Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Root surface demineralization is widely used as an adjunct to periodontal treatment. To clarify the influence of citric acid root conditioning on periodontal wound healing, the effects of citric acid and associated extracellular acidosis on the viability (MTT assay), attachment and protein synthesis ([3H]-proline incorporation into trichloroacetic acid-precipitated proteins) of human gingival fibroblasts (GF) were investigated. A concentration of 47.6 mmol/L of citric acid (pH 2.3) in water led to total cell death within three minutes of incubation. Media containing 23.8 mmol/L and 47.6 mmol/L of citric acid exerted strong cytotoxicity (47 to 90 per cent of cell death) and inhibited protein synthesis (IC50 = 0.28 per cent) of GF within three hours of incubation. Incubation of cells in a medium containing 11.9 mmol/L of citric acid also suppressed the attachment and spreading of fibroblasts on culture plates and Type I collagen, with 58 per cent and 22 per cent of inhibition, respectively. Culture medium supplemented with 11.9, 23.8 and 47.6 mmol/L of citric acid also led to extracellular acidosis by decreasing the pH value from 7.5 to 6.3, 5.2 and 3.8, respectively. In addition, it was confirmed that the toxic effect of media containing citric acid was due to their acidity rather than the citrate content. Most of the citric acid-induced cell death could be prevented by adjusting the pH value of the culture medium to pH 7.5. Sodium citrate, at a concentration of 47.6 mmol/L, also exerted little cytotoxicity. The results suggested that toxicity of citric acid in specific stages of the healing process must be considered prior to its clinical application. Careful management of citric acid in order to avoid contact with tissue or the development of other demineralizing agents is important in enhancing periodontal wound healing.
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PMID:The effects of extracellular citric acid acidosis on the viability, cellular adhesion capacity and protein synthesis of cultured human gingival fibroblasts. 1045 69

The attachment of blood platelets to the surface of bare and protein-coated thickness-shear mode acoustic wave devices operating in a flow-through configuration has been studied. Platelets in washed from bind to the gold electrodes of such sensors, but the resulting frequency shifts are far less than predicted by the conventional mass-based model of device operation. Adherence to albumin and various types of collagen can be produced by on-line introduction of protein or by a pre-coating strategy. Differences in attachment of platelets to collagen types I and IV and the Horm variety can be detected. Platelets attached to collagen yield an interesting delayed, but reversible signal on exposure to a flowing medium of low pH. Scanning electron microscopy of sensor surfaces at various time points in this experiment reveals that originally intact platelets are eventually destroyed by the high acidity of the medium. The reversible frequency is attributed to the presence of removable platelet granular components at the sensor-liquid interface.
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PMID:Blood platelet adhesion to protein studied by on-line acoustic wave sensor. 1128 36

Poorly crystalline apatite (PCA) crystals introduced into bone tissue should be stable for a definite period before they are dissolved as a result of a host response. In this report, the dissolution of PCA crystals by the action of osteoclasts was studied on artificial thin films. These consisted of PCA crystals having similar crystallographic properties to bone crystals which were developed for assaying the osteoclast activity in vitro. The dissolution of minerals by osteoclasts decreased along with the decreased amount of labile phosphate and hydrogen phosphate domains of apatite crystals, which were caused by the crystal maturation temperature. A profound effect on mineral dissolution by pH in the culture medium was also shown. Low acidity considerably increased mineral dissolution, whereas a slight alkalinity totally blocked mineral dissolution. There was little difference in the mineral dissolution behavior of osteoclasts near the physiologic pH. In addition, it was determined whether mineral dissolution by osteoclasts was dependent on the destruction of the organic matrix. Nocodazole was introduced to inhibit the secretion of hydrolytic enzymes, and acetazolamide was added to inhibit acid production by the osteoclasts. There was no significant change as a result of nocodazole addition on mineral dissolution or by the addition of acetazolamide on degradation of collagen. These results indicate that small changes in the physicochemical properties of apatite crystals can decrease resorption by osteoclasts, which can be highly activated at low pH. These results also suggest that mineral dissolution and organic degradation by osteoclasts are self-regulating.
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PMID:Dissolution of poorly crystalline apatite crystals by osteoclasts determined on artificial thin-film apatite. 1134 May 96

Ascorbic acid has been associated with the slowing of osteoarthritis progression in guinea pig and man. The goal of this study was to evaluate transcriptional and translational regulation of cartilage matrix components by ascorbic acid. Guinea pig articular cartilage explants were grown in the presence of L-ascorbic acid (L-Asc), D-isoascorbic acid (D-Asc), sodium L-ascorbate (Na L-Asc), sodium D-isoascorbate (Na D-Asc), or ascorbyl-2-phosphate (A2P) to isolate and analyze the acidic and nutrient effects of ascorbic acid. Transcription of type II collagen, prolyl 4-hydroxylase (alpha subunit), and aggrecan increased in response to the antiscorbutic forms of ascorbic acid (L-Asc, Na L-Asc, and A2P) and was stereospecific to the L-forms. Collagen and aggrecan synthesis also increased in response to the antiscorbutic forms but only in the absence of acidity. All ascorbic acid forms tended to increase oxidative damage over control. This was especially true for the non-nutrient D-forms and the high dose L-Asc. Finally, we investigated the ability of chondrocytes to express the newly described sodium-dependent vitamin C transporters (SVCTs). We identified transcripts for SVCT2 but not SVCT1 in guinea pig cartilage explants. This represents the first characterization of SVCTs in chondrocytes. This study confirms that ascorbic acid stimulates collagen synthesis and in addition modestly stimulates aggrecan synthesis. These effects are exerted at both transcriptional and post-transcriptional levels. The stereospecificity of these effects is consistent with chondrocyte expression of SVCT2, shown previously to transport L-Asc more efficiently than D-Asc. Therefore, this transporter may be the primary mechanism by which the L-forms of ascorbic acid enter the chondrocyte to control matrix gene activity.
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PMID:The effects of ascorbic acid on cartilage metabolism in guinea pig articular cartilage explants. 1185 33

The natural resin collected from the trunk wood of Protium heptaphyllum is used in folk medicine to treat inflammatory conditions and to hasten wound repair. In the search of new potential anti-inflammatory agents with gastroprotective property, the present study evaluated its effects in experimental models of gastric ulcer and inflammation. In mice, the resin (200 and 400 mg/kg) significantly attenuated the gastric damage induced by ethanol or acidified ethanol (HCl/ethanol), in a manner similar to N-acetyl-L-cysteine (NAC), a replenisher of sulfhydryls. Unlike NAC the resin failed to restore the ethanol-induced depletion of non-protein sulfhydryl content, indicating a different mechanism of gastroprotection. However, in 4-h pylorus-ligated rats, the resin significantly reduced the total acidity without much change in gastric secretory volume. In rats, at similar doses the resin did not modify the hind-paw edema induced by carrageenan, but effectively reduced the formation of cotton pellet-induced granuloma, suggesting its inhibitory effect on collagen formation but not on acute edema. Furthermore, the vascular permeability increase induced by acetic acid was significantly reduced in mice that received 400 mg/kg resin. The resin demonstrated no overt toxicity in mice up to an oral dose of 5 g/kg. Phytochemical analysis revealed the presence of alpha- and beta-amyrins as principal triterpenoid constituents of resin, which were previously described to have anti-ulcer property. These findings indicate the potential gastroprotective and anti-inflammatory property of P. heptaphyllum resin and further support its popular use in gastrointestinal disorders.
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PMID:Gastroprotective and anti-inflammatory effects of resin from Protium heptaphyllum in mice and rats. 1464 90

Alendronate (ALD) causes serious gastrointestinal adverse effects. The aim of this study was to investigate whether taurine (TAU), a semi-essential amino acid and an antioxidant, improves the alendronate-induced gastric injury. Rats were administered 20 mg/kg ALD by gavage for 4 days, either alone or following treatment with TAU (50 mg/kg, i.p.). On the last day of treatment, following drug administration, pylorus ligation was performed and 2 h later, rats were killed and stomachs were removed. Gastric acidity and tissue ulcer index values, lipid peroxidation and glutathione (GSH) levels, myeloperoxidase (MPO) activity as well as the histologic appearance of the stomach tissues were determined. Chronic oral administration of ALD induced significant gastric damage, increasing lipid peroxidation, MPO activity and collagen content, as well as decreasing tissue GSH levels. Treatment with TAU prevented the damage and also the changes in biochemical parameters. Findings of the present study suggest that ALD induces oxidative gastric damage by a local irritant effect, and that TAU ameliorates this damage by its antioxidant and/or membrane-stabilizing effects.
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PMID:Protective effect of taurine against alendronate-induced gastric damage in rats. 1566 Sep 65

Paracetamol is regarded as a relatively safe drug in the gastro-duodenal region of humans but recent epidemiological investigations have suggested that at high doses there may be an increased risk of ulcers and bleeding. To investigate the possibility that inflammatory conditions and gastric acidity may play a role in potentiating development of gastric mucosal injury from paracetamol in rats (as noted previously with various non-steroidal anti-inflammatory drugs) we studied the gastric irritant effects of paracetamol and some phenolic and non-phenolic analgesics and antipyretics in rats with adjuvant or collagen II induced arthritis or zymosan-induced paw inflammation and given 1.0 ml hydrochloric acid (HCl) 0.1 M and/or an i. p. injection of the cholinomimetic, acetyl-beta-methyl choline chloride 5.0 mg/kg. Gastric lesions were determined 2 h after oral administration of 100 or 250 mg/kg paracetamol or at therapeutically effective doses of the phenolic or non-phenolic analgesics/antipyretics. The results showed that gastric mucosal injury occurred with all these agents when given to animals that received all treatments so indicating there is an adverse synergy of these three factors, namely: (i) intrinsic disease; (ii) hyperacidity; and (iii) vagal stimulation for rapidly promoting gastric damage, both in the fundic as well as the antral mucosa, for producing gastric damage by paracetamol, as well as the other agents. Removing one of these three predisposing factors effectively blunts/abolishes expression of this paracetamol-induced gastrotoxicity in rats. These three factors, without paracetamol, did not cause significant acute gastropathy.
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PMID:Paracetamol [acetaminophen]-induced gastrotoxicity: revealed by induced hyperacidity in combination with acute or chronic inflammation. 1698 95

Painful degenerative disc disease is a major health problem and for successful tissue regeneration, MSCs must endure and thrive in a harsh disc microenvironment that includes matrix acidity as a critical factor. MSCs were isolated from bone marrow of Sprague-Dawley rats from two different age groups (<1 month, n=6 and 4-5 months, n=6) and cultured under four different pH conditions representative of the healthy, mildly or severely degenerated intervertebral disc (pH 7.4, 7.1, 6.8, and 6.5) for 5 days. Acidity caused an inhibition of aggrecan, collagen-1, and TIMP-3 expression, as well as a decrease in proliferation and viability and was associated with a change in cell morphology. Ageing had generally minor effects but young MSCs maintained greater mRNA expression levels. As acidic pH levels are typical of increasingly degenerated discs, our findings demonstrate the importance of early interventions and predifferentiation when planning to use MSCs for reparative treatments.
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PMID:MSC response to pH levels found in degenerating intervertebral discs. 1913 33

Detailed analysis of copper compounds migration in the corneal stroma are presented. The biochemical conditions of the middle periphery of the cornea is found to inhibit copper ions movement to the center in patients with keratoconus due to increased tear alkalinity. Low concentration of dichlorocuprate (I) ion in the center of cornea results in inactivation of lysyl oxidase, an enzyme that catalyzes collagen cross-linking, and thus promotes keratoconus. Revealed association of tear acidity and copper distribution in cornea offers new opportunities in pathogenic treatment of keratoconus.
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PMID:[The role of tear acidity and Cu-cofactor of lysyl oxidase activity in the pathogenesis of keratoconus]. 2172 Dec 63

Fluoropolymer surfaces are unique in view of the fact that they are quite inert, have low surface energies, and possess high thermal stabilities. Attempts to modify fluoropolymer surfaces have met with difficulties in that it is difficult to control the modification to maintain bulk characteristics of the polymer. In a previously described method, the replacement of a small fraction of surface fluorine by acid groups through radio frequency glow discharge created a surface with unexpected reactivity allowing for attachment of proteins in their active states. The present study demonstrates that 1-ethyl-3-[3-dimethylaminopropyl] carbodiimide hydrochloride (EDC) reacts with the acid groups on fluoropolymer surfaces in a novel reaction not previously described. This reaction yields an excellent leaving group in which a primary amine on proteins can substitute to form a covalent bond between a protein and these surfaces. In an earlier study, we demonstrated that collagen IV could be deposited on a modified PTFE surface using EDC as a linker. Once collagen IV is attached to the surface, it assembles to form a functional stratum resembling collagen IV in native basement membrane. In this study, we show data suggesting that the fluorine to carbon ratio determines the acidity of the fluoropolymer surfaces and how well collagen IV attaches to and assembles on four different fluoropolymer surfaces.
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PMID:Radio frequency glow discharge-induced acidification of fluoropolymers. 2188 36


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