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PubMed2004

Flow cytometric determination of neutrophil respiratory burst activity in workers exposed to formaldehyde.

AIM: The aim of the study was to investigate neutrophil respiratory burst activity (NRBA) in workers who were occupationally exposed to formaldehyde. METHODS: NRBA, spontaneous and stimulated with E. coli, N-formyl-methionyl-leucyl-phenylalanine (fMLP) and phorbol 12-myristate 13-acetate (PMA), was studied by means of quantitative flow cytometric determination in 29 workers who were occupationally exposed to formaldehyde; 21 healthy subjects, not exposed to formaldehyde, served as controls. All subjects underwent clinical assessment, including a review of a summary of their medical history and a physical examination. Routine haematological tests were performed. RESULTS: A statistically significant predominance of subjective symptoms and objective clinical findings of chronic upper respiratory tract inflammation, as well as decreased resistance to infections, was observed in the 29 workers exposed to formaldehyde, compared with the controls (chi2 = 9.28, P = 0.02). No statistically significant difference in the spontaneous and stimulated NRBA between the exposed workers and the control group was observed. The spontaneous NRBA (percentage oxidizing cells) was significantly lower in the group of exposed workers with upper respiratory tract findings and frequent and long-lasting infectious inflammatory relapses (median and range 0.45 (0.02-2.03), mean values 0.65 +/- 0.74) than in the healthy controls (median and range 1.35 (0.07-8.69), mean values 2.42 +/- 2.47; P < 0.05), and in the group of exposed workers with rare and short, acute, inflammation of the upper respiratory tract or without any inflammations (median and range 1.00 (0.02-8.67), mean values 1.67 +/- 2.08; P < 0.05). A significant negative correlation between the duration of occupational exposure to formaldehyde and erythrocyte count and haematocrit was found. CONCLUSIONS: The observed decrease of spontaneous NRBA in workers with a history and clinical findings of frequent and long-lasting relapses of chronic inflammation of the upper respiratory tract could be due to formaldehyde exposure and individual susceptibility. The results obtained suggest that functional changes in polymorphonuclear neutrophil granulocytes could serve as an early indicator of an impact of formaldehyde on NRBA. The applied method might be used for identifying groups at increased toxicological risk.

Adult↗
PubMed1992

Effect of formaldehyde on the efficiency of hybridization of DNA immobilized on nitrocellulose filters.

We report in this study that under certain conditions formaldehyde interacts with DNA and makes it more efficient for hybridization on nitrocellulose filters. Hybridization signals of formaldehyde-treated DNA are stronger (up to 10 fold) as compared with that of the heat- or alkali-denatured DNA. Various parameters of the DNA-formaldehyde reaction are optimized as follows: (a) 6 x SSC, 10% formaldehyde, 60 degrees C, 20-30 min, reaction volume 10-200 microliters or (b) 6 x SSC, 5% formaldehyde, 98 degrees C, 15 min, reaction volume 10-200 microliters. Treatment of agarose gels after electrophoresis with formaldehyde improved both the transfer of DNA and the efficiency of hybridization. The following conditions are recommended for gel treatment: denaturation in 0.3 N NaOH, 1 M NaCl followed by neutralization with 0.5 M phosphate buffer, pH 7.0, containing 10% formaldehyde at 60 degrees C for 20 min.

Collodion↗
PubMed1984

Inhibition of the oxidation of acetaldehyde and formaldehyde by hepatocytes and mitochondria by crotonaldehyde.

Crotonaldehyde was oxidized by disrupted rat liver mitochondrial fractions or by intact mitochondria at rates that were only 10 to 15% that of acetaldehyde. Although a poor substrate for oxidation, crotonaldehyde is an effective inhibitor of the oxidation of acetaldehyde by mitochondrial aldehyde dehydrogenase, by intact mitochondria, and by isolated hepatocytes. Inhibition by crotonaldehyde was competitive with respect to acetaldehyde, and the Ki for crotonaldehyde was about 5 to 20 microM. Crotonaldehyde had no effect on the oxidation of glutamate or succinate. Very low levels of acetaldehyde were detected during the metabolism of ethanol. Crotonaldehyde increased the accumulation of acetaldehyde more than 10-fold, indicating that crotonaldehyde, besides inhibiting the oxidation of added acetaldehyde, also inhibited the oxidation of acetaldehyde generated by the metabolism of ethanol. Formaldehyde was a substrate for the low-Km mitochondrial aldehyde dehydrogenase, as well as for a cytosolic, glutathione-dependent formaldehyde dehydrogenase. Crotonaldehyde was a potent inhibitor of mitochondrial oxidation of formaldehyde, but had no effect on the activity of formaldehyde dehydrogenase. In hepatocytes, crotonaldehyde produced about 30 to 40% inhibition of formaldehyde oxidation, which was similar to the inhibition produced by cyanamide. This suggested that part of the formaldehyde oxidation occurred via the mitochondrial aldehyde dehydrogenase, and part via formaldehyde dehydrogenase. The fact that inhibition by crotonaldehyde is competitive may be of value since other commonly used inhibitors of aldehyde dehydrogenase are irreversible inhibitors of the enzyme.

Acetaldehyde↗
PubMed1984

Oxidation of formaldehyde and acetaldehyde by NAD+-dependent dehydrogenases in rat nasal mucosal homogenates.

Homogenates of respiratory and olfactory tissue from the rat nasal cavity were examined for their capacity to catalyze the NAD+-dependent oxidation of formaldehyde (in the presence and absence of glutathione) and of acetaldehyde. Both aldehydes were oxidized efficiently by nasal mucosal homogenates, and formaldehyde dehydrogenase (FDH) and aldehyde dehydrogenase (AldDH) were tentatively identified in both tissue samples. At least two isozymes of AldDH, differing with respect to their apparent Km and Vmax values with acetaldehyde as substrate, were found in the nasal mucosa, one of which may catalyze the oxidation of both formaldehyde and acetaldehyde. The specific activity of FDH in the olfactory mucosa was twice that in the respiratory mucosa, whereas the specific activity of the higher Km isozyme of AldDH was five to eight times greater in respiratory than in olfactory tissue. The specific activity of the lower Km isozyme of AldDH was similar in respiratory and olfactory homogenates. Repeated exposures of rats to formaldehyde (15 ppm, 6 hr/day, 10 days) or to acetaldehyde (1500 ppm, 6hr/day, 5 days) did not substantially affect the specific activities of FDH and AldDH in nasal mucosal homogenates. Glutathione is a cofactor for FDH; the concentration of nonprotein sulfhydryls in respiratory mucosal homogenates was approximately 2.8 mumoles/g and was not changed significantly by repeated exposures to formaldehyde (15 ppm, 6hr/day, 9 days). These data indicate that the rat nasal mucosa, which is the major target site for both aldehydes in inhalation toxicity studies, can metabolize both formaldehyde and acetaldehyde, and that the specific activities of formaldehyde and aldehyde dehydrogenase in homogenates of the nasal mucosa are essentially unchanged following repeated exposures to toxic concentrations of either compound.

Acetaldehyde↗
PubMed1984

Lack of bronchomotor response to up to 3 ppm formaldehyde in subjects with asthma.

A study was undertaken to determine whether exposure to concentrations of formaldehyde occasionally encountered in polluted indoor air would cause bronchoconstriction in subjects with mild asthma. In seven subjects the increase in specific airways resistance (SRaw) caused by inhalation of 1 ppm formaldehyde for 10 min was compared with the response caused by inhalation of formaldehyde-free air. Also, the increase in SRaw caused by inhalation of 1 and 3 ppm formaldehyde during moderate exercise for 10 min was compared with the response caused by inhalation of formaldehyde-free air during exercise for 10 min. Inhalation of formaldehyde at rest and during exercise did not cause a significant increase in SRaw in the subjects. It is concluded that brief exposure to these concentrations of formaldehyde, even in association with moderate exercise, is unlikely by itself to cause significant bronchoconstriction in most subjects with mild asthma.

Adolescent↗
PubMed1983

Formaldehyde production promoted by rat nasal cytochrome P-450-dependent monooxygenases with nasal decongestants, essences, solvents, air pollutants, nicotine, and cocaine as substrates.

To identify compounds which might be metabolized to formaldehyde in the nasal cavity, 32 potential substrates for cytochrome P-450-dependent monooxygenases were screened with rat nasal and, for comparison, liver microsomes. Tested substrates included 6 nasal decongestants, cocaine, nicotine, 9 essences, 3 potential air pollutants, and 12 solvents. Each test substrate, with the possible exception of the air pollutants, contained one or more N-methyl, O-methyl, or S-methyl groups. Eighteen of the tested materials were metabolized to produce formaldehyde by nasal microsomes. Five substrates, namely, the solvents HMPA and dimethylaniline, cocaine, and the essences dimethyl anthranilate and p-methoxyacetophenone, were metabolized to produce formaldehyde at rates exceeding 1000 pmol/mg microsomal protein/min by nasal microsomes. Eight substrates, including four nasal decongestants, nicotine, and an extract of diesel exhaust particles, were metabolized to produce formaldehyde at rates of 200 to 1000 pmol/mg microsomal protein/min. Five other substrates were metabolized to formaldehyde at detectable rates. The results indicate that a variety of materials which often come in contact with the nasal mucosa can be metabolized to formaldehyde by nasal enzymes. The released formaldehyde may influence the irritancy of inhaled compounds and has been suggested to play a role in the tumorigenicity of some compounds.

Air Pollutants↗
PubMed1985

Carcinogenicity of formaldehyde and hydrogen chloride in rats.

Previous studies in this laboratory have shown that the combined exposure of hydrogen chloride (HCI) and formaldehyde vapors (HCHO) elicited a significant incidence of nasal cancer in rats. In studies performed elsewhere, it has been demonstrated that exposure to formaldehyde alone induced a high nasal cancer response in rats. We wished to determine whether concurrent exposure of hydrogen chloride would enhance the tumorigenic effects of formaldehyde. Two exposure techniques were used. In one hydrogen chloride and formaldehyde were premixed at high concentrations before entry into the exposure chambers in order to maximize the formation of reactive alkylating agents. In the second the hydrogen chloride and formaldehyde were introduced separately into the exposure chamber. Appropriate control exposures consisting of formaldehyde alone or hydrogen chloride alone or air alone were also performed. The results show that nasal cancer incidences were induced in all animals receiving HCHO regardless of concurrent exposure to hydrogen chloride. The tumors were predominantly squamous cell type arising from the anterior portion of the nasal cavity. This study demonstrates that hydrogen chloride does not appreciably influence the nasal carcinogenicity of formaldehyde.

Animals↗
PubMed1987

Isotope effects and their implications for the covalent binding of inhaled [3H]- and [14C]formaldehyde in the rat nasal mucosa.

DNA-protein crosslinks were formed in the nasal respiratory mucosa of Fischer-344 rats exposed for 3 hr to selected concentrations of [3H]- and [14C]formaldehyde (3HCHO and H14CHO) (M. Casanova and H. d'A. Heck (1987). Toxicol. Appl. Pharmacol. 89, 105-121). In rats depleted of glutathione (GSH) and exposed to 10 ppm of 3HCHO and H14CHO, the 3H/14C ratio of the fraction of the DNA that was crosslinked to proteins was significantly (39 +/- 6%) higher than that of the inhaled gas. This suggests an isotope effect, either on the formation of DNA-protein crosslinks by labeled HCHO or on the oxidation of labeled HCHO catalyzed by formaldehyde (FDH) or aldehyde dehydrogenase (AldDH). The possibility of an isotope effect on the formation of crosslinks was investigated using rat hepatic nuclei incubated with [3H]- and [14C]formaldehyde (0.1 mM, 37 degrees C). A small (3.4 +/- 0.9%) isotope effect was detected on this reaction, which slightly favored 3HCHO over H14CHO in binding to DNA. The magnitude of this isotope effect cannot account for the high isotope ratio observed in the crosslinked DNA in vivo. The possibility of an isotope effect on the oxidation of 3HCHO and H14CHO catalyzed by FDH was investigated using homogenates of the rat nasal mucosa incubated with [3H]- and [14C]formaldehyde at total formaldehyde concentrations ranging from 0.1 to 11 microM, NAD+ (1 mM), GSH (15 mM), and pyrazole (1 mM). The experiments showed that 3HCHO is oxidized significantly more slowly than H14CHO under these conditions (Vmax/Km (H14CHO) divided by Vmax/Km (3HCHO) = 1.82 +/- 0.11). A similar isotope effect was observed in the absence of GSH, presumably due to the oxidation of 3HCHO and H14CHO catalyzed by AldDH. These results suggest that the residual (unoxidized) formaldehyde present in the nasal mucosa of rats exposed to [3H]- and [14C]formaldehyde may be "enriched" in 3HCHO relative to H14CHO, which can bind to DNA resulting in an isotope ratio higher than that of the inhaled gas. The isotope effect on the oxidation of 3HCHO and H14CHO suggests that previous estimates of the amount of HCHO covalently bound to nasal mucosal DNA (M. Casanova-Schmitz, T. B. Starr, and H. d'A. Heck (1984). Toxicol. Appl. Pharmacol. 76, 26-44) may have been too large, especially at low airborne concentrations and that the shape of the concentration-response curve for DNA-protein crosslinking is more nonlinear than reported previously.

Administration, Inhalation↗
PubMed1985

Formaldehyde asthma--rare or overlooked?

A total of 230 persons who had been exposed to formaldehyde and suffered from asthma-like respiratory symptoms were examined between January 1, 1977, and May 31, 1983. All the subjects had a bronchial provocation test with formaldehyde. On the basis of the medical and occupational history of the patients, the specific bronchial provocation test, and other test results, 12 cases were considered to be caused by specific sensitization to formaldehyde. All subjects had been exposed occupationally. An exposure period of between 1 mo and 19 yr preceded the onset of symptoms. Three persons displayed no bronchial hyperreactivity as assessed with a histamine or metacholine provocation test. Eleven of the 12 reactions were triggered by about 2.5 mg/m3 and one reaction by about 1.2 mg/m3 of formaldehyde. The late reaction in 1 patient was completely blocked by the inhalation of 100 micrograms of beclomethasone di-isoproprionate before the challenge with formaldehyde. Seventy-one of the 218 subjects who did not react when they were challenged with formaldehyde demonstrated bronchial hyperreactivity. We conclude that formaldehyde asthma, although apparently a rare disease, is under reported. Removal from exposure has a favorable effect on the symptoms. Low domestic exposures, however, may maintain the symptoms in individuals already sensitized.

Adult↗
PubMed1993

Evaluation of a worker with possible formaldehyde-induced asthma.

BACKGROUND: We describe the evaluation of a worker with clinical symptoms compatible with bronchospasm caused by formaldehyde exposure. METHODS: The worker was evaluated by means of enzyme-linked immunosorbent assay, cutaneous tests, and methacholine and formaldehyde inhalation challenges. The worker's serum was injected intradermally into the skin of a normal rhesus monkey to determine whether hypersensitivity could be transferred from human to primate. RESULTS: An enzyme-linked immunosorbent assay showed that the worker had positive IgE and IgG titers to formaldehyde-human serum albumin. The worker had a positive cutaneous test for formaldehyde-human serum albumin, and this cutaneous reactivity was transferred to a rhesus monkey through the worker's serum. The worker had a negative methacholine challenge at 25 mg/ml and negative formaldehyde inhalation challenges at 0.3, 1, 3, and 5 ppm for 20 minutes. It is possible that the worker would have had a positive result if a higher concentration of F were used for the challenge, but it is more probable that the worker's symptoms were not caused by immunologically mediated asthma. We have studied individuals exposed to formaldehyde, their clinical syndromes, and serologic results for a decade. This worker is the one subject with the most compatible history and immunology, but the worker had a negative challenge. CONCLUSION: Immunologically mediated asthma caused by formaldehyde is extremely rare, if it exists at all.

Asthma↗
PubMed1992

Perspectives on formaldehyde toxicity: separating fact from fantasy.

Formaldehyde (IUPAC name, methanal) is one of the simplest, most ubiquitous molecules in our environment and troposphere. Exposure to large amounts of formaldehyde can produce a variety of respiratory and dermatologic problems in humans, in both the home and the workplace. However, in spite of anecdotal reports on formaldehyde-induced illness over the past 20 years there is a paucity of data regarding its potential as either an allergen or an antigen in humans. In addition, many of our current impressions about formaldehyde are based on studies of dubious scientific validity. In this review, we discuss the biological and chemical properties of formaldehyde and its presence in materials which we come in contact with, and finally attempt to put in perspective our current understanding of the detrimental effects of formaldehyde on our health, or lack thereof. There is no evidence at present that formaldehyde causes immunological diseases. Finally, and unfortunately, many of the studies have drawn invalid conclusions and are based on poorly controlled anecdotal observations.

Animals↗
PubMed1994

Biochemical and histopathological changes in nasal epithelium of rats after 3-day intermittent exposure to formaldehyde and ozone alone or in combination.

To get a better insight into the pathophysiology of the nasal changes induced by formaldehyde-ozone mixtures, a 3-day inhalation study was carried out in rats, using intermittent exposure to formaldehyde (3.6 ppm) and ozone (0.4 ppm) alone or in combination and focusing on biochemical and histopathological changes in rat nasal respiratory epithelium. Formaldehyde dehydrogenase, glutathione S-transferase, glutathione reductase, and glucose-6-phosphate dehydrogenase activities in this epithelium were not affected by the individual compounds. However, combined exposure to formaldehyde and ozone resulted in slightly decreased activities of these enzymes. Formaldehyde was found to induce rhinitis, degeneration, frank necrosis, hyperplasia and squamous metaplasia of the ciliated and non-ciliated nasal respiratory epithelium, while ozone induced disarrangement, flattening and slight basal cell hyperplasia of the non-ciliated cuboidal epithelium accompanied by influx of neutrophils. Proliferating cell nuclear antigen (PCNA) expression was elevated not only in nasal areas showing ozone-induced histopathological changes but also in the otherwise normal-appearing epithelium of the nasal septum. No interactive effects were found with respect to proliferative response of the nasal respiratory epithelium after exposure to the formaldehyde-ozone mixture. The present study did not provide evidence of a major role of glutathione and glutathione-dependent enzymes in the pathogenesis of nasal lesions induced by formaldehyde and/or ozone, demonstrated the potential of ozone to affect the mucociliary epithelium lining the nasal septum, and suggested that PCNA expression is a sensitive tool for detection of early effects of respiratory irritants.

Administration, Inhalation↗
PubMed2006

Housing characteristics and indoor concentrations of nitrogen dioxide and formaldehyde in Quebec City, Canada.

Concentrations of nitrogen dioxide and formaldehyde were determined in a study of 96 homes in Quebec City, Canada, between January and April 2005. In addition, relative humidity, temperature, and air change rates were measured in homes, and housing characteristics were documented through a questionnaire to occupants. Half of the homes had ventilation rates below 7.5 L/s person. Nitrogen dioxide (NO2) and formaldehyde concentrations ranged from 3.3 to 29.1 microg/m3 (geometric mean 8.3 microg/m3) and from 9.6 to 90.0 microg/m3 (geometric mean of 29.5 microg/m3), respectively. The housing characteristics documented in the study explained approximately half of the variance of NO2 and formaldehyde. NO2 concentrations in homes were positively correlated with air change rates (indicating a significant contribution of outdoor sources to indoor levels) and were significantly elevated in homes equipped with gas stoves and, to a lesser extent, in homes with gas heating systems. Formaldehyde concentrations were negatively correlated with air change rates and were significantly elevated in homes heated by electrical systems, in those with new wooden or melamine furniture purchased in the previous 12 months, and in those where painting or varnishing had been done in the sampled room in the previous 12 months. Results did not indicate any significant contribution of indoor combustion sources, including wood-burning appliances, to indoor levels of formaldehyde. These results suggest that formaldehyde concentrations in Quebec City homes are caused primarily by off-gassing, and that increasing air change rates in homes could reduce exposure to this compound. More generally, our findings confirm the influence of housing characteristics on indoor concentrations of NO2 and formaldehyde.

Air Movements↗
PubMed2005

Absorption of lean formaldehyde from air with Na2SO3 solution.

Formaldehyde is a major indoor pollutant over the world and its high release over the national standards in developing countries, such as China, harms people's health seriously. In this work, an investigation is carried out in a stirred vessel with a plain gas-liquid interface for the absorption of lean formaldehyde from pollution air by Na(2)SO(3) solution at 25 degrees C. Experiments are conducted with Na(2)SO(3) concentrations of 0.01-0.30kmolm(-3). The results show that the Na(2)SO(3) solution is an effective absorbent to remove lean formaldehyde from polluted air. The experiments reveal that the absorption rate is considerably influenced by the gas flow rate and formaldehyde concentration. The Na(2)SO(3) concentration has little effect on the absorption rate, and the loading content of formaldehyde reduces the absorption rate only if the formaldehyde concentration approaches or exceeds the concentration of Na(2)SO(3) solution. A theoretical model is developed and used to successfully calculate the absorption rate with the overall relative deviation of less than 15% to the experimental data. A possible process of the absorption method is also proposed in this paper. The analysis shows that the proposed process is feasible in removing formaldehyde from indoor air.

Absorption↗
PubMed1988

Comparison of health of occupants and characteristics of houses among control homes and homes insulated with urea formaldehyde foam. II. Initial health and house variables and exposure-response relationships.

A health survey was conducted on 1726 occupants of urea formaldehyde foam insulated (UFFI) houses and 720 residents of control homes. The occupants of the UFFI houses showed a modest excess of many symptoms relative to the controls. This excess of complaints was contributed mainly by the residents of households which were intending to have their UFFI removed and by onsets which followed the installation of UFFI. There were no associated abnormalities in nasal airway resistance, sense of smell, pulmonary function, or patch tests for allergy to formaldehyde. However, the UFFI subjects intending to have their UFFI removed demonstrated a small increase in nasal epithelial squamous metaplasia. The indoor formaldehyde levels of the UFFI houses were about 20% higher than in the controls, while the carbon dioxide levels were similar in both groups. The UFFI subjects showed positive relationships between level of formaldehyde exposure and the presence of a number of symptoms, which were largely dependent on a small group of formaldehyde values that were in excess of 0.12 ppm. A number of the exposure-response relationships were enhanced by UFFI. These results suggested that some adverse health effects of UFFI were explained by formaldehyde alone while others were related to the combined effects of formaldehyde and an additional UFFI-related factor(s) which was not identified.

Carbon Dioxide↗
PubMed2000

Formaldehyde neurotoxicity in animal experiments.

The aim of this study was to determine whether the inhalation of formaldehyde has a neurotoxicological impact. Forty Wistar rats (Lew.1/K) were trained to find food in a maze within a particular time. When all animals were at an equal level, 13 rats inhaled 2.6 ppm and 13 others inhaled 4.6 ppm formaldehyde 10 min/d, 7 d/week for 90 d. The control group comprised 14 animals inhaling water steam according to the same exposure pattern. During the exposure period and the post-trial observation stage (30 d), the time required to find the food and the number of mistakes made on the way were recorded. Between the animals exposed to formaldehyde and the control group a statistically significant difference for both parameters was observed (p < 0.05). The animals exposed to formaldehyde needed more time and made more mistakes than the animals of the control group while going through the maze. The results underline the necessity for a systematic observance of precautions in case of occupational or dwelling-related formaldehyde exposure, and allow us to classify formaldehyde as "probably neurotoxic". Further investigations are required to assess the neurotoxicologic impact of subchronic formaldehyde exposure.

Administration, Inhalation↗
PubMed1994

Oxidation of glycerol to formaldehyde by microsomes: are glycerol radicals produced in the reaction pathway?

Microsomes and reconstituted systems containing cytochrome P450 can oxidize glycerol to formaldehyde in a reaction catalyzed by an oxidant produced from the interaction of nonheme iron with H2O2. To evaluate the mechanism for this oxidation, the generation of glycerol radicals by various systems was compared to rates of formaldehyde production from glycerol. Photolysis of H2O2, oxidation of xanthine by xanthine oxidase in the presence of iron catalysts, or NADPH-dependent microsomal electron transfer in the presence of ferric-EDTA produced hydroxyl radicals. In the presence of glycerol these reaction systems produced DMPO-glycerol radical adducts which were detected by ESR spectroscopy. Despite the production of .OH and glycerol spin-trapped adducts by these reaction systems, very low amounts or nondetectable amounts of formaldehyde were produced from the glycerol. However, significant amounts of formaldehyde were observed when microsomes were incubated in the presence of ferric ammonium sulfate or ferric-ATP, although .OH production was lower with these iron catalysts than with ferric-EDTA. These results fail to support correlation between .OH production and oxidation of glycerol to formaldehyde. Under conditions in which glycerol was oxidized to formaldehyde, no glycerol radical species could be observed with DMPO as the spin-trapping agent. These results suggest the oxidant (not .OH) derived from the interaction of H2O2 with iron apparently cleaves glycerol to formaldehyde without the formation of a radical intermediate. Alternatively, the radical intermediate may be produced at a too low concentration to be detected or the radical intermediate may not be formed as a free species and therefore cannot be spin-trapped.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Histone redistribution and conformational effect on chromatin induced by formaldehyde.

Histone redistributions between endogenous DNA in calf thymus chromatin and exogenous DNA from Clostridium perfringens (69% A + T) or from Micrococcus luteus (30% A + T) induced by 0.6 M NaCl or by 2% formaldehyde were studied by thermal denaturation. The observed redistribution occurred on histone Hl when the exogenous DNA was (A + T)-richer than the DNA in chromatin, and when the mixture was exposed to 0.6 M NaCl or formaldehyde. When a (G + C)-richer DNA was added as the acceptor for histones, no substantial transfer of histones from chromatin DNA to exogenous DNA was found. Thus the activation energy of histone dissociation from chromatin DNA seems to be substantially lowered by 0.6 M NaCl or formaldehyde such that histones (mostly histone Hl) can be dissociated and bind the (A + T)-richer DNA and form a more stable complex. It is suggested that the formaldehyde effect on histones may be due to the loss of positive charges on lysine and arginin residues (probably more on lysine than on arginine) in histones after their rapid reaction with formaldehyde. Formaldehyde treatment of chromatin also distorts the DNA conformation, as revealed by circular dichroism (CD) studies. This structural effect occurs mainly on those base pairs bound by histones other than Hl, or within the chromatin subunit. Histone redistribution is treated as a thermodynamic phenomenon of histone binding to DNA. The validity of using formaldehyde to study chromatin structure is discussed.

Animals↗