal circulation, the actual therapeutic dose taken by patients is critical.

Adult↗
PubMed1997

Comparative in vitro oxygen radical scavenging ability of zinc methionine and selected zinc salts and antioxidants.

1. The concentration-dependent scavenging abilities of zinc DL-methionine, zinc sulfate, zinc gluconate, zinc picolinate and selected free radical scavengers, including superoxide dismutase (SOD), catalase, mannitol, allopurinol and DL-methionine, were examined against biochemically generated superoxide anion, hydroxyl radical and hypochlorite radical plus hypochlorous acid, by chemiluminescence and cytochrome c reduction. 2. Zinc methionine was the most effective of the zinc compounds that were tested. Following incubations with superoxide anion, hydroxyl radical, and hypochlorite radical-generating systems, in the presence of 50 microM zinc DL-methionine approximately 38%, 47% and 28% inhibition in reactive oxygen species generation was observed, respectively, compared to control groups. 3. The protective abilities of various zinc salts, as well as selected free radical scavengers and antioxidants were also assessed on phorbol ester (TPA)-induced lactate dehydrogenase (LDH) release from cultured PC-12 cells. Preincubation showed better protection than coincubation. Approximately 45% and 50% inhibition in TPA-induced LDH leakage was observed following preincubation with 50 microM zinc DL-methionine and 50 microM vitamin E succinate, respectively. Zinc DL-methionine exhibited better protection against LDH leakage than any other zinc salt tested. 4. The results indicate that zinc DL-methionine can attenuate the biochemical consequences of oxygen free radicals, and is comparable to other well-known antioxidants and free radical scavengers in the in vitro system that was employed.

Animals↗
PubMed1986

Zinc and its deficiency diseases.

The pervasive role of zinc in the metabolic function of the body results from its function as a cofactor of a multitude of enzymes. Zinc is found in every tissue in the body, and because zinc metalloenzymes are found in every known class of enzymes, the metal has a function in every conceivable type of biochemical pathway. Symptoms resulting from zinc deficiency are as diverse as the enzymes with which the metal is associated. If chronic, severe, and untreated, zinc deficiency can be fatal. Less drastic symptoms include infections, hypogonadism, weight loss, emotional disturbance, dermatitis, alopecia, impaired taste acuity, night blindness, poor appetite, delayed wound healing, and elevated blood ammonia levels. Many symptoms of zinc deficiency result from poor diet consumption, but often the most severe symptoms result from other factors including excessive alcohol use, liver diseases, malabsorption syndromes, renal disease, enteral or parenteral alimentation, administration of sulfhydryl-containing drugs, and sickle cell disease. The most severe symptoms of zinc deficiency occur in young children affected with the autosomal-recessive trait, acrodermatitis enteropathica. This disease results in decreased synthesis of picolinic acid which causes an impaired ability to utilize zinc from common food. Because simple laboratory analyses are often not reliable in determining zinc nutriture of a patient, those symptoms caused by suspected zinc deficiency are best verified by the oral administration of zinc dipicolinate. This zinc compound is efficacious and safe and would provide an accurate means of identifying symptoms that do result from zinc deficiency.

Humans↗
PubMed2001

Solid-substrate room-temperature phosphorescence study on zinc(II) and tin(IV) protoporphyrins and their interaction with DNA.

The solid-substrate room-temperature phosphorescence (SS-RTP) of two commercially available metalloporphyrin compounds, zinc(II) protoporphyrin (ZnPP) and tin(IV) protoporphyrin (SnPP) has been studied. Strong and stable RTP signals of the two metalloporphyrins in neutral to weakly basic solutions can be simply induced on filter paper without addition of external heavy atom perturbers. Their emission bands appeared at 723 nm for ZnPP and 718 nm for SnPP at an excitation wavelength of 417 nm. Compared with SnPP, ZnPP is a better RTP probe for DNA because its RTP enhancement effect is much higher under the same experimental conditions. The interaction of ZnPP with DNA at pH 8.5 gives an apparent binding constant of 9.1 x 10(3) which is similar to that of the cationic porphyrin absorption probe CuTMPyP (copper (II)- tetrakis(4-N-methylpyridyl)porphine complex). Hydrogen bonding between the monocarboxylic acid substituent of ZnPP and the base pairs of DNA plays a crucial role in the binding.

DNA↗
PubMed2002

Delineation of the protective action of zinc sulfate on ulcerative colitis in rats.

The protective action of zinc compounds in Crohn's disease-like inflammatory bowel disease in animals has been shown. A similar action of zinc sulfate on ulcerative colitis has not been defined. The present study aimed to delineate the protective action of zinc sulfate and the pathogenic mechanisms of 2,4-dinitrobenzene sulfonic acid (DNBS)-induced ulcerative colitis in rats. Zinc sulfate at different concentrations was given either orally (p.o.) or rectally (p.r.) to rats at 42, 48, 66 and 72 h following the induction of colonic inflammation by DNBS. Rats were killed 96 h after instillation of DNBS rectally to assess the severity of colonic damage, myeloperoxidase and xanthine oxidase activities. The involvement of mast cell degranulation and histamine release in the pathogenesis of DNBS-induced colitis was determined by using a mast cell stabilizer (ketotifen) and histamine receptor blockers (terfenadine and ranitidine). DNBS given rectally produced inflammation and ulceration in rats with a pathology resembling ulcerative colitis. Myeloperoxidase activity but not xanthine oxidase activity was sharply increased by this agent. Intrarectal administration of zinc solution and parenteral injection of histamine blockers significantly reduced tissue damage and myeloperoxidase but not xanthine oxidase activity. Ketotifen, a mast cell stabilizer, also significantly decreased mucosal injury and myeloperoxidase activity in the colon. In conclusion, mast cell degranulation followed by histamine release plays an important role in the pathogenesis of DNBS-induced ulcerative colitis. Zinc given rectally has a therapeutic effect against this colitis model, perhaps through the reduction of inflammation and inhibition of the above pathogenic mechanisms.

Animals↗
PubMed2005

Zinc absorption from zinc oxide, zinc sulfate, zinc oxide + EDTA, or sodium-zinc EDTA does not differ when added as fortificants to maize tortillas.

The fortification of staple foods with zinc may play an important role in achieving adequate zinc intakes in countries at risk of zinc deficiency. However, little is known about the relative bioavailability of different zinc compounds that may be used in food fortification. The objective of this study was to measure and compare fractional zinc absorption from a test meal that included a maize tortilla fortified with zinc oxide, zinc sulfate, zinc oxide + EDTA, or sodium-zinc EDTA. A double isotopic tracer ratio method ((67)Zn as oral tracer and (70)Zn as intravenous tracer) was used to estimate zinc absorption in 42 Mexican women living in a periurban community of Puebla State, Mexico. The test meal consisted of maize tortillas, yellow beans, chili sauce, and milk with instant coffee; it contained 3.3 mg zinc and had a phytate:zinc molar ratio of 17. Fractional zinc absorption did not differ significantly between the test groups (ANOVA; P > 0.05). Percent absorptions were (mean +/- SD) zinc oxide, 10.8 +/- 0.9; zinc sulfate, 10.0 +/- 0.02; zinc oxide + EDTA, 12.7 +/- 1.5; and sodium-zinc EDTA, 11.1 +/- 0.7. We conclude that there was no difference in zinc absorption from ZnO and ZnSO(4) when added as fortificants to maize tortillas and consumed with beans and milk. The addition of EDTA with zinc oxide or the use of prechelated sodium-zinc EDTA as fortificants did not result in higher zinc absorption from the test meal.

Chelating Agents↗
PubMed1995

Zinc deficiency delays gastric ulcer healing in rats.

Zinc is an important element in wound healing. Zinc compounds hasten the healing of gastric ulcers, by an unknown mechanism(s). We studied the effect of the induction of zinc deficiency on gastric ulcer healing. Rats were given a control or zinc-deficient diet for six weeks and then subjected to the induction of acetic acid-induced chronic gastric ulcers. Four days later, zinc-deficient rats were divided into two groups. In the first group, the zinc-deficient diet was continued. In the second group, the diet was changed to the control diet. Zinc-deficient rats had a mean serum zinc concentration approximately 70% of that in controls. Zinc deficiency did not affect the formation of gastric ulcers; however, it reduced cell proliferation by day 4 and delayed ulcer healing. Zinc supplementation brought zinc to control levels within a week, but failed to reverse the delay in ulcer healing. We conclude that zinc is crucial for healing of gastric ulcers, especially at the early stage.

Acetates↗
PubMed1978

An impurity in the buffer 2-amino-2-methyl-1-propanol, which correlates with depression of measured alkaline phosphatase activity.

Recent findings indicate that the buffer 2-amino-2-methyl-1-propanol, widely used in clinical measurement of alkaline phosphatase activity, contains an impurity that inhibits the activity of the enzyme. Analysis of several lots of 2-amino-2-methyl-1-propanol has demonstrated the presence of a material, the concentration of which correlates well with alkaline phosphatase activity. Mass spectral analysis of this material indicates that it is a substituted ethylenediamine compound. Zinc chelation is discussed as a possible mode of its inhibition. Further work is in progress to separate and characterize this and other compounds in the buffer and to determine their modes and degrees of alkaline phosphatase inhibition.

Alkaline Phosphatase↗
PubMed1997

The protective effect of zinc sulphate pretreatment against duodenal ulcers in the rat.

Exogenously administered zinc compounds have been shown to possess antiulcer activity in the development of gastric lesions. The aim of this study was to investigate the effects of zinc sulphate pretreatment of rats on cysteamine-induced duodenal ulcers and to correlate them with changes in zinc serum and tissue levels. Atomic absorption spectrophotometry was used to determine zinc serum and tissue concentrations in all animal groups. Cysteamine produced marked duodenal ulceration in control animals 24 h after application, with an increase in endogenous zinc tissue concentrations and a marked decrease in serum concentrations. Zinc sulphate (20, 40 or 80 mg kg-1) applied per os one hour prior to cysteamine application inhibited the development of duodenal lesions in a dose-related manner. The application of zinc sulphate in a single intraperitoneal (i.p.) application (80 mg kg-1) did not, however, prevent the formation of duodenal lesions. In order to assess zinc absorption from the gastrointestinal tract, one group of rats received a single oral dose of zinc sulphate (80 mg kg-1) without cysteamine application. The observations of this study seem to indicate that zinc plays an important cytoprotective role in duodenal ulcer disease.

Administration, Oral↗
PubMed1994

[Role of metallothionein in cancer chemotherapy].

Metallothionein (MT) shows a protective effect against toxic actions of some antitumor drugs and gamma-irradiation in animals. Preadministration of bismuth subnitrate, an MT inducing drug, significantly reduced side effects of antitumor drugs without affecting antitumor activity of the drugs. This specific effect of bismuth on the toxicity of antitumor drugs appears to be attributable to its specific induction of MT in normal tissues, but not in tumor tissue. Preinduction of MT synthesis in the lung also prevented mice from carcinogenesis caused by cisplatin and melphalan in the lung. On the other hand, zinc compound induced MT synthesis in the tumor, and significantly suppressed the antitumor activity of some antitumor drugs. Propargylglycine (PPG), an inhibitor of cystathionine pathway, significantly inhibited MT induction by zinc in the tumor inoculated in mice, and, consequently, PPG could diminish cisplatin resistance acquired by an increase in the tumor MT levels.

Alkynes↗
PubMed1982

Zinc-sulfur bonds of aspartate transcarbamylase studied by x-ray absorption spectroscopy.

X-ray absorption spectra have been recorded for aspartate transcarbamylase [unligated and ligated with the transition-state analogue N-(phosphonoacetyl)-L-aspartate] and for the model compound zinc dimethyldithiocarbamate. The spectra confirm that, in the enzyme, the zinc atom is ligated to four sulfur atoms, with a mean distance of 2.34 +/- 0.03 A. A spread in bond lengths of 0.1 +/- 0.03 A is possible, due to thermal and/or static disorder. No significant difference was found between the spectra of the ligated and unligated enzymes.

Aspartate Carbamoyltransferase↗
PubMed1988

Inhibitory effect of zinc on nickel subsulfide carcinogenesis in Fischer rats.

The effects of zinc oxide (ZnO) and zinc acetate (ZnAcet) administered i.m. together with nickel subsulfide (Ni3S2), a potent muscle carcinogen, were observed over 66 weeks in male F344/NCr rats. The rats (20/group) received a single injection of 2.5 mg Ni3S2 (equal to 31 mumol Ni) alone or combined with different molar proportions of ZnO or ZnAcet (8-60 mumol Zn) into both thighs. One more group of rats given i.m. Ni3S2 received s.c. ZnO (60 mumol Zn) at the nape of the neck. Control rats were treated with i.m. ZnO (60 mumol Zn) or the injection vehicle, water. In rats given Ni3S2 alone the incidence of local tumors reached 100% in 40 weeks. In rats treated locally with Ni3S2 + ZnO or ZnAcet, the tumor incidence at week 40 was only 40-60%; it reached 85-100% in 66 weeks, with no significant differences among the treatments. Treatment with i.m. Ni3S2 + s.c. ZnO resulted in 100% muscle tumors at week 58. One local tumor was found in rats given ZnO alone and none in the water injected animals. Statistical analysis revealed highly significant differences in the tumor occurrence rates between rats treated with Ni3S2 alone and rats treated with Ni3S2 combined with ZnO or ZnAcet, whereas the final tumor incidences at week 66 were not different. The first tumors were found at weeks 24-31 regardless of the treatment. Hence, administration of zinc slows the carcinogenic process induced by nickel. This effect has a systemic character and is produced by both water-soluble and insoluble zinc compounds despite their different retention times in the muscle. The half-lives of ZnO and ZnAcet in the muscle were approx. 24 days and 2.5 days, respectively; that of Ni3S2 was 21 days. Zinc in either form exerted no apparent influence upon the retention of nickel at the injection site and did not significantly affect the early local cellular reactions to nickel.

Acetates↗
PubMed1996

Endogenous zinc concentrations in cysteamine-induced duodenal ulcers in the rat.

Exogenously administered zinc compounds have been shown to possess anti-ulcer activity against a wide variety of ulcerogenic agents, both in laboratory animal models and in human peptic ulcer disease. However, a strong possibility exists that endogenous zinc may also play an important role during noxious events by various mechanisms. Therefore, the aim of this study was to focus on the changes of endogenous zinc serum and tissue concentrations in cysteamine-induced duodenal lesions. We used atomic absorption spectrophotometry to determine the tissue and serum concentrations of zinc in normal (control) rats and those with cysteamine-induced duodenal ulcers. The results obtained in this study indicated that the onset, development and spontaneous healing of ulcer lesions were associated with certain shifts in zinc serum and tissue concentrations. Prior to ulcer formation, a significant increase was noted in serum zinc values. With the onset of duodenal lesions, zinc serum concentrations significantly decreased, while there was a significant increase in duodenal tissue concentrations when compared to healthy control animals. Zinc tissue concentrations decreased and returned to starting values by the end of the first week of spontaneous healing. This decrease in zinc tissue concentration corresponded to the healing rate of the duodenal ulcers. Serum zinc concentrations also returned to starting values within the first week period. These observations indicate and confirm that zinc could play an important role in duodenal ulcer disease and represent a natural defense system in the body.

Animals↗
PubMed2003

Zinc as a potential enteroprotector in oral rehydration solutions: its role in nitric oxide metabolism.

Zinc has been recognized as an antioxidant with potential for chronic and acute effects. Oxidative damage produced by free radicals, including nitric oxide (NO), is responsible for certain types of intestinal malabsorption syndromes and diarrhea. Under physiologic or mildly stimulatory conditions for NO synthesis, the small intestine characteristically is in a proabsorptive state; however, an excessive production of NO triggers formation of cyclic nucleotides, which cause secretion and malabsorption. In this study, we hypothesized that low-molecular-weight, soluble zinc chelates could modulate the effects of induced NO excess on the small intestine. In vitro experiments demonstrated that zinc-citrate or zinc-histidine at > or =0.66 mM, as well as a known NO scavenger, 2-[carboxyphenyl]-4,4,4,4-tetramethylimidazoline-1-oxyl-3-oxide, at 2 microM, were effective at removing chemically generated NO. In vivo jejunal perfusions, conducted in healthy rats under anesthesia, showed that c-PTIO reduced the proabsorptive effects produced by 1 mM L-arginine, the precursor of NO. In a standard oral rehydration solution, 1 mM zinc-citrate partially reversed the antiabsorptive effects on potassium caused by an excess of NO generated from 20 mM L-arginine but did not alter sodium or water absorption. The data are consistent with the view that soluble zinc compounds incorporated into an oral rehydration solution may deserve further attention as a means to scavenge NO with fluids used for the treatment of chronic or acute diarrhea, especially in malnourished children who are often zinc deficient.

Animals↗
PubMed2000

Specific toxins destabilize virus inhibitors (e.g. AIDS viruses).

There are two approaches to the study of viral infections - the A-Z hypothesis of Sprietsma involving thiol-zinc inhibition of protease activation in the virus coat, and the activity of toxins in depleting the cell of thiols, or the activity of toxins activating (not detoxifying) the mixed function oxidase (MFO) system. Both of these systems generate free radicals and utilize thiols in the process. Zinc forms stable mercaptides with thiols, inhibits cyclic reduction-autoxidation of thiols and superoxide generation. When the MFO system acts as an activator and not as a detoxifier in that intermediate products are more toxic than the original compound, zinc inhibits the oxidation. An example of increased toxicity with increased MFO activity is the toxin 3-methylindole (3-MI), a toxic product of intestinal bacterial putrefaction which reactivates the infectious bovine rhinotracheitis virus (IBR). Zinc reduces MFO activity and in this regard it functions synergistically with antioxidants in protecting cell membranes. It is hypothesized that stable zinc complexes inhibit activity of proteases in the virus nucleocapside (NC) proteins in the virus coat, both directly and indirectly because zinc also inactivates some toxins that are thiol depleters or virus reactivators.

Animals↗
PubMed1976

Effects of zinc chloride on gastric secretion and ulcer formation in pylorus-occluded rats.

The effects of 10-day pretreatment with i.p. injections of zinc chloride, 16 mg/kg, on gastric secretion and on gastric ulceration induced by stress or by acid accumulation were examined in pylorus-occluded rats. Zinc chloride pretreatment significantly reduced the volume of gastric secretion and the total acid output as well as the incidence of gastric ulcers induced either by stress or by acid accumulation. The findings support the idea zinc compounds may be useful in the treatment of gastric ulcers.

Animals↗
PubMed1991

The hypothesis of zinc deficiency in the pathogenesis of neurofibrillary tangles.

Neurofibrillary tangles (NFT) in human encephalopathies of various etiologies may result from a common pathogenetic mechanism: a functional zinc decrease leading to a deficiency of the DNA metabolizing zinc-enzymes, giving rise to abnormal neuronal DNA and synthesis of pathological proteins: NFT. In encephalopathia Saturnica, zinc decreases in the hippocampus displaced by lead; in Guam's encephalopathy, calcium deficiency permits the entry in the brain of toxic metals that may displace zinc; in Boxer's dementia and some viral encephalitides, blood-brain-barrier (BBB) is altered and abnormal metals may reach the brain; in Down's syndrome and Alzheimer's disease precapillary and capillary amyloidosis disturbs the BBB, metals (iron and aluminium) are encrusted in the amyloid and their brain level increases, whereas zinc decreases especially in the hippocampus. A deficiency of the zinc enzymes of neuronal detoxication, of glutamate catabolism and of some neurotransmitters metabolisms may also contribute in the neuronal dysfunction of these encephalopathies. A non-toxic zinc compound crossing the BBB may be useful for the treatment of these encephalopathies and especially for Alzheimer's disease.

Alzheimer Disease↗
PubMed2002

Coordination chemistry and reactivity of monomeric alkoxides and amides of magnesium and zinc supported by the diiminato ligand CH(CMeNC(6)H(3)-2,6-(i)Pr(2))(2). A comparative study.

The preparation and characterization of a series of closely related magnesium and zinc compounds are reported: LMg(N(i)Pr(2))(THF), 1; LZn(N(i)Pr(2)), 2; LMg(O(t)Bu)(THF), 3; LZn(O(t)Bu), 4; and LZn(OSiPh(3))(THF), 6; where L = CH(CMeNC(6)H(3)-2,6-(i)Pr(2))(2). Their dynamic solution behavior has been examined by variable-temperature NMR studies and reveals that THF reversibly dissociates in toluene-d(8) or CD(2)Cl(2) and that exchange with free THF occurs by a dissociative process. Compounds 1-4 and 6 all initiate and subsequently sustain ring-opening polymerization (ROP) of lactides. For a related series of compounds LMX(THF)(n)(), where n = 1 or 0, the rate of initial ring-opening follows the order M = Mg > Zn and X = O(t)Bu > N(i)Pr(2) > NSi(2)Me(6) > OSiPh(3). In THF at 25 degrees C, compounds 3 and 4 polymerize 100 equiv of rac-lactide to >95% conversion in 5 and 80 min for M = Mg and Zn, respectively, and yield ca. 90% heterotactic PLA, (isi + sis tetrads). The reactions proceed faster in methylene chloride, but for M = Mg, a Bernoulian distribution of tetrads is formed from rac-lactide (3iii:2isi:sii:sis:iis) prior to trans-esterification. Polymerization of L-LA in toluene-d(8) and THF-d(8) by 3 and 4 have been studied by VT (1)H NMR spectroscopy: the resting state for zinc is proposed to be a monomeric species akin to LZn(eta(2)-OCHMeC(O)OMe), whereas the magnesium complex appears to be dimeric LMg(mu-OP)(2)MgL. None of the compounds is capable of initiating homopolymerization of propylene oxide (PO) or cyclohexene oxide (CHO), although the magnesium amide 1 effects ring-opening by allylic proton abstraction and the dimeric compound [LMg(mu-OC(6)H(9))](2), 7, is formed. Reactions with carbon dioxide are also described, along with the characterization of LZnO(2)CN(i)Pr(2), 8, which is shown to be inert with respect to CHO and PO at room temperature. All the compounds are hydrolytically sensitive, and LZn(mu-OH)(2)ZnL, 5, has been isolated from hydrolysis of compound 4. The crystal and molecular structures are reported for compounds 1-5, 7, and 8. These results are compared with those recently reported by Coates et al.

Journal Article↗