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PubMed1993

Molecular structure and genetic regulation of SFA, a gene responsible for resistance to formaldehyde in Saccharomyces cerevisiae, and characterization of its protein product.

A 3.7 kb DNA fragment of yeast chromosome IV has been sequenced that contains the SFA gene which, when present on a multi-copy plasmid in Saccharomyces cerevisiae, confers hyper-resistance to formaldehyde. The open reading frame of SFA is 1158 bp in size and encodes a polypeptide of 386 amino acids. The predicted protein shows strong homologies to several mammalian alcohol dehydrogenases and contains a sequence characteristic of binding sites for NAD. Overexpression of the SFA gene leads to enhanced consumption of formaldehyde, which is most probably the reason for the observed hyper-resistance phenotype. In sfa::LEU2 disruption mutants, sensitivity to formaldehyde is correlated with reduced degradation of the chemical. The SFA gene shares an 868 bp divergent promoter with UGX2 a gene of yet unknown function. Promoter deletion studies with a SFA promoter-lacZ gene fusion construct revealed negative interference on expression of SFA by upstream sequences. The upstream region between positions -145 and -172 is totally or partially responsible for control of inducibility of SFA by chemicals such as formaldehyde (FA), ethanol and methyl methanesulphonate. The 41 kDa SFA-encoded protein was purified from a hyper-resistant transformant; it oxidizes long-chain alcohols and, in the presence of glutathione, is able to oxidize FA. SFA is predicted to code for a long-chain alcohol dehydrogenase (glutathione-dependent formaldehyde dehydrogenase) of the yeast S. cerevisiae.

Alcohol Dehydrogenase↗
PubMed1985

Depletion of nasal mucosal glutathione by acrolein and enhancement of formaldehyde-induced DNA-protein cross-linking by simultaneous exposure to acrolein.

Incubation of homogenates of rat nasal mucosa with acrolein resulted in the apparent formation of DNA-protein cross-links. However, inhalation exposure of male Fischer-344 rats to acrolein (2.0 ppm, 6 h) did not cause detectable DNA-protein cross-linking in the nasal respiratory mucosa. Simultaneous exposure of rats to both acrolein (2.0 ppm) and formaldehyde (6.0 ppm) for 6 h resulted in a significantly higher yield of DNA-protein cross-links than was obtained following exposure to formaldehyde (6.0 ppm) alone. Acrolein exposure at concentrations of 0.1, 0.5, 1.0, or 2.5 ppm resulted in a concentration-dependent depletion of nonprotein sulfhydryl groups in the nasal respiratory mucosa. A plausible explanation for the enhancement of DNA-protein cross-links by simultaneous exposure to formaldehyde and acrolein may be that depletion of glutathione by acrolein inhibited the oxidative metabolism of formaldehyde, leading to an increase of formaldehyde-induced DNA-protein cross-links.

Acrolein↗
PubMed1990

Exposure to formaldehyde and glutardialdehyde in operating theatres.

The disinfection of operating theatres and adjoining areas is carried out with chemical disinfectants containing not only formaldehyde but also glutardialdehyde. The cleaning staff is therefore unavoidably exposed to these two substances. Adequate and correct evaluation of staff exposure must be based on exact quantification of these aldehydes in room air. The statutory MAK-levels of 0.5 ppm (formaldehyde) and 0.2 ppm (glutardialdehyde) call for highly sensitive and specific analytical methods for monitoring exposure that should be suited for personal measuring as well. Since previous methods have failed to meet these requirements, we have adapted a newly developed method for the specific measurement of formaldehyde and other aldehydes and ketones for the personal monitoring of formaldehyde and glutardialdehyde. Detailed personal measurings over whole shifts and of short-term peaks have yielded the following results: During routine disinfection activities in operating theatres using low concentrations of disinfectants, the limits prescribed by MAK can be respected. Disinfections to prevent notifiable infectious diseases in accordance with the Federal Epidemic Law (Bundesseuchengesetz) involving the use of higher disinfectant concentrations are liable to exceed the MAK limits for formaldehyde and glutardialdehyde. If for reasons of hygiene this excess exposure cannot be avoided, effective protection of the cleaning staff from unacceptably high concentrations of these substances can be ensured only by providing personal protective outfits.

Air Pollutants, Occupational↗
PubMed1979

Quantitative fluorescence histochemistry of combined formaldehyde-chloral-induced fluorescence of amino-terminal tryptophyl-peptide in model experiments and in the pars intermedia of the rat hypophysis.

The relationship between the intensity of combined formaldehyde-chloral vapour-induced fluorescence and the concentration of amino-terminal tryptophyl-peptide in model experiments was found to be non-linear. At a certain concentration the intensity began to increase more slowly than the concentration, and when the concentration further increased the intensity even began to decrease. Based on the studies previously reported and on the above findings it seems that fluorescence induced by combined formaldehyde-chloral vapour, glyoxylic acid vapour and possibly also other combined formaldehyde and carbonyl compounds in the hypophyseal cells containing amino-terminal tryptophyl-peptides is quenched in normal conditions due to the high local concentration. Thus, small to moderate changes in the amounts of amino-terminal tryptophyl-peptides cannot be observed by measuring the fluorescence intensity. In tissue experiments the intensity of combined formaldehyde-chloral vapour-induced fluorescence in the rat pars intermedia was measured after reserpine treatment, which decreases the number of hormone storage granules as demonstrated electron microscopically. The fluorescence intensity measurements were combined with an estimation of the amounts of amino-terminal tryptophyl-peptides extracted from hypophyses and separated in thin-layer chromatography, and subsequently demonstrated by combined formaldehyde-chloral vapour and a protein stain (amido black). Reserpine treatment decreased the fluorescence intensity in the pars intermedia and in thin-layer chromatography, and the staining of the fluorescent band with amido black was also decreased. Amino-terminal tryptophyl-peptides appeared to be depleted from the pars intermedia cells together with endorphins and other hormones of the ACTH/MSH cells containing tryptophan.

Animals↗
PubMedDate not supplied

Formaldehyde fixation and microwave irradiation.

Formaldehyde is the most commonly used fixative in pathology laboratories. However, due to time pressures, this fixative is often not optimally exploited. The majority of biopsies are only partly fixed when histoprocessing is started, with adverse effects. This paper reports how formaldehyde fixation is improved, by using 1.5 min of microwave irradiation of tissue previously soaked for four hours in the fixation solution. It is argued that this beneficial effect of microwave irradiation can be attributed to the acceleration of the reaction of formaldehyde to the tissue. Formation of free formaldehyde, by the dehydration of methylene glycol present in the tissue when the irradiation starts, is also enhanced. Five different formaldehyde-containing fixatives were evaluated, using five different working protocols. Spleen was taken as a suitable tissue for these tests. The technique described leads to uniform microscopical results. It is a simple method and is suitable for use in routine laboratories.

Formaldehyde↗
PubMed1979

Haemolysis due to formaldehyde-induced anti-N-like antibodies in haemodialysis patients.

During reuse of formaldehyde sterilized Kiil-dialysers, red cell survival, measured by means of 51Cr t/2, was significantly reduced (p less than 0.001) in 16 patients with anti-N-like positive sera, when compared with 19 antibody negative control patients (mean +/- SD: 16.5 +/- 2.7 versus 22.4 +/- 3.1 days.) In antibody negative patients (n = 10) replacement of formaldehyde sterilized dialysers by ethylene-oxide sterilized disposable dialysers resulted in a significant increase (p less than 0.002) of 51Cr t/2 (Mean +/- SD, days: Kiildialyser 16.3 +/- 1.9; disposable dialyser 20.3 +/- 3.5). This improvement took place, although antibody titres persisted during the 51Cr-measurements and declined thereafter only slowly. In antibody negative patients (n = 6) red cell survival did not increase, when formaldehyde as a sterilant was avoided. In antibody positive patients mean haematocrit rose significantly (p less than 0.05), whereas in none of the antibody negative patients a definite change of haematocrit occurred. The data demonstrate, that formaldehyde sterilisation of dialysers may cause antibody-mediated haemolysis contributing to the extent of renal anaemia. This immunohaemolysis may be corrected, in spite of continuing antibody persistance, when formaldehyde exposure is totally avoided, or possibly when minimized.

Antibody Formation↗
PubMed1992

Formation of formaldehyde and malonaldehyde by photooxidation of squalene.

Formaldehyde and malonaldehyde were identified upon exposure of squalene to ultraviolet (UV) irradiation at 300 nm. Formaldehyde was derivatized by reaction with cysteamine to form thiazolidine; malonaldehyde was derivatized by reaction with N-methylhydrazine to produce N-methylpyrazole. The derivatives were subsequently analyzed with a gas chromatograph equipped with a fused silica capillary column and a nitrogen/phosphorus detector. The levels of formaldehyde and malonaldehyde produced increased with irradiation time. The amount of formaldehyde produced reached a maximum of 3.40 nmol/mg squalene after 7 hr irradiation; the maximum amount of malonaldehyde generated, 0.92 nmol/mg, was found after 5 hr of irradiation. Prior to this study, formaldehyde had not been reported as a photoproduct of squalene. Acetaldehyde and acetone were also detected in the irradiated squalene, which may be formed via a 6-methyl-5-hepten-2-one intermediate. 6-Methyl-5-hepten-2-one can also undergo breakdown to form malonaldehyde.

Formaldehyde↗
PubMed1990

Pulmonary function and bronchial reactivity in asthmatics during low-level formaldehyde exposure.

This study evaluated whether formaldehyde, at concentrations similar to those found in the indoor environment, could produce adverse effects on the lower airway of 15 asthmatic persons with documented bronchial hyperresponsiveness who were exposed for 90 min in a climate chamber to clean air containing formaldehyde vapor at levels of 0.85 mg/m3, 0.12 mg/m3, and 0.008 mg/m3. No significant changes in forced expiratory volume in 1 sec (FEV1), airway resistance (Raw), specific airway resistance (SRaw), and flow-volume curves could be detected during formaldehyde exposure. Furthermore, histamine challenge tests performed immediately after formaldehyde exposure showed no evidence of changes in bronchial reactivity. No late reactions were registered during the first 14-16 hr after exposure. The results suggest that residential levels of formaldehyde are of minor importance in the emergence of pulmonary symptoms. Discrepancies between the present study and previous data may be due to differences in environmental conditions.

Adolescent↗
PubMed2005

The detection of formaldehyde in textiles using interdigitated microelectrode array diffusion layer titration with electrogenerated hypobromite.

An interdigitated microelectrode array (IDA) was applied to the determination of formaldehyde released from textiles produced in industry. The proposed method is based on formaldehyde reaction with hypobromite which is formed in weakly basic media by control current electrooxidation of bromide on the generator segment of the IDA array. The unreacted hypobromite diffuses through the gap between individually polarisable IDA segments and it is amperometrically detected on the collector segment of the IDA. The efficiency of this nonconvective transfer process in the absence of formaldehyde was substantially higher (78%) in comparison with that when using the rotating ring disc electrode. The influence of the added formaldehyde on the transfer process can be utilised to develop a simple and sensitive analytical procedure for formaldehyde detection with a detection limit of 4 x 10(-6) mol dm(-3).

Bromine Compounds↗
PubMed2002

Formaldehyde removal in synthetic and industrial wastewater by Rhodococcus erythropolis UPV-1.

Rhodococcus erythropolis strain UPV-1 is able to grow on phenol as the only carbon and energy source and to remove formaldehyde completely from both synthetic and industrial wastewater. The rate of formaldehyde removal is independent of either initial biomass or formaldehyde concentration. The presence of viable, intact cells is strictly necessary for this removal to take place. Discontinuous and continuous formaldehyde-feed systems were successfully tested with synthetic wastewater in shaken flasks. Once biodegradation was well established in model synthetic wastewater, a real wastewater sample was obtained from a local phenolic and melamine resin-manufacturing company. Incubation of biomass with this wastewater at subtoxic concentrations of formaldehyde resulted in the complete removal of the pollutant. Parameters, such as chemical oxygen demand and toxicity, were assessed as indicators of wastewater cleanup progress.

Biodegradation, Environmental↗
PubMed2003

Elevated levels of secretoneurin in the rabbit aqueous humor in response to formaldehyde irritation.

BACKGROUND: Secretoneurin, a 33-amino-acid neuropeptide, is generated by proteolytic processing of secretogranin II, which belongs to the chromogranin family. This study aimed to investigate whether secretoneurin is present in the uninflamed rabbit aqueous humor and whether it is released in response to treatment with topical formaldehyde, an agent known to release sensory peptides originating from the trigeminal ganglion. METHODS: Blood samples and aqueous humor of eyes pretreated with neutral formaldehyde and untreated controls were analyzed for secretoneurin immunoreactivity by a highly sensitive radioimmunoassay. Furthermore, the molecular form of the secretoneurin immunoreactivity was characterized by gel filtration high-performance liquid chromatography (HPLC). RESULTS: In the blood, secretoneurin levels were found to be below the detection limit of 2 fmol/100 microl. In the aqueous humor, secretoneurin-immunoreactivity was detected in moderate but significant amounts. The mean concentration of secretoneurin was 8.1 (+/-0.34) fmol/100 microl in controls and 7.8 (+/-0.1) fmol/100 microl 15 min after formaldehyde application. Thirty minutes after treatment, the secretoneurin levels were significantly elevated by 63%. Gel filtration HPLC revealed that the main molecular form corresponded to the free peptide secretoneurin. CONCLUSIONS: The neuropeptide secretoneurin has been detected in the anterior segment of the eye for the first time. The elevation of secretoneurin in formaldehyde-treated eyes may be induced by an enhanced release from the iris/ciliary body complex, as formaldehyde is known to provoke neurogenic inflammation in the anterior segment via release of sensory peptides originating from the trigeminal ganglion. This is why our results indicate a sensory origin of secretoneurin in the eye.

Animals↗
PubMed1991

Role of iron, hydrogen peroxide and reactive oxygen species in microsomal oxidation of glycerol to formaldehyde.

Rat liver microsomes can oxidize glycerol to formaldehyde. This oxidation is sensitive to catalase and glutathione plus glutathione peroxidase, suggesting a requirement for H2O2 in the overall pathway of glycerol oxidation. Hydrogen peroxide can not replace NADPH in supporting glycerol oxidation; however, added H2O2 increased the NADPH-dependent rate. Ferric chloride or ferric-ATP had no effect on glycerol oxidation, whereas ferric-EDTA was inhibitory. Certain iron chelators such as desferrioxamine, EDTA or diethylenetriaminepentaacetic acid, but not others such as ADP or citrate, inhibited glycerol oxidation. The inhibition by desferrioxamine could be overcome by added iron. Neither superoxide dismutase nor hydroxyl radical scavengers had any effect on glycerol oxidation. With the exception of propyl gallate, several antioxidants which inhibit lipid peroxidation had no effect on formaldehyde production from glycerol. The inhibition by propyl gallate could be overcome by added iron. In contrast to glycerol, formaldehyde production from dimethylnitrosamine was not sensitive to catalase or iron chelators, thus disassociating the overall pathway of glycerol oxidation from typical mixed-function oxidase activity of cytochrome P450. These studies indicate that H2O2 and nonheme iron are required for glycerol oxidation to formaldehyde. The responsible oxidant is not superoxide, H2O2, or hydroxyl radical. Cytochrome P450 may function to generate the H2O2 and reduce the nonheme iron. There may be additional roles for P450 since rates of formaldehyde production by microsomes exceed rates found with model chemical systems. Elevated rates of H2O2 production by certain P450 isozymes, e.g., P450 IIE1, may contribute to enhanced rates of glycerol oxidation.

Animals↗
PubMed1993

Mutagenicity of formaldehyde in Chinese hamster lung fibroblasts: synergy with ionizing radiation and N-nitroso-N-methylurea.

Cultured Chinese hamster V79 cells, a widely utilized model system in risk assessment of environmental agents, have been utilized to measure toxicity and mutagenicity of formaldehyde with or without previous exposure to either the alkylating agent N-nitroso-N-methylurea or to ionizing radiation. Each of these agents caused a dose-dependent decrease in colony forming efficiency and a parallel increase in 6-thioguanine resistant colonies. Significant mutant frequencies were induced by 0.3 up to 1 mM formaldehyde, 2 and 4 Gy of radiation and 0.2 and 0.5 mM N-nitroso-N-methylurea. Exposure of cells to ionizing radiation or N-nitroso-N-methylurea followed by submutagenic concentrations of formaldehyde potentiated both the cytotoxicity and the mutagenicity as compared with the corresponding separate effects caused by each of these agents. Taken together, these studies clearly demonstrate genotoxic effects in vitro of three recognized carcinogens, i.e. formaldehyde, N-nitroso-N-methylurea and ionizing radiation. Moreover, the synergies now demonstrated in regards to cytopathic consequences indicate interactive effects between formaldehyde and these agents, representing both a chemical and a physical carcinogen.

Animals↗
PubMed1992

Reduction of carbon monoxide to formaldehyde by the terminal oxidase of the marine bacterium Pseudomonas nautica strain 617.

When exposed to CO, the aerobic respiratory system of the marine bacterium Pseudomonas nautica strain 617, previously reduced with dithionite, undergoes reoxidation. When dealing with the purified oxidase (dithionite reduced) exposure of the enzyme to CO induces its reoxidation (collapse of its alpha band). Under our experimental conditions, this form of the oxidase could not be reduced again by dithionite. Addition of formaldehyde to the native oxidized enzyme resulted in full inhibition of the oxidase reduction by dithionite, presumably due to complex formation. We hypothesized a reduction of CO into formaldehyde and a locking of the active site by the reaction product. By using flash photolysis, it was possible to turn over the enzyme, accumulate the reaction product and identify it as formaldehyde. When using the membrane-bound enzyme, formaldehyde accumulated without the help of flash photolysis. This unusual reduction of CO to formaldehyde could be related to the previously reported uncommon features of the P. nautica oxidase, in particular O2 reduction into H2O2 as end product [(1989) FEBS Lett. 247, 475-479].

Carbon Monoxide↗
PubMed1979

Genetic effects of formaldehyde in yeast. III. Nuclear and cytoplasmic mutagenic effects.

Low concentrations of formaldehyde induce nuclear mutations when yeast cells are allowed to grow in the presence of this compound. The induction of reversions is a linear function of the concentration and depends upon the repair capacities of the treated cells. A strain defective in excision-repair (rad3-12) is more mutable by formaldehyde than the isogenic wild-type whereas a strain blocked in the mutagenic pathway (rad6-1) is not mutable after the same treatment. Allele specificities were found. In particular the lys1-1 mutation is not reversible by formaldehyde. Higher concentrations of formaldehyde induce efficiently the cytoplasmic "petite" mutation in non-growing conditions when a lethal effect is noticeable. The growth phase as well as the physiological state influence this mutagenic effect. The mutagenic effect of formaldehyde in yeast is discussed in relation with the repair processes involved.

DNA Repair↗
PubMed1988

Formaldehyde mutagenesis of the eT1 balanced region in Caenorhabditis elegans: dose-response curve and the analysis of mutational events.

In this study we have generated a dose-response curve for the formaldehyde induction of recessive lethal mutations in the eT1(III;V)-balanced region of C. elegans. We have mapped 96 out of 112 formaldehyde-induced lesions to either LGIII or LGV and genetically analyzed 31 lesions that mapped to LGV. Our findings showed that a 4-h treatment with 0.1% formaldehyde gave the best mutation induction frequency with the least side effects. We found that formaldehyde induced putative point mutations, deficiencies and more complex lesions in C. elegans. We isolated 11 putative point mutations, 3 of which defined new genes and 8 were alleles of known genes. One of the new genes, let-450, is currently the left-most known gene on LGV. We also isolated 5 deficiencies. Our formaldehyde-induced lesions increased the number of zones in the eT1-balanced region of LGV from 22 to 34.

Alleles↗
PubMed1988

Effect of the homokaryotic state of the uvs-2 allele in Neurospora crassa on formaldehyde-induced killing and ad-3 mutation.

Formaldehyde was tested for its killing and mutagenic activities in the ad-3 forward-mutation test in Neurospora crassa. The test was conducted in 3 two-component heterokaryons (dikaryons) of N. crassa in order to determine the effect of the uvs-2 allele, which causes a defect in nucleotide excision repair, on formaldehyde-induced killing and the induction of ad-3 mutants. These dikaryons were homokaryotic for uvs-2+ (H-12), homokaryotic for usv-2 (H-59), and heterokaryotic for uvs-2 (H-71). Formaldehyde induced killing and ad-3 mutants in H-12, but the presence of uvs-2 in the homokaryotic state (H-59) resulted in a 9-fold increase in killing and a 40-fold increase in the induction of ad-3 mutants. This increased sensitivity to formaldehyde-induced killing and mutation conferred by uvs-2 in the homokaryotic state (H-59 vs. H-12) is similar to that noted by others in Escherichia coli. Salmonella typhimurium and Saccharomyces cerevisiae. The dikaryon heterokaryotic for uvs-2 (H-71) has the same sensitivity to formaldehyde-induced ad-3 mutation as H-12, indicating that uvs-2 is recessive to uvs-2+.

DNA Repair↗
PubMed1986

Effects of formaldehyde on bronchial ion transport.

The functions of the epithelium that lines mammalian airways are potential targets for the toxic effects of reactive chemicals such as formaldehyde. We examined the effects of formaldehyde on bioelectric properties and ion permeation of excised canine and human bronchial epithelium. Concentration-dependent reductions in short-circuit current were induced in both tissues. Sodium absorption and transcellular chloride fluxes across canine bronchial epithelium were inhibited by 65 and 35%, respectively, by 10(-3) M formaldehyde. The QO2 of isolated dog bronchial epithelial cells was reduced by 32% by 10(-3) M formaldehyde. These results are consistent with an action of formaldehyde on cellular ion permeability but effects secondary to metabolic inhibition cannot be dismissed.

Animals↗