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Biosynthesis of acetyl--aspartic acid.

Cirla et al. (1984) carried out a clinical evaluation of 100 workers in synthetic polyurethane leather produc tion exposed to a mean TWA concentration (determined by personal sampling) of 22 mg/m3 (range 8–58 mg/m3) (mean TWA 7 ppm; range 3–19 ppm). The mean expo sure period was 5 years (range 1–15 years).The workers were also exposed to small (but unspecified) quantities of toluene, methyl ethyl ketone (MEK), ethyl acetate, and isopropyl and isobutyl alcohol. Study subjects were selected to minimize large variations in exposure; those with histories of possible accidental exposures were also excluded. The referent group was 100 workers at the same or similar factories, without exposure to any solvents or toxic metals, matched by sex, age group, alcohol history, smoking habits, coffee intake, socio economic status, residence, and dietary customs. Clinical evaluation was carried out and a laboratory assessment was performed for blood cell counts and serum AP, AST, ALT, and -GT. Serum -GT was abnormally high in 25/100 exposed and only 10/100 referents ( Several symptoms, including headache, dyspepsia, and digestive impairment, characteristic of effects on the liver were also associated with exposure to DMF.

N-Acetylaspartic acid - Wikipedia

In female Sprague-Dawley rats administered a single oral dose of 100 mg 14C-labelled DMF/kg body weight on day 12 or 18 of pregnancy, 60–70% of the radioactivity was excreted in urine and 3–4% in faeces at 48 h (Saillenfait et al., 1997). Approximately 4% of the dose was present in the liver at 0.5 h after dosing at both gestation times, with 8 and 13% in the gastrointes tinal tract (stomach and intestine) and 0.7 and 0.8% in the kidneys, respectively. Plasma radioactivity was relatively constant from 0.5 to 4 h after dosing (approximately 0.4–0.5% of the dose) but declined rapidly thereafter. By 48 h, only the liver (0.5 and 0.6%) and intestine (0.2 and 0.3%) retained any significant activity. In animals exposed on day 12 of gestation, approximately 1.5% of the dose was present in the uterus, placenta, embryo, and amniotic fluid at between 0.5 and 4 h, which rapidly declined to less than 0.1% at 24 h. In rats exposed on day 18 of gestation, fetal tissues accounted for 6% of the administered dose. HPLC analysis performed at intervals from 1 to 24 h indicated that unchanged DMF and metabolites were readily transferred to the embryonic and fetal tissues, where levels were generally equal to those in maternal plasma. The parent compound accounted for most of the radioactivity until 4–8 h and then decreased.

N acetyl aspartate | Sigma-Aldrich

The major metabolic pathway for DMF in mam malian species is oxidation by the cytochrome P-450- dependent mixed-function oxidase system to HMMF (Figure 1). This can generate NMF and formaldehyde (see review by Gescher, 1993). Further cytochrome P- 450-mediated oxidation of NMF and/or HMMF results in the formation of -(-methylcarbamoyl)glutathione (SMG), the conjugate of the presumed reactive (toxic) intermediate, methyl isocyanate, excreted as - acetyl--(-methylcarbamoyl)cysteine (AMCC). Results of studies with liver microsomes from acetone-treated rats (Mráz et al., 1993; Chieli et al., 1995) and mice (Chieli et al., 1995) and with reconstituted enzyme systems indicate that cytochrome P-450 2E1 mediates the metabolism of DMF to HMMF and, subsequently, to the proposed reactive intermediate, methyl isocyanate.

In a number of early studies, the effects of co- administration of ethanol on blood concentrations of DMF, NMF, ethanol, and acetaldehyde were investigated. Although there were variations in results depending on dose, time interval between administration of DMF and ethanol, and routes of exposure, there were increases in concentrations of DMF, NMF, ethanol, or acetaldehyde in blood upon co-exposure. These results may be attributable to inhibition by DMF of the activity of alcohol dehydrogenase observed both and (Eben & Kimmerle, 1976; Hanasono et al., 1977; Sharkawi, 1979) and of aldehyde dehydrogenase observed (Elovaara et al., 1983).

Search results for N acetyl aspartate at Sigma-Aldrich

DMF is used commercially as a solvent in vinyl resins, adhesives, pesticide formulations, and epoxy formulations; for purification and/or separation of acetylene, 1,3-butadiene, acid gases, and aliphatic hydrocarbons; and in the production of polyacrylic or cellulose triacetate fibres and pharmaceuticals (WHO, 1991; IARC, 1999). DMF is also used in the production of polyurethane resin for synthetic leather (Fiorito et al., 1997).

In 1996, just over 16 tonnes of DMF were released from various industrial locations in Canada, of which 93% (15 079 kg) were emitted to the atmosphere and the remainder to water (245 kg), wastewater (204 kg), landfill sites (26 kg), or deep-well injection (669 kg) (Environment Canada, 1998). The Canadian market for DMF is quite small, with an estimated domestic con sumption in the range of less than 1000 tonnes/year (SRI International, 1994; Environment Canada, 1998). The petrochemical sector was responsible for 84% (12.7 tonnes) of the reported atmospheric releases. Releases from the pharmaceutical industry accounted for 87% (0.212 tonnes) of total releases to water. Total release volumes from Canadian industrial sectors include 13.3 tonnes from the petrochemical sector, 1.2 tonnes from manufacture of pharmaceuticals, 0.7 tonnes from dye and pigment manufacture, 0.6 tonnes from polyvinyl chloride coating operations, 0.1 tonnes from its use as a solvent in pesticide manu facture, 0.07 tonnes from paint/finisher and paint remover manufacture, and 0.09 tonnes from other mis cellaneous industrial sectors.For 1996, a reported total quantity of 0.056 tonnes was released (0.023 tonnes to air, 0.033 tonnes to water) by the producer during chemical synthesis of DMF (Environment Canada, 1998). Less than 1 tonne of DMF was released from wastewater treatment facilities and in landfills (Envi ronment Canada, 1998). With a few exceptions, most industries reported little to no seasonal variation in releases (Environment Canada, 1998).

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Suppressing N-acetyl-L-aspartate (NAA) synthesis …

Although the database for carcinogenicity is limited to two adequately conducted bioassays in rats and mice, there have been no increases in the incidence of tumours following chronic inhalation exposure to DMF. The weight of evidence for genotoxicity is over whelmingly negative, based on extensive investigation in assays, particularly for gene mutation, and a more limited database In studies with laboratory animals, DMF has induced adverse reproductive effects only at concentra tions greater than those associated with adverse effects on the liver, following both inhalation and oral expo sure. Similarly, in well conducted and reported primarily recent developmental studies, fetotoxic and teratogenic effects have been consistently observed only at maternally toxic concentrations or doses. Available data are inadequate as a basis for assessment of the neurological or immunological effects of DMF.The focus of this CICAD and the sample risk characterization is primarily effects of indirect exposure in the general environment. Air in the vicinity of point sources appears to be the greatest potential source of exposure of the general population to DMF. Based on the results of epidemiological studies of exposed workers and supporting data from a relatively extensive database of investigations in experimental animals, the liver is the critical target organ for the toxicity of DMF. A tolerable concentration of 0.03 ppm (0.1 mg/m3) has been derived on the basis of increases in serum hepatic enzymes.Data on the toxicity of DMF to terrestrial vascular plants have not been identified. Effect concentrations for indicators of the potential sensitivities of trees, shrubs, and other plants are high; hence, it is unlikely that terres trial plants are particularly sensitive to DMF. For other terrestrial organisms, an estimated no-effects value of 15 mg/m3 has been derived based on a critical toxicity value for hepatic toxicity in mice divided by an application factor. Comparison of this value with a conserva tive estimated exposure value indicates that it is unlikely that DMF causes adverse effects on terrestrial organisms in the sample country.,-Dimethylformamide (CAS No. ) is a colourless liquid at room temperature with a faint amine odour (BUA, 1994). There are many synonyms for this compound, the most common being the acronym DMF. The molecular mass of DMF is 73.09, as calculated from its empirical formula (C3H7NO). DMF sold commer cially contains trace amounts of methanol, water, formic acid, and dimethylamine (BUA, 1994).

N-Acetylaspartic acid - an overview | ScienceDirect Topics

DMF is readily absorbed following oral, dermal, or inhalation exposure. Following absorption, DMF is uniformly distributed, metabolized primarily in the liver, and relatively rapidly excreted as metabolites in urine. The major pathway involves the hydroxylation of methyl moieties, resulting in -(hydroxymethyl)-- methylformamide (HMMF), which is the major urinary metabolite in humans and animals. HMMF in turn can decompose to -methylformamide (NMF). In turn, enzymatic -methyl oxidation of NMF can produce - (hydroxymethyl)formamide (HMF), which further degenerates to formamide. An alternative pathway for the metabolism of NMF is oxidation of the formyl group, resulting in -acetyl--(-methylcarbamoyl) cysteine (AMCC), which has been identified as a urinary metabolite in rodents and humans. A reactive interme diate, the structure of which has not yet been determined (possibly methyl isocyanate), is formed in this pathway; while direct supporting experimental evidence was not identified, this intermediate is suggested to be the putatively toxic metabolite. Available data indicate that a greater proportion of DMF may be metabolized by the putatively toxic pathway in humans than in experimental animals. There is metabolic interaction between DMF and alcohol, which, though not well understood, may be due, at least in part, to its inhibitory effect on alcohol dehydrogenase.

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