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PubMed2004

Metals accelerate production of the aberrant splicing isoform of the presenilin-2.

Oxidative stress is a major risk factor for Alzheimer's disease (AD) and other neurodegenerative disorders. Metals are known to be one of the factors that contribute to oxidative stress. Recently, we reported that the aberrant splicing isoform (PS2V) generated by skipping exon5 of the presenilin-2 (PS2) gene is a diagnostic feature of sporadic AD (SAD). PS2V is inducible by exposure of human neuroblastoma to hypoxia. We examined whether this aberrant splicing was caused by metal-induced oxidative stress, such as exposure to aluminum. As a result, we demonstrated that exposure to aluminum accelerated PS2V production induced by hypoxia. This acceleration of the production of PS2V to hypoxia was caused by chronic aluminum exposure, but was not related to the intracellular content of aluminum. HMGA1a is a mediator of PS2V production, and it was induced by aluminum as well as by hypoxia. Induction of HMGA1a was increased by chronic exposure to aluminum, and a nuclear extract containing HMGA1a bound to a specific sequence on exon5 of PS2 pre-mRNA, as reported previously. Finally, the acceleration of PS2V production induced by aluminum under hypoxic conditions reflected, but has not yet been directly shown to cause, vulnerability to endoplasmic reticulum stress. These results suggest that exposure to some metals can accelerate and enhance PS2V generation, and that hypoxia plus chronic exposure to metals may promote the development of AD.

Alternative Splicing↗
PubMed1996

Sensitization of Escherichia coli to nisin by maltol and ethyl maltol.

When used separately, 20 mmol l-1 maltol or 1600 AU ml-1 nisin resulted in a 0-0.6 log10 reduction in viable counts of Escherichia coli in a buffer system. However, when added in combination they yielded a 1.8-5.5-log-cycle reduction in viable counts of E. coli at pH 5.0 and 6.8 respectively. It is postulated that maltol (and ethyl maltol) destabilizes the cell outer membrane by chelation of Mg2+ and/or Ca2+, thus permeabilizing the E. coli cell to nisin.

Anti-Bacterial Agents↗
PubMed1991

Evidence for regulatory control of iron uptake from ferric maltol across the small intestine of the rat.

1. 59Fe absorption from the novel iron compound, ferric maltol, was studied in rats pretreated twice daily for two weeks with non-radioactive ferric maltol in oral doses containing 7 mg elemental iron. Tissue accumulation of 59Fe 2 h after administration of radioactive ferric maltol into the stomach was significantly lower in iron pretreated animals than in saline-treated controls. 2. 59Fe uptake from ferric maltol into isolated fragments of ileum and of duodenum was of similar magnitude in control animals but in iron-treated animals, duodenal uptake was significantly lower than that of the ileum. 3. Absorption of 59Fe was also investigated in anaesthetized rats after intestinal perfusion with saline (controls) or with 5 mM chenodeoxycholate to render the intestines more permeable. 4. Changes in permeability of the small intestine were monitored by estimating the amount of [14C]-mannitol absorbed and fluid secreted with reference to the non-absorbable [3H]-inulin in the perfusate effluents. 5. Despite the increased permeability of the intestines after bile salt treatment, there was little difference from control in the tissue accumulation of 59Fe from ferric maltol 2 h after intraduodenal administration. However 59Fe absorption from ferrous sulphate was significantly increased after bile salt treatment. 6. Gel filtration profiles of plasma made 5 and 60 min after intraduodenal administration of [59Fe]-ferric [3H]-maltol demonstrated that metal and ligand do not enter the circulation as the complex even when intestinal permeability is increased. 7. Uptake of 59Fe was investigated in isolated fragments of rat small intestine after saline or bile salt perfusion. Although 59Fe uptake from ferric maltol was somewhat greater in the bile salt-treated intestinal fragments, saturable kinetics were still observed. By contrast, "Fe uptake from ferrous sulphate: ascorbate was greatly enhanced by bile salt pretreatment and a very large diffusional component of uptake was evident. 8. It is concluded that iron uptake from ferric maltol may well be under endogenous regulatory control even in damaged intestines, so it is unlikely that this novel iron compound can bring about iron overload when administered orally.

Animals↗
PubMed1991

Dissociation of a ferric maltol complex and its subsequent metabolism during absorption across the small intestine of the rat.

1. The fate and disposition of [59Fe]-ferric [3H]-maltol after intravenous administration were investigated in anaesthetized rats. Immediate dissociation of ferric iron from maltol took place in the circulation even with high doses of ferric maltol (containing 1 mg elemental iron). In plasma samples withdrawn within 1 min of injection and subjected to gel filtration, 59Fe eluted with the high molecular weight proteins whilst the tritium was associated with low molecular weight material. 2. The rates of elimination of 59Fe and of tritium from the plasma and their ultimate fate were very different. The half life for 59Fe in the plasma was around 70 min and 59Fe appeared mainly in the bone marrow and liver. There was an initial rapid exit of tritium from the plasma with a half life of around 12 min. This was followed either by a plateau or by a rise in tritium levels, involving entry of maltol metabolites into the circulation. These metabolites could be recovered in the urine. 3. Entry of 59Fe and of tritium into the blood plasma after intraduodenal administration of [59Fe]-ferric [3H]-maltol was also very different. At low doses of ferric maltol (containing 100 micrograms elemental iron), the tritium appeared in the plasma in highest amounts within seconds and then decreased whilst there was a slow rise in 59Fe levels. At higher doses of ferric maltol (containing 7 mg elemental iron), levels of 59Fe in the plasma were highest at 5 min and then fell whereas tritium levels rose steadily. Mucosal processing of 59Fe prevented further entry of iron at high dose into the circulation. 4. Initial rates of uptake of [3H]-maltol into isolatcd intestinal fragments were measured over a range of concentrations and revealed that maltol alone could diffuse freely into the tissues whereas maltol complexed to iron showed saturable uptake kinetics similar to those seen with the iron itself. 5. After intestinal uptake, 59Fe and tritium were associated with different subcellular fractions, maltol itself being metabolized to the glucuronide conjugate within the intestinal mucosa. 6. It is concluded that dissociation of metal and ligand takes place before entry into the intestinal mucosa. Iron is then taken up on the endogenous carrier and processed in the normal way whilst maltol enters by diffusion, its rate of entry being limited by the degree of dissociation. It is subsequently metabolized by conjugation and eliminated rapidly from the body in the urine.

Animals↗
PubMed2005

3,4-di-deoxyglucosone-3-ene promotes leukocyte apoptosis.

BACKGROUND: Heat-sterilized, single-chambered, glucose-containing peritoneal dialysis solutions promote neutrophil apoptosis and impair the peritoneal antibacterial response. It has been proposed that glucose degradation products may be responsible for this effect. However, the precise contribution of individual glucose degradation products had not been addressed. METHODS: The effect of individual glucose degradation products on apoptosis in cultured human neutrophils and peripheral blood mononuclear cells was studied. RESULTS: Peritoneal dialysis solutions with a high content of both glucose and glucose degradation products accelerated neutrophil and mononuclear cell apoptosis. Among the different glucose degradation products, 3,4-di-deoxyglucosone-3-ene (3,4-DGE) accelerated apoptosis in neutrophils and peripheral blood mononuclear cells at concentrations (25 micromol/L) in the range found in heat-sterilized, single-chambered, 4.25% glucose peritoneal dialysis fluids. Apoptosis induced by 3,4-DGE was caspase-dependent and could be prevented by the broad-spectrum caspase inhibitor benzyloxycarbonyl-Val-Ala-DL-Asp-fluoromethylketone (zVAD-fmk). By contrast, no cytotoxicity was observed following the addition of methylglyoxal, acetaldehyde, formaldehyde, or 3-deoxyglucosone at concentrations found in peritoneal dialysis solutions. CONCLUSION: 3,4-DGE appears to be the main proapoptotic factor in high glucose peritoneal dialysis solutions. 3,4-DGE may impair peritoneal defenses by accelerating leukocyte apoptosis.

Apoptosis↗
PubMed1996

The combination of glycolic acid and hydroquinone or kojic acid for the treatment of melasma and related conditions.

BACKGROUND: Melasma continues to be a difficult problem. Although the cause is genetic, the condition is aggravated with sunlight, birth control pills, and pregnancy. Although hydroquinone is effective and has been available for years, a new product, kojic acid, has the advantage of being pharmaceutically more stable and, also, a tyrosinase inhibitor. OBJECTIVE: To evaluate on melasma and related conditions two similar formulations of glycolic acid/hydroquinone and glycolic acid/kojic acid. The therapeutic index of the two formulations is examined. METHODS: Thirty-nine patients were treated with kojic acid on one side of the face and hydroquinone in a similar vehicle on the other side of the face. The results were documented by a clinical investigator and with Wood's light examination combined with ultraviolet light photography. RESULTS: Fifty-one percent of the patients responded equally to hydroquinone and kojic acid. Twenty-eight percent had a more dramatic reduction in pigment on the kojic acid side; whereas 21% had a more dramatic improvement with the hydroquinone formulation. These results were not statistically different. The kojic acid preparation was more irritating. CONCLUSION: Both glycolic acid/kojic acid and glycolic acid/hydroquinone topical skin care products are highly effective in reducing the pigment in melasma patients. Both formulations should be available to the dermatologist to satisfy the patient's preferences.

Adult↗
PubMed1988

The effect of synthetic iron chelators on bacterial growth in human serum.

The effect of synthetic iron chelators of the 1-alkyl-3-hydroxy-2-methylpyrid-4-one class (the L1 series) and 1-hydroxypyrid-2-one (L4) on bacterial growth in human serum was compared with those of the plant iron chelators mimosine and maltol and of the microbial siderophore desferrioxamine. None of the synthetic chelators enhanced growth of 3 Gram-negative organisms (Yersinia enterocolitica, Escherichia coli and Pseudomonas aeruginosa); in some cases they were even inhibitory. L4 strongly stimulated growth of Staphylococcus epidermidis, but the L1 series had only a marginal effect. Maltol was mildly inhibitory to all 4 bacterial species, while mimosine enhanced the growth of S. epidermidis and Y. enterocolitica but had little effect on E. coli or P. aeruginosa. Desferrioxamine enhanced the growth of all except E. coli. These results suggest that the chelators of synthetic or plant origin may carry less risk of increasing susceptibility to bacterial infection in patients undergoing chelation therapy for iron overload than does desferrioxamine, the drug currently in clinical use.

Bacteria↗
PubMed1999

Effect of tyrosinase inhibitors on Tuber borchii mycelium growth in vitro.

This paper reports the effect of the tyrosinase (monophenol o-diphenol:oxygen oxidoreductase; EC 1.14.18.1) inhibitors diethyldithiocarbamate (DETC), L-tropolone, kojic acid, phenylthiourea (PTU) and L-mimosine on the in vitro growth of Tuber borchii (a white truffle) mycelium. A significant inhibitory effect on mycelium growth was observed for DETC, PTU and L-tropolone (0% growth compared to control at 100 microg ml(-1) DETC, PTU and L-tropolone and at 10 microg ml(-1) DETC and L-tropolone). As a comparison the action of the same inhibitors was also tested on the growth and pigmentation of the mould Cladosporium sphaerospermum. In the presence of CuSO(4) 10(-6) M T. borchii mycelium acquired pigmentation (as rounded aggregates compared to control revealed by SEM microscopy). Tyrosinase activity in the extract from T. borchii mycelium (18-day culture) was detected spectrophotometrically.

Ascomycota↗
PubMed2006

Reduction in solanapyrone phytotoxin production by Ascochyta rabiei transformed with Agrobacterium tumefaciens.

Agrobacterium tumefaciens was used to transform Ascochyta rabiei, the causal agent of chickpea blight. Employing a T-DNA containing a hygromycin resistance gene (hph), 908 transformants were obtained from germinated pycnidiospores on a selective medium containing hygromycin. Transformants were confirmed using PCR and Southern analyses and of four of these that were tested, two had integrated multicopies of the hph gene, one had two copies and one had a single insertion. Transformants were tested for the production of solanapyrone A toxin using a microtitre plate assay. Loss of toxin production by transformants was confirmed by reversed phase high-performance liquid chromatography. Sixteen transformants out of 668 tested produced significantly less solanapyrone A than the wild-type strain.

Agrobacterium tumefaciens↗
PubMedDate not supplied

Phospholipase A2 modulates respiratory burst developed by neutrophils in patients with rheumatoid arthritis.

Activated by bacterial peptides, phorbol esters, calcium ionophores and other agonists, neutrophils (PMNs) release the proinflammatory mediator, arachidonic acid (AA) via the intervention of phospholipase A(2) (PLA(2)). AA may play an essential role in activation of NADPH-oxidase, which is involved in the generation of superoxide anion by neutrophils. The present study is focused on the involvement of PLA(2) in the respiratory burst developed by PMNs isolated from patients with rheumatoid arthritis (RA). PLA(2) exists in very high levels in diseases such as rheumatoid arthritis and may cause acute inflammatory and proliferative changes in synovial structures. The respiratory burst was evaluated as superoxide anion release, using an amplified chemiluminescence method. The assays were performed using PMNs untreated or treated with different doses of stimulatory reagents (phorbol 12-myristate-13-acetate (PMA), calcium ionophore (A23187)). Our data suggested that PMA stimulated the production of superoxide anion in a dose-response manner, as compared with A23187, which did not induce a significant release of superoxide anion in PMNs-RA. The exogenous addition of AA significantly amplified the superoxide anion release by PMNs-RA stimulated with PMA and to a lesser extent, by PMNs stimulated with A23187. AA has also reversed the inhibitory effect of arachidonyl-trifluorometylketone and E-6-(bromomethylene)tetrahydro-3-(1-naphthalenyl)2H-pyran-2-one (BEL) on the superoxide anion release by PMNs-RA. In conclusion, the differential responses to these two agents suggested that different isoforms of PLA(2) were activated by A23187 or PMA, and support the idea that activation of these different PLA(2) served distinct functions of PMNs. Therefore, the inhibition of PLA(2) enzymes might be of great importance in the immunotherapy of rheumatoid arthritis.

Arachidonic Acid↗
PubMed1995

Effect of kojic acid on the oxidation of DL-DOPA, norepinephrine, and dopamine by mushroom tyrosinase.

Kojic acid inhibits effectively the rate of formation of pigmented product(s) and of oxygen uptake when DL-DOPA, norepinephrine and dopamine are oxidized by mushroom tyrosinase. In addition to the direct effect of kojic acid on the enzyme, kojic acid also affects the UV-VIS spectrum of the final product(s) formed, this being due to the ability of the o-quinones of these substrates to oxidize kojic acid to a yellow product(s). Kojic acid can thus prevent the conversion of the o-quinones of DL-DOPA, norepinephrine and dopamine to their corresponding melanin.

Basidiomycota↗
PubMed1997

Effect of maltol on the oxidation of DL-DOPA, dopamine, N-acetyldopamine (NADA), and norepinephrine by mushroom tyrosinase.

Maltol (3-hydroxy-2-methyl-4H-pyran-4-one) appears to inhibit the rate of oxidation of DL-DOPA, dopamine, NADA and epinephrine by tyrosinase when assayed spectrophotometrically but not when assayed polarographically. Maltol has an effect on the spectrum of product(s) formed when each catecholamine was oxidized by tyrosinase showing that maltol hastens the disappearance of the quinones, possibly by conjugating with them. Indeed, at relatively high concentrations, maltol prevented the conversion of DL-DOPA, dopamine, and norepinephrine to their corresponding melanins via tyrosinase.

Basidiomycota↗
PubMed1998

Arbutin increases the pigmentation of cultured human melanocytes through mechanisms other than the induction of tyrosinase activity.

We assessed the effects of arbutin on the pigmentation of cultured normal human melanocytes. As indicated by a cell-blotting assay, arbutin at concentrations in the range of 0.5-8 mM increased the pigmentation of the cultured melanocytes, while kojic acid at concentrations in the range of 0.5-4 mM decreased the pigmentation. The pigmentation-augmenting effect of arbutin was further confirmed by the results of a cell-pelleting assay, the traditional method of assessment. Treatment of the cells with arbutin increased the melanin content of the cells and the protein content as well. On the other hand, the tyrosinase activity in the cells was reduced by arbutin treatment. The levels of transcription of tyrosinase and tyrosinase related protein-1 genes were not affected by arbutin treatment as indicated by a semi-quantitative reverse transcription-polymerase chain reaction assay. These results demonstrate that arbutin promotes an increase in pigmentation of cultured human melanocytes that is not mediated by augmented tyrosinase activity.

Arbutin↗