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At least 1,207 records · Page 67Linked to original sources
PubMed1994

Formaldehyde-free collagen glue in experimental lung gluing.

Because of the well-known limitations of the adhesive strength of fibrin glue, it is imperative to develop a stronger glue with acceptable biocompatibility. This was accomplished by removing the formaldehyde component from gelatin-resorcinol-formaldehyde glue and replacing it by two less toxic aldehydes--pentanedial and ethanedial. To evaluate the adhesive strength of this new glue, GR-DIAL, lung incisions in rabbit hybrids were glued together. Each group (n = 5) was examined histologically after 2 days and 1, 2, and 4 weeks. The glue disintegrated gradually with good bioresorption when the incision was closed with a thin layer of glue. The healing process was favorable, indicating good biocompatibility. Therefore, GR-DIAL glue is capable of enhancing the use of surgical glues in the field of thoracic surgery by enabling surgeons to close larger parenchymal lesions than with fibrin glue.

Animals↗
PubMed1985

Differential inhibition of A, B and C fibres in the rat vagus nerve by lidocaine, eugenol and formaldehyde.

Evoked compound-action potentials (cAP) in all three fibre types of the isolated nerve were reversibly depressed by exposure to the drugs. After 20 min exposure, lidocaine (0.5 mM) depressed the amplitude of the A and B fibre potentials significantly more than the C fibre potential. With eugenol (0.8 mM), there was no significant difference in depression of A, B and C fibre activity. With formaldehyde (4.5 mM), the latency was longer, and the C fibres were initially significantly more depressed than the A and B fibres. As dull pain from a chronically-inflamed pulp is believed to be mediated through C fibres, these results may explain the difficulties in obtaining complete local analgesia with lidocaine. They indicate that application of low concentrations of eugenol and formaldehyde to the pulp-dentine organ may have an analgesic effect on pain mediated through both A and C fibres.

Action Potentials↗
PubMed1985

Pyruvate prevents the ATP depletion caused by formaldehyde or calcium-chelator esters in the human red cell.

Formaldehyde released during hydrolysis of calcium-chelator esters incorporated into cells blocks glycolysis in the human erythrocyte (Tiffert, T., García-Sancho, J. and Lew, V.L. (1984) Biochim. Biophys. Acta 773, 143-156). This blockade is due to the inhibition of glyceraldehyde-3-phosphate dehydrogenase by NAD+ depletion caused by enzymatic oxidation of formaldehyde coupled to NADH production. The addition of pyruvate to the incubation medium prevents or reverts ATP depletion.

Adenosine Triphosphate↗
PubMed1985

Description of microparticles in urea-formaldehyde foam insulation products.

Thousands of families living in homes insulated with urea-formaldehyde foam (UFF) have complained of various health problems. This product is now banned from the market both in Canada and the United States. Formaldehyde gas emitted by the product has been considered to be the source of these health problems but this cause-effect relationship has not been confirmed as yet. It has been suggested that other contaminants released by the foam could be involved. Work initiated to verify this possibility has permitted the observation of microparticles of less than 1 micron in diameter in foam samples obtained from various houses. The microparticles can easily be removed from the foam by passing air through it or, simply, by immersing it in water. These particles have been studied by different microscopy techniques and their morphological characteristics are described. They may represent a potential health risk.

Construction Materials↗
PubMed1985

B-Z transition in poly(dG-dC).poly(dG-dC) in the presence of formaldehyde amino derivatives.

It was shown by circular dichroism that the B-Z transition of poly(dG-dC).poly(dG-dC) in high NaCl concentrations occurred more rapidly in the presence of formaldehyde and Tris. The product of formaldehyde and glycine interaction induces changes in the poly(dG-dC).poly(dG-dC) CD spectral characteristics of a 'B-like' conformation. It is supposed that the B-Z transition occurs without large-scale hydrogen bond breakage.

Circular Dichroism↗
PubMed1996

Formaldehyde produced endogenously via deamination of methylamine. A potential risk factor for initiation of endothelial injury.

Methylamine can be converted by semicarbazide-sensitive amine oxidase (SSAO) to formaldehyde and hydrogen peroxide, which have been proven to be toxic towards cultured endothelial cells. We investigated whether or not these deaminated products from methylamine can exert potentially hazardous toxic effects in vivo. Long lasting residual radioactivity in different tissues was detected following administration of [14C]-methylamine in the mouse. Approximately 10% of the total administered radioactivity could even be detected 5 days after injection of [14C]-methylamine. Eighty percent of the formation of irreversible adducts can be blocked by a highly selective SSAO inhibitor, (E)-2-(4-fluorophenethyl)-3-fluoroallylamine hydrochloride (MDL-72974A). The residual radioactivity was primarily associated with the insoluble tissue components and the soluble macromolecules. Radioactively labelled macromolecules were fragmented following enzymatic proteolysis. Results suggest that the formaldehyde derived from methylamine interacts with proteins in vivo. In the streptozotocin-induced diabetic mice, both SSAO activity and the formation of residual radioactivity were found to be significantly increased in the kidney. Chronic administration of methylamine enhances blood prorenin level, which strongly suggests that uncontrolled deamination of methylamine may be a risk factor for initiation of endothelial injury, and subsequent genesis of atherosclerosis.

Allyl Compounds↗
PubMed1993

Denture adhesives: cytotoxicity, microbial contamination, and formaldehyde content.

Denture adhesives are extensively used to enhance retention of dentures. Denture adhesives and their leachable components are ingested, but reports on the biologic aspects of denture adhesives are scarce. This study investigated some biological properties of 19 commercially available denture adhesives. The adhesives were assessed by the agar overlay technique and analyzed for microbial contamination and formaldehyde content. In the agar overlay test, all of the materials caused severe cytotoxic effects. Sabouraud dextrose agar was used for cultivation of fungi and tryptone soya broth for cultivation of aerobes, including fungi. Most of the samples tested showed microbial growth. The formaldehyde test revealed the presence of substantial amounts in four products and minor amounts in two products.

Adhesives↗
PubMed1975

Genetic effects of formaldehyde in yeast. I. Influence of the growth stages on killing and recombination.

In random cultures, stationary phase cells of Saccharomyces cerevisiae are more resistant to killing induced by formaldehyde than are exponentially growing cells. It is shown that this compound induces intra- and intergenic recombination in this eucaryotic organism. In synchronized populations the lag and G1 phases demonstrate the higher resistance to both killing and induction of recombinants by formaldehyde whereas maximal sensitivity occurs during the end of G2 and/or the mitotic division. This pattern in contrast with that found after treatments by ionizing or ultraviolet radiations.

Formaldehyde↗
PubMed1980

Biochemical analysis of damage induced in yeast by formaldehyde.

Cross-links between DNA and proteins were induced by formaldehyde treatment in yeast cells. This damage can be repaired by post-treatment incubation of cells or protoplasts in nutrient medium. This repair was observed for wild-type cells as well as for a UV-sensitive, excision-deficient mutant (rad1-3), also sensitive to the lethal effect of formaldehyde.

DNA Repair↗
PubMed1989

Liquid holding increases mutation induction by formaldehyde and some other cross-linking agents in Escherichia coli K12.

The induction by some cross-linking agents of forward mutations leading to nalidixic acid resistance in Escherichia coli K12/343/113 was considerably enhanced when a 24-h period of liquid holding was interpolated between treatment and growth phase. Liquid holding increased the mutagenic effectiveness of nor-nitrogen mustard (NNM) 28-fold, of phosphoramide mustard (PAM) 10-fold, and of tris-ethyleneimino)-phosphineoxide (TEPA), tris(chloroethyl)amine (TCEA) and chloroacetaldehyde (CAA) 3-fold, over the complete concentration range. By contrast, the activities of cisplatin (CDDP), transplatin (TDDP) and chloracetamide-N-metholol (CAM) were slightly decreased after liquid holding. Liquid holding did not measurably influence the mutagenicity of formaldehyde at low concentrations, whereas at higher concentrations an 8-fold increase was observed. As opposed to the considerable activity in the Uvr+ strain, formaldehyde was found not to be mutagenically active in an E. coli strain carrying a deletion of the uvrB gene.

Cross-Linking Reagents↗
PubMed1992

Formaldehyde, glyoxal, urethane, methyl carbamate, 2,3-butanedione, 2,3-hexanedione, ethyl acrylate, dibromoacetonitrile and 2-hydroxypropionitrile induce chromosome loss in Saccharomyces cerevisiae.

Induction of mitotic chromosome loss could be demonstrated for the dialdehyde glyoxal, the diketones 2,3-butanedione and 2,3-hexanedione, ethyl and methyl carbamate, ethyl acrylate, dibromoacetonitrile, 2-hydroxypropionitrile and formaldehyde, but only when they were combined with subacute concentrations of propionitrile, which is a strong inducer of chromosomal malsegregation. The same chemicals did not induce mitotic chromosome loss when applied in pure form. However, glyoxal, ethyl acrylate, dibromoacetonitrile and formaldehyde when applied in pure form also induced mitotic recombination. Respiratory deficiency was induced, in the absence of propionitrile, by these recombinogenic agents and also by 2,3-hexanedione and 2-hydroxypropionitrile which are not recombinogenic.

Acetonitriles↗
PubMed1977

Repair of postextraction sockets: influence of homogeneous bone implants preserved by formaldehyde. An experimental study in dogs.

Small bone sticks from a dog, fixed in formaldehyde from 1 to 4 weeks, were used as homoimplants in the left postextraction sockets of dogs, and the right sockets were allowed to heal as ungrafted controls. The animals were killed 5, 11, 22, and 60 days after implantation. No obvious differences were discovered, either clinically or radiographically, between the repair of the control sockets and that of the experimental sockets. However, appreciable histologic differences could be noted. The presence of the implant disturbed and retarded both the organization of the granulation tissue and the process of intra-alveolar ossification. The attempt to use homogeneous bone implants that had been preserved in formaldehyde in order to stimulate osteogenesis in the host produced unsatisfactory results, since it retarded the process of postextraction alveolar repair.

Alveolar Process↗
PubMed1984

Formaldehyde emitted by chemical vapor sterilizers.

Formaldehyde has been identified as a potential occupational carcinogen and is a component of chemical solutions used in chemical vapor sterilizers. This study evaluated room air for formaldehyde in rooms where chemical vapor sterilizers were in use.

Air Pollutants↗
PubMed1984

Differentiation between metabolic incorporation and covalent binding in the labeling of macromolecules in the rat nasal mucosa and bone marrow by inhaled [14C]- and [3H]formaldehyde.

The mechanisms of labeling of macromolecules (DNA, RNA, and protein) in the respiratory and olfactory mucosa, and in the bone marrow (femur) of male Fischer-344 rats exposed to [14C]- and [3H]formaldehyde [( 14C]- and [3H]CH2O) were investigated. Animals were exposed for 6 hr to atmospheres containing [14C]- and [3H]CH2O at concentrations of 0.3, 2, 6, 10, or 15 ppm, 1 day following a single pre-exposure to the same concentration of unlabeled CH2O. The major route of nucleic acid labeling at all concentrations and in all tissues was metabolic incorporation; protein labeling in the respiratory mucosa was mainly due to covalent binding at the higher CH2O concentrations. Incorporation of [14C]CH2O into DNA in the respiratory mucosa was maximal at 6 ppm but decreased at higher concentrations, whereas labeling of DNA in the olfactory mucosa and bone marrow increased monotonically with concentration. Evidence for covalent binding of CH2O to respiratory mucosal DNA was obtained at CH2O concentrations equal to or greater than 2 ppm. The concentration of CH2O covalently bound to DNA at 6 ppm was 10.5-fold higher than at 2 ppm, indicating significant nonlinearity of DNA binding with respect to the inhaled formaldehyde concentration under these conditions. Covalent binding to proteins increased in an essentially linear manner with increases in the airborne concentration. No evidence was obtained for the formation of covalent adducts with macromolecules in the olfactory mucosa or bone marrow. The nonlinear increase in covalent binding to respiratory mucosal DNA with increasing CH2O concentrations may be explained either by a decrease in the efficiency of defense mechanisms or by an increase in the availability of reaction sites on the DNA resulting from increased cell turnover.

Animals↗
PubMed1984

Induction of formaldehyde sensitivity in guinea pigs.

Occupational exposure to formaldehyde (HCHO) has been implicated in development of both dermal hypersensitivity and pulmonary hypersensitivity. The purpose of this study was to assess the route of exposure most likely to cause sensitization in animals and the potency of formaldehyde as a sensitizing chemical. Three routes of exposure were utilized: inhalation, dermal, and injection (with Freund's complete adjuvant). For inhalation exposure, groups were exposed to 6 ppm (Group I) or 10 ppm HCHO (Group II) for 6 hr/day or 8 hr/day (Group III) on 5 consecutive days. Animals were evaluated for skin sensitivity, production of anti-HCHO antibody, and respiratory sensitivity (both immediate- and delayed-onset) to HCHO. Of the animals receiving inhalation exposure, two of four animals in Group III displayed dermal sensitivity. No antibodies or pulmonary sensitivity were detected in any animals in any of these groups. Animals exposed to HCHO by injection displayed extensive dermal reactions when skin tested. In addition, two of four animals in this group developed antibodies to HCHO in low titer. No pulmonary sensitivity was detected. Animals exposed to HCHO by dermal contact developed neither pulmonary sensitivity nor antibodies to HCHO. However, all of these animals developed skin sensitivity. The severity of the contact sensitivity response, as well as the percentage of animals sensitized, increased with exposure dose. These results indicated that HCHO was a skin sensitizer in the guinea pig without causing detectable respiratory hypersensitivity.

Administration, Topical↗
PubMed1985

Sensory irritation response to inhaled aldehydes after formaldehyde pretreatment.

Pretreatment of Fischer-344 (F-344) rats with formaldehyde (HCHO) induces significant cross tolerance to the sensory irritation properties of Cl2. The purpose of this study was to determine if HCHO pretreatment would cause sensory irritation cross tolerance to other inhaled aldehydes. Male F-344 rats, weighing 190 to 210 g, were pretreated with 15 ppm HCHO, 6 hr/day for 9 days, and challenged on the 10th day with a saturated (acetaldehyde, propionaldehyde, and butyraldehyde), unsaturated (acrolein and crotonaldehyde), or cyclic (cyclohexanecarboxaldehyde, 3-cyclohexene-1-carboxaldehyde, and benzaldehyde) aldehyde. The sensory irritation response in these animals was quantified by measuring respiratory rate depression in a head-only inhalation chamber using plethysmographic techniques. Control animals were challenged identically without prior pretreatment. In naive (nonpretreated) animals, the concentration eliciting a 50% decrease in respiratory rate (RD50) was 23 ppm or less for unsaturated aliphatic aldehydes. For cyclic and saturated aliphatic aldehydes, the RD50 ranged from 600 to 1000 ppm and 3000 to 6800 ppm, respectively. Formaldehyde pretreatment resulted in cross tolerance only with acetaldehyde (RD50 increased 3.5-fold) and acrolein (RD50 increased 5-fold). These results indicate that the development of cross tolerance following HCHO pretreatment is not a general phenomenon. Prediction of acceptable concentrations of occupational exposure for the prevention of sensory irritation in humans has been based primarily on RD50 data for mice. Comparison of the RD50 values obtained for rats in this investigation with previously published results for mice varied by over one-half an order of magnitude, thereby disputing the usefulness of data from F-344 rats in setting threshold limit values for the prevention of sensory irritation.

Aldehydes↗
PubMed1986

More precise localization of nasal tumors associated with chronic exposure of F-344 rats to formaldehyde gas.

Considerable interest and research have resulted from the finding that squamous cell carcinomas, polypoid adenomas, and a small number of other nasal neoplasms occurred in F-344 rats following chronic inhalation exposure to formaldehyde. These tumors were reported to originate in the anterior portion of the nasal cavity but their precise location in the nose was not determined. Histologic sections from the nasal passages of these rats have been reexamined and the location of each tumor has been recorded. The majority of squamous cell carcinomas occurred on the anterior portion of the lateral aspect of the nasoturbinate and adjacent lateral wall (57%) or the midventral nasal septum (26%). Polypoid adenomas were confined to a small region of the anterior nasal cavity and were restricted to the free margins of the naso-and maxilloturbinates and lateral wall adjacent to these margins. One neoplasm, considered to be the malignant counterpart of the polypoid adenoma, originated on the dorsal margin of the maxilloturbinate in the same region of the nose. Remaining neoplasms were generally too large or too poorly preserved for assessment of their site of origin. Mechanistic studies directed toward a better understanding of the nasal carcinogenicity of formaldehyde, or other nasal carcinogens. should take into account the anatomic sites of origin of the neoplasms whenever this can be determined.

Animals↗
PubMed1986

A simple procedure for the extraction of the native chromophore of visual pigments: the formaldehyde method.

The chromophore of visual pigments was efficiently extracted in its original isomeric conformation by dichloromethane/hexane in the presence of excess formaldehyde. This new method of extraction (the formaldehyde method) in combination with HPLC is useful for the determination of the chromophore composition of visual pigments. The chromophore isolated by this method is biologically active and can be used for regeneration experiments.

Animals↗