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PubMed1989

Nasal tumours in rats after severe injury to the nasal mucosa and prolonged exposure to 10 ppm formaldehyde.

To study the significance of damage to the nasal mucosa for the induction of nasal tumours by formaldehyde in rats, a long-term inhalation study was conducted in which male rats with severely damaged or undamaged nose were exposed 6 h/day for 5 days/week to 0, 0.1, 1.0 or 10 ppm formaldehyde vapour for 28 months, or for 3 months followed by a 25-month observation period. The damage to the nasal mucosa was induced by bilateral intranasal electrocoagulation. The total number of rats used was 720, 480 with damaged and 240 with intact nose. Compound-related degenerative, inflammatory and hyperplastic changes of the nasal respiratory and olfactory mucosa were invariably observed when rats with intact nose were exposed to 10 ppm but not when exposed to 1.0 or 0.1 ppm formaldehyde. Nasal electrocoagulation increased the incidences of formaldehyde-induced rhinitis, hyper- and metaplasia of the respiratory epithelium, and degeneration and hyper- and metaplasia of the olfactory epithelium. In addition, exposure to 10 ppm formaldehyde for 28 months produced nasal squamous cell carcinomas in rats with damaged nose (15/58) but not in rats with intact nose. Three months of exposure to 10 ppm formaldehyde or exposure to 0.1 or 1.0 ppm formaldehyde for 28 months had no such effect. It was concluded that severe damage to the nasal mucosa may contribute to the induction of nasal tumours by formaldehyde.

Animals↗
PubMed1985

On the chemistry of formaldehyde fixation and its effects on immunohistochemical reactions.

Formalin has been recommended as an innocuous fixative for immunohistochemistry. However, several studies demonstrated impairment or blocking of antigenic activity of certain proteins. Formalin fixation was discovered accidentally by F. Blum in 1893 and its deleterious effects on various tissue structures were discussed extensively during the following decades. More recently, some authors assumed that formaldehyde bound to tissues can be largely or completely removed by washing and dehydration. According to chemical data, formaldehyde forms highly reactive methylols with uncharged amino groups. Such methylol groups yield methylene bridges with suitably spaced amides, arginine and aromatic amino acid sidechains. Only loosely bound formaldehyde is removed by washing for several hours. Residual bound formaldehyde cannot be dislodged by washing for weeks, but some formaldehyde is gradually removed when tissues are stored in water for an extended number of years. Methylene crosslinks resist treatment with high concentrations of urea, and can be broken only by drastic hydrolysis. It appears unlikely that such firmly bound formaldehyde is removed by conventional washing and dehydration procedures used in histochemistry. The superiority of methacarn, alcohol or acetone over formaldehyde fixation for immunohistochemical demonstration of prekeratin, myosin, type I and type IV collagen, laminin and fibronectin can be ascribed to the irreversible alterations of tissue proteins by formaldehyde.

Fixatives↗
PubMed1999

Activity of O6-methylguanine DNA methyltransferase in mononuclear blood cells of formaldehyde-exposed medical students.

A recent study reported that exposure of student embalmers in Cincinnati to high concentrations of formaldehyde (2 mg/m3) reduced the activity of the DNA repair protein O6-methylguanine DNA methyltransferase (MGMT). Reduction in a DNA repair enzyme may strongly increase the cancer risk not only with respect to the repair-enzyme causing agent but with respect to all carcinogens causing lesions subject to repair by the enzyme in question. Thus, we examined whether formaldehyde exposure of 57 medical students during their anatomy course at two different Universities in Germany influenced MGMT activity in mononuclear blood cells. Mean formaldehyde exposure of 41 students was 0.2 +/- 0.05 mg/m3 for 6 h per week. MGMT activity was 133.2 +/- 14.9 fmol MGMT/10(6) cells before the beginning of the formaldehyde exposure, 131.1 +/- 15.8 fmol MGMT/10(6) cells after 50 days (P = 0.56) and 128.2 +/- 19.0 fmol MGMT/10(6) cells after 111 days of exposure (P = 0.92). Similarly, no significant influence of formaldehyde exposure was observed, when smoking habits, alcohol consumption, allergic disease and sex of students were considered. In addition no significant difference was obtained in MGMT activity between 16 students with mean formaldehyde exposure of 0.8 +/- 0.6 mg/m3 and students without formaldehyde exposure (n = 51; P = 0.37). In conclusion, exposure of the medical students in western Europe to formaldehyde did not decrease MGMT activity in mononuclear blood cells.

Adult↗
PubMed2003

Potential biological indicators for glutaraldehyde and formaldehyde sterilization processes.

The present study aimed to isolate, select, and evaluate bacterial isolates with potential for use as biological indicators for sterilization with glutaraldehyde and/or formaldehyde. A total of 340 local Bacillus isolates were screened for glutaraldehyde and/or formaldehyde resistance by determination of minimum inhibitory concentrations (MICs), minimum bactericidal concentrations (MBCs), and extinction time and were compared with B. subtilis (var. niger) ATCC 9372, the biological indicator for ethylene oxide sterilization, as reference. Of these, 85 isolates had glutaraldehyde MICs of 0.5% or higher, while 29 had formaldehyde MICs of 0.04% or higher. Of the 29 resistant isolates, 15 had MBCs of 0.05% or more. Extinction times were used to evaluate the bactericidal/sporicidal activity of glutaraldehyde. Eight had inactivation times of more than 5 h in 2% glutaraldehyde (pH 8), whereas 12 had inactivation times of more than 3 h in l% formaldehyde, with one isolate in common. These 19 isolates were selected and evaluated as potential biological indicators for aldehydes by determination of the decimal reduction times ( D values), compared with the reference strain. Eight glutaraldehyde-resistant isolates exhibited D values 2.0- to 3.5-fold higher than the reference strain (30 min.). Only five of 12 formaldehyde resistant isolates had D values higher than that of the reference strain. Using six resistant isolates, temperature coefficient values between 2.11 and 3.02 were obtained for 2% formaldehyde. Finally, 14 isolates were tested for potential pathogenicity and were identified to species level. All of the eight glutaraldehyde-resistant isolates, including the isolate with dual resistance, and three formaldehyde-resistant isolates were B. licheniformis, while two other formaldehyde-resistant isolates were B. cereus. Six of the selected B. licheniformis isolates are potential biological indicators for sterilization processes using aldehydes. Three can be suggested for glutaraldehyde only and three for both aldehydes.

Bacillus subtilis↗
PubMed1990

Oxidation of glycerol to formaldehyde by rat liver microsomes. Effects of cytochrome P-450 inducing agents.

Glycerol was shown recently to be metabolized to formaldehyde by microsomes from chowfed control rats (Winters et al., Biochem Biophys Res Commun 153: 612-617, 1988). In the present study, experiments were carried out to evaluate the oxidation of glycerol by microsomes isolated from rats treated with inducers of different isozymes of cytochrome P-450. The oxidation of glycerol to formaldehyde was increased in microsomes from rats treated with pyrazole, ethanol or acetone relative to their respective controls, but not after treatment with phenobarbital or 3-methylcholanthrene. This reaction was sensitive to inhibition by carbon monoxide and was inhibited by compounds known to be effective substrates for P-450j, e.g. aniline, ethanol, pyrazole and 4-methylpyrazole. Treatment with pyrazole caused an increase in Vmax for glycerol oxidation but did not affect affect the Km (about 15 mM) for glycerol, as compared to saline controls. Evidence that the product of glycerol metabolism is formaldehyde was provided by the observation that this product served as a substrate for the glutathione-dependent formaldehyde dehydrogenase, and the amount of formaldehyde detected was identical to that detected by the Nash reaction. By utilizing [14C]glycerol, and coupling the formaldehyde dehydrogenase reaction to the formate dehydrogenase reaction, 14CO2 could be detected, indicating that the formaldehyde produced was derived from the added glycerol. These results suggest that that glycerol is not metabolically inert when added to microsomes but serves as an effective substrate for the cytochrome P-450j isozyme, extending the alcohol substrate specificity of this enzyme to poly-ols. The production of formaldehyde from glycerol may require caution since glycerol is often present in microsomal or reconstituted systems.

Acetone↗
PubMed1986

Genotoxicity of formaldehyde and an evaluation of its effects on the DNA repair process in human diploid fibroblasts.

Formaldehyde treatment of human fibroblasts gave rise to DNA damage detected by a nick translation assay. This damage was not repaired by typical 'long-patch'-type excision repair as evidenced by the failure of DNA repair inhibitor post-treatment to elevate the amount of DNA strand breakage. In addition, the effects of formaldehyde on DNA repair were examined in light of a recent report suggesting that formaldehyde inhibited the repair of X-ray-induced strand breaks and UV- and benzo [a]pyrene diol epoxide-induced unscheduled DNA synthesis in human bronchial cells. We report that formaldehyde (1) was ineffective at inhibiting the sealing of X-ray- or bleomycin-induced DNA strand breaks, (2) did not inhibit the removal of pyrimidine dimers from cellular DNA at short treatment times, and (3) that the previously observed inhibition of unscheduled DNA synthesis was most likely due to the inhibition of uptake of labeled precursor into formaldehyde-treated cells. Thus, our findings are not consistent with the notion that formaldehyde inhibits the repair process in human fibroblasts. Finally, formaldehyde was shown to elevate the level of misincorporation of bases into synthetic polynucleotides catalyzed by E. coli DNA polymerase I, indicating that the mutagenicity of formaldehyde may be due to covalent alteration of DNA bases.

Bleomycin↗
PubMed1992

Allergic contact dermatitis from formaldehyde resins in permanent press clothing: an underdiagnosed cause of generalized dermatitis.

BACKGROUND AND METHODS: Formaldehyde resins have been used to impart wrinkle resistance to clothing fabrics since 1926. After several patients with positive patch tests to formaldehyde resins had been examined, a study was undertaken of the records of all patch tests performed at the University of Louisville Patch Test Clinic and the Allergy Section of the Skin and Cancer Clinic of New York University Medical Center from January 1988 through April 1990 to determine the prevalence of positive patch-test reactions to formaldehyde-based textile resins and the clinical and demographic patterns associated with textile resin allergy. RESULTS: Seventeen patients were identified at the two centers. Twelve were allergic to formaldehyde as well as to formaldehyde textile resins. Several clinical patterns were found, including accentuation of dermatitis in areas of tight clothing, primary occurrence in clothing-covered areas, and a chronic recalcitrant course. Ethylene urea melamine formaldehyde resin was the best screening agent with 14 definite positive reactions and one equivocal reaction. CONCLUSION: Formaldehyde textile resin allergy is more common than has been previously recognized. Patch testing with one or more formaldehyde textile resins is indicated in patients with a particular pattern of dermatitis.

Adult↗
PubMed2005

Maximum exposure levels for xylene, formaldehyde and acetaldehyde in cars.

Although millions of individuals are exposed to emissions from articles inside cars, relatively little has been published about possible adverse health effects and about exposure levels that can be considered safe or "acceptable". Xylene, formaldehyde and acetaldehyde represent typical examples of relevant volatile organic substances (VOC) released from articles inside cars. Recently, a concept for derivation of maximum exposure levels for volatile organic substances in cars has been published. In the present study we applied this concept to derive maximum exposure levels for xylene, formaldehyde and acetaldehyde and compared the resulting concentrations to exposure levels usually found inside of cars. We derived Short Term Exposure Levels Inside Automotive Vehicles (STELIA) of 29, 0.125 and 15.3 mg/m(3) for xylene, formaldehyde and acetaldehyde, respectively. These STELIAs should not be exceeded during short-term exposures, for instance when starting a car that had been heated up during parking in the sun. Exposure Levels Inside Automotive Vehicles (ELIA, chronic) for chronic exposure to non-genotoxic substances were 8.8, 0.125 and 0.635 mg/m(3) for systemic as well as 17.6, 0.125 and 1.7 mg/m(3) for local exposure to xylene, formaldehyde and acetaldehyde, respectively. Although, it is known that exposure limits for carcinogenic substances should be treated with caution, encouraged by the well documented threshold mechanisms we nevertheless derived ELIAs for Carcinogenic and Mutagenic Substances (ELIA, cm) resulting in 0.125 and 0.635 mg/m(3) for formaldehyde and acetaldehyde. If these ELIAs are matched against average concentrations of xylene, formaldehyde and acetaldehyde found in cars at 23 degrees C (1.22, 0.048 and 0.042 mg/m(3)), there is no reason for concern. With respect to STELIAs and extrapolated concentrations at 65 degrees C (14.7, 1.47 and 1.68 mg/m(3), for xylene, formaldehyde and acetaldehyde, respectively), however, a reduction of the concentration of formaldehyde may be necessary.

Acetaldehyde↗
PubMed2005

Reevaluation of mortality risks from nasopharyngeal cancer in the formaldehyde cohort study of the National Cancer Institute.

OBJECTIVE: To determine whether the National Cancer Institute's (NCI) recent suggestion of a causal association between formaldehyde exposure and mortality from nasopharyngeal cancer (NPC) is robust with respect to alternative methods of data analysis and alternative categorizations of formaldehyde exposure. METHODS: The original authors provided the cohort data. We computed U.S. and local county (regional) rate-based standardized mortality ratios (SMRs) and internal cohort rate-based relative risks (RR) by categories of four formaldehyde exposure metrics (highest peak, average intensity, cumulative, and duration of exposure), using both NCI categories and an alternative categorization based on tertiles of all NPC deaths among exposed subjects. We computed SMRs and RRs for each of 10 study plants and by plant group (Plant 1 (n = 4261) vs. Plants 2-10 (n = 21,358)). RESULTS: Six of 10 NPC deaths observed in the NCI study occurred in only one plant (Plant 1) and the remaining four cases occurred individually in four of the other nine plants studied. A large, statistically significant, regional rate-based NPC SMR of 10.32 (95% CI = 3.79-22.47) among formaldehyde-exposed workers in Plant 1 contrasted sharply with a 35% deficit in NPC deaths (SMR = .65, 95% CI = .08-2.33) among exposed workers in Plants 2-10 combined. The statistically significant exposure-response relationship with formaldehyde and NPC reported in the NCI study for highest peak exposure was driven entirely by a large, statistically significant excess NPC risk in Plant 1 for the highest peak exposure category (4+ ppm). For the remaining nine plants, RRs for all non-baseline highest peak exposure categories were less than 1.0, and we observed no evidence of an exposure-response relationship. Most of the observed NPC excesses for the non-baseline categories of the other exposure metrics (average intensity, cumulative, and duration of formaldehyde exposure) were concentrated in Plant 1, and by contrast to the NCI findings, none of the corresponding exposure-response relationships was statistically significant. CONCLUSIONS: Overall, our reanalysis provided little evidence to support NCI's suggestion of a causal association between formaldehyde exposure and mortality from NPC. NCI's conclusion of a possible causal association was driven heavily by anomalous findings in one study plant (Plant 1). An independent and larger study of Plant 1 by the current authors concluded the NPC excess was not associated with formaldehyde exposure. Our findings cast considerable additional uncertainty regarding the validity of NCI's suggested causal association.

Academies and Institutes↗
PubMed2001

Formaldehyde in human cancer cells: detection by preconcentration-chemical ionization mass spectrometry.

A rapid and highly sensitive method for the detection of formaldehyde utilizing selected ion flow tube-chemical ionization mass spectrometry is reported. Formaldehyde in aqueous biological samples is preconcentrated by distillation and directly analyzed using gas-phase thermal energy proton transfer from H30+; this procedure can be performed in 30 min. The method detection limit for formaldehyde based on seven replicate measurements of reference water samples (2.5 mL) is 80 nM at the 99% confidence level. Detection is linear up to 130 microM. This technique allows the first measurement of natural formaldehyde levels in human cancer cells in vitro. Elevated levels of formaldehyde relative to the reference water are observed for doxorubicin-sensitive cells (MCF-7 breast cancer, K562 leukemia, HeLa S3 cervical cancer) with estimated intracellular formaldehyde concentrations ranging from 1.5 to 4.0 microM, whereas formaldehyde in doxorubicin-resistant MCF-7/Adr breast cancer cells is essentially at reference level. This trend is inverted for prostate cancer cells LNCaP (sensitive) and DU-145 (resistant). Correlation of natural formaldehyde level with doxorubicin cytotoxicity is a function of the expression of enzymes that neutralize oxidative stress and the drug efflux pump, P-170 glycoprotein.

Formaldehyde↗
PubMed2002

Chemical pretreatment of formaldehyde-containing effluents.

Lime was found in this study to be an efficient reagent to lower the concentration of formaldehyde in highly concentrated effluents down to and below the limits suitable for biological treatment systems. The results show that the reactions leading to formaldehyde elimination can be divided in two steps. In the first step, the reaction is relatively slow. More than two-thirds of the original formaldehyde disappears in the second step in a period as short as one-third of the first step. Such trend is followed in a temperature range of up to 92 degrees C. Economical considerations suggest maintaining the conditions of the process around the ambient temperature with no heat requirement. It was noticed that the efficiencies of formaldehyde removal better than 99% could be achievable even around room temperature. However, these efficiencies would result in quite a shorter period of time if the temperature was raised. The mathematical representation for the rate of formaldehyde removal was found to appear with an exponential behavior. It will be seen that the rate of formaldehyde removal is strongly dependent on temperature. The present survey proves that the formaldehyde-containing effluents can be treated in a pretreatment step by lime to maintain the formaldehyde concentration in a range that is safe for biological treatment systems.

Calcium Compounds↗
PubMed2002

Characterization and reduction of formaldehyde emissions from a low-VOC latex paint.

The patterns of formaldehyde emission from a low volatile organic compound (VOC) latex paint applied to gypsum board were measured and analyzed by small environmental chamber tests. It was found that the formaldehyde emissions resulted in a sharp increase of chamber air formaldehyde concentration to a peak followed by transition to a long-term slow decay. A semi-empirical first-order decay in-series model was developed to interpret the chamber data. The model characterized the formaldehyde emissions from the paint in three stages: an initial "puff" of instant release, a fast decay, and a final stage of slow decay controlled by a solid-phase diffusion process that can last for more than a month. The model was also used to estimate the peak concentration and the amount of formaldehyde emitted during each stage. The formaldehyde sources were investigated by comparing emission patterns and modeling outcomes of different paint formulations. The biocide used to preserve the paint was found to be a major source of the formaldehyde. Chamber test results demonstrated that replacing the preservative with a different biocide for the particular paint tested resulted in an approximate reduction of 55% of formaldehyde emissions. But the reduction affected only the third-stage long-term emissions.

Air Pollution, Indoor↗
PubMed1985

Formaldehyde kinetics and bacteriology in dialyzers.

The kinetics of formaldehyde washout in new and reused dialyzers with 2% (w/v) and 4% formaldehyde solution was studied. Using a standard method of rinsing, the concentration of formaldehyde decreases exponentially, but the rate of decrease and the steady-state level depends on the type of dialyzer. The residual quantity of formaldehyde using a 4% solution is more than twice that seen with a 2% solution in similar dialyzers. Bacteriological tests on water-adapted, formaldehyde-resistant organisms indicate that a significant proportion of these organisms can survive a 4-hr incubation with 4% formaldehyde at 20 degrees C. However, increasing the temperature of incubation to 40 degrees C or the addition of ethanol up to 8% (v/v) improved the bacteriological efficacy of formaldehyde. Under these conditions, a 1% formaldehyde solution allows eradication of all organisms tested. Similar results were observed in multiple-use dialyzers inoculated with the same organisms. There was no effect of incubation at 40 degrees C on the in vitro clearance determinations of new and reused dialyzers.

Disinfection↗
PubMed1999

An automatic monitor of formaldehyde in air by a monitoring tape method.

An automatic monitor has been developed for measuring formaldehyde in air using a sensitive tape for formaldehyde. It is based on the color change of the tape on reaction with formaldehyde. The porous cellulose tape, containing silica gel as an absorbent and impregnated with the processing solution containing hydroxylamine sulfate, Methyl Yellow (pH indicator; pH 2.9-4.0, red-yellow), glycerin and methanol, was found to be a highly sensitive means of detecting formaldehyde and maintains a stable sensitivity. When the tape was exposed to a sample of air containing formaldehyde, the color of the tape changed from yellow to red. The degree of color change was proportional to the concentration of formaldehyde at a constant sampling time and flow rate, and it could be recorded by measuring the intensity of reflected light (555 nm). The tape could be used to detect down to 0.08 ppm (World Health Organization standard) of formaldehyde with a sampling time of 30 min and a flow rate of 100 mL min-1. Reproducibility tests showed that the relative standard deviation of response (n = 10) was 3.8% for 0.1 ppm formaldehyde. The monitor is simple, specific, capable of unattended operation and is recommended for both laboratory and field operation.

Air Pollution, Indoor↗
PubMed2000

Indoor and outdoor formaldehyde concentrations in homes in residential areas in Greater Cairo.

Indoor and outdoor measurements of formaldehyde were conducted at seven flats located in residential areas in Greater Cairo, during spring and summer seasons 1999. The mean daytime formaldehyde concentrations in kitchens, bedrooms and living rooms were 89, 100 and 100 ppb, respectively, in the seven flats. Significant positive correlations were found between the concentrations of formaldehyde found in these three rooms. On the other hand, no significant differences were found between the mean formaldehyde concentrations in these three rooms. The maximum mean concentration of formaldehyde (147 ppb) was recorded in a new flat, while the minimum concentration (43 ppb) was observed in an old flat. The maximum hourly and daytime concentrations were 350 and 225 ppb, respectively. Air temperature, relative humidity and the age of the flat are factors affecting the emission and concentration of formaldehyde. The maximum indoor and outdoor formaldehyde concentrations were recorded during the summer season. During the spring, 38% of the samples indicated that the concentration of formaldehyde in the seven flats exceeded 0.1 ppm, the American Society of Heating, Refrigerating, and Air Conditioning Engineers' (ASHRAE) standard; in the summer, this figure increased to 53%.

Air Pollution, Indoor↗
PubMed2003

Identification of formaldehyde-induced modifications in proteins: reactions with model peptides.

Formaldehyde is a well known cross-linking agent that can inactivate, stabilize, or immobilize proteins. The purpose of this study was to map the chemical modifications occurring on each natural amino acid residue caused by formaldehyde. Therefore, model peptides were treated with excess formaldehyde, and the reaction products were analyzed by liquid chromatography-mass spectrometry. Formaldehyde was shown to react with the amino group of the N-terminal amino acid residue and the side-chains of arginine, cysteine, histidine, and lysine residues. Depending on the peptide sequence, methylol groups, Schiff-bases, and methylene bridges were formed. To study intermolecular cross-linking in more detail, cyanoborohydride or glycine was added to the reaction solution. The use of cyanoborohydride could easily distinguish between peptides containing a Schiff-base or a methylene bridge. Formaldehyde and glycine formed a Schiff-base adduct, which was rapidly attached to primary N-terminal amino groups, arginine and tyrosine residues, and, to a lesser degree, asparagine, glutamine, histidine, and tryptophan residues. Unexpected modifications were found in peptides containing a free N-terminal amino group or an arginine residue. Formaldehyde-glycine adducts reacted with the N terminus by means of two steps: the N terminus formed an imidazolidinone, and then the glycine was attached via a methylene bridge. Two covalent modifications occurred on an arginine-containing peptide: (i) the attachment of one glycine molecule to the arginine residue via two methylene bridges, and (ii) the coupling of two glycine molecules via four methylene bridges. Remarkably, formaldehyde did not generate intermolecular cross-links between two primary amino groups. In conclusion, the use of model peptides enabled us to determine the reactivity of each particular cross-link reaction as a function of the reaction conditions and to identify new reaction products after incubation with formaldehyde.

Chromatography, Liquid↗
PubMed1981

The digestion by cattle of grass silage made with formic acid and formic acid-formaldehyde.

1. A primary growth crop of perennial ryegrass (Lolium perenne L., cv. S23) was partially wilted and ensiled after the application of either formic acid-water (1:3, w/v; 7.11 l/t fresh herbage; control diet C) or formic acid-formaldehyde (1:1, w/w; 8.8 l/t fresh herbage; formaldehyde treated diet F) which supplied 50 g HCHO/kg crude protein (nitrogen (N) x 6.25). The two silages were fed separately and a third diet comprising formaldehyde-treated silage, supplemented with urea (20 g/kg dry matter DM) at the time of feeding was also examined (diet FU). 2. The three diets were fed at a level of 16 g DM/kg live weight to six 3- to six-month-old cattle fitted with rumen and re-entrant duodenal cannulas in two 3 x 3 Latin Square experiments, and measurements were made of the digestion of energy, carbohydrate and N. 3. The formaldehyde-treated silage had a lower content of fermentation acids and ammonia-N, and a higher content of water-soluble carbohydrate and total amino acids. The apparent digestibility of organic matter, energy and N were depressed (P less than 0.05, P less than 0.05 and P less than 0.01 respectively) by treatment with formaldehyde, but cellulose and neutral-detergent fibre digestibility were unaffected. 4. Within the rumen the digestion of organic matter, cellulose and neutral-detergent fibre were unaffected by formaldehyde treatment or supplementation with urea. Microbial protein synthesis in the rumen was similar for the three diets (average 131 g/kg apparently digested organic matter in the rumen). 5. The application of formic acid-formaldehyde increased (P less than 0.05) the amount of food protein escaping degradation in the rumen (4.76 diet C, 6.89 diet F; 7.07 diet FU g/kg protein intake). The contribution of amino acids of dietary origin at the duodenum increased (P less than 0.05) from 50 (diet C) to 80 (diet F) and 82 (diet FU) g/kg DM intake, and the flow of total amino acids at the duodenum was 33% higher (P less than 0.001) in cattle fed formic acid-formaldehyde silage diets compared with the control silage due to the reduction in degradation of protein at ensiling and in the rumen.

Amino Acids↗
PubMed1989

Mechanistic study on formaldehyde-induced hepatotoxicity.

In isolated, hemoglobin-free perfused livers of fasted rats, formaldehyde at an initial concentration of 10 mmol/l produced toxicity as evidenced by a release of enzymes (GPT, SDH) and of glutathione (mainly GSSG) into the perfusate, an accumulation of calcium in the liver, and a depletion of hepatic glutathione. Formaldehyde also led to an enhanced release of malondialdehyde into the perfusate, indicating peroxidative processes and decreased hepatic oxygen consumption by about 50-70%. The electron microscopic investigation of formaldehyde-exposed livers showed a destruction of the mitochondria (ruptured membranes, loss of the cristae) and some damage of the rough endoplasmic reticulum. Feeding the rats prior to surgery attenuated the hepatotoxic effects of 10 mmol/l formaldehyde. At an initial concentration of 3 mmol/l, formaldehyde did not release enzymes from livers of fed or fasted rats but only from those whose glutathione content had been depleted by treatment with phorone (250 mg/kg ip 2 h earlier). Formaldehyde liberated glucose and lactate from the livers of fed but not from those of fasted rats, indicating anaerobic energy supply in the fed state. The hepatotoxic action of formaldehyde is not due to its metabolism to formate or to the 10% methanol added as a stabilizing agent to the commercially available 37% solution named formalin. In conclusion, by destruction of mitochondria, formaldehyde inhibits aerobic energy supply and thereby presumably produces hepatocellular damage.

Alanine Transaminase↗