Determination of Hemoglobin Adducts in Humans Occupationally Exposed to Acrylamide

Bergmark, Emma; Calleman, Carl Johan; He, Fengsheng; Costa, Lucio G.

doi:10.1006/taap.1993.1085

Cited by 195 publications

(128 citation statements)

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“…The assumption that GA is the genotoxic agent in AA exposure implies that it is important also to measure the ratio between internal doses of AA and GA. The data so far published indicate that the ratio between the adduct levels to N-terminal valine of GA and AA is about 1:1 [11,45], however with a lower value obtained by Licea-Perez et al [13].…”

mentioning

confidence: 79%

“…Exposure to AA in work environments has been studied by measurements of stable reaction products (adducts) to hemoglobin (Hb), as a measure of internal dose [11][12][13][14][15]. In exposed workers dose-response relationships between Hb adducts and neurotoxic effects have been demonstrated [14,16].…”

Section: Introductionmentioning

confidence: 99%

“…In the case of AA, Calleman [55] has estimated the rate of detoxification in humans from studies at relatively high exposure levels to approximately 0.15 h -1 . Using detoxification rate and the rate constant for the formation of adducts determined by Bergmark et al [11], a background level of 0.030 nmol/g Hb of the AA adduct would correspond to an intake of 1.2 µg/kg bw and day. This is higher than the estimated intake (0.5 µg/kg bw and day) from food consumption statistics and measured AA levels in food.…”

mentioning

confidence: 99%

“…A ratio of 1:1 between the adduct levels of GA and AA would according to rate constants determined by Bergmark mean that the dose (i.e. concentration × time) of GA is about 30 % of the dose of AA [11]. The reaction-kinetic parameters underlying these calculations, however, have to be further evaluated.…”

mentioning

confidence: 99%

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Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake, smoking habits and gender

Hagmar

Wirfält

Paulsson

et al. 2005

Mutation Research/Genetic Toxicology and Environmental Mutagene

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mentioning

confidence: 79%

Section: Introductionmentioning

confidence: 99%

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confidence: 99%

mentioning

confidence: 99%

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Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake, smoking habits and gender

Hagmar

Wirfält

Paulsson

et al. 2005

Mutation Research/Genetic Toxicology and Environmental Mutagene

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“…In animal experiments, dietary intake of AA has been shown to increase the AA adduct level in Hb (Tareke et al, 2000;Vikström et al, 2005), and to give reliable quantitative measures of the internal dose of AA; reviewed by Törnqvist et al (2006). Exposure-related increases in Hb AA adducts have been shown in workers with occupational exposure to AA (Bergmark et al, 1993;Hagmar et al, 2001;Jones et al, 2006), and in tobacco smokers (Bergmark, 1997;Schettgen et al, 2004). An human study with oral exposure (in aqueous solution) at the level of high occupational exposures showed a clearcut relationship between exposure and the increased level of the Hb AA Estimated AA-intakes and Hb AA-adducts E Wirfält et al adduct .…”

Section: Discussionmentioning

confidence: 99%

Associations between estimated acrylamide intakes, and hemoglobin AA adducts in a sample from the Malmö Diet and Cancer cohort

et al. 2007

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Objective: To examine the coherence of estimated intakes of acrylamide (AA) from foods, with hemoglobin (Hb) AA adduct levels, an objective marker of environmental AA exposure. Design: A cross-sectional study. Setting: The Malmö Diet and Cancer study, a large population-based prospective cohort (n ¼ 28 098) in the south of Sweden. Subjects: A sample of non-smoking (n ¼ 70) and smoking (n ¼ 72) women and men selected to obtain large variation in Hb AA adducts. Methods: Self-reported data on the usual consumption of foods were combined with published data on the AA content in Swedish foods. The Hb AA adduct levels were determined by a modified Edman degradation method. Linear regression and correlation analysis examined associations between estimated AA intakes, and Hb AA adducts. Results: In randomly selected individuals (n ¼ 40), the estimated median AA intake was 28 mg per day. In linear regression models, adjusting for sex, significant associations were seen in non-smokers between Hb AA adducts and estimated AA from foods (P ¼ 0.006). In smokers both AA from foods (P ¼ 0.006) and the calculated amount of tobacco consumed (P ¼ 0.003) were significantly associated with Hb AA adducts. Positive partial correlations between dietary AA estimates and Hb AA adducts were seen in smoking men (r ¼ 0.37) and women (r ¼ 0.59), and in non-smoking men (r ¼ 0.60), but not in non-smoking women. Conclusions: This study suggests that both diet and tobacco are important sources of the environmental AA exposure, although the lack of correlations in non-smoking women cast doubt on the validity of dietary AA intake estimates used in cancer epidemiology, or suggest that unrecognized factors may influence the internal dose measure of AA exposure.

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Probing acrylamide alkylation sites in cysteine-free proteins by matrix-assisted laser desorption/ionisation time-of-flight

Bordini¹,

Hamdan²,

Righetti³

2000

Rapid Commun. Mass Spectrom.

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It is recognised that gel-separated proteins can experience a frequent modification provoked by the interaction of unpolymerized acrylamide monomers with the thiol group of cysteine to form a beta-cysteinyl-S-propionamide adduct. Other groups which have been implicated in this reaction include the hydroxyl group of tyrosine, the straightepsilon-amino group of lysine, and the free N-terminus. In a series of recent publications it has been demonstrated that at pH approximately 9.5 and in the presence of cysteine, none of these groups experienced measurable interaction with acrylamide monomers. To emphasise this conclusion we have used matrix-assisted laser desorption/ionisation with a reflectron time-of-flight mass spectrometer to examine a number of cysteine-free proteins incubated for various intervals with 30 mM acrylamide monomers at pH 9.5. These high resolution data suggest that, for short incubation times (>/=1 hour) and in the absence of cysteine, the straightepsilon-NH(2) group of lysine is the likely adduction site of acrylamide. Longer incubation times (>/=24 hours) with acrylamide monomers rendered the role of Cys as the favourite alkylation site less evident.

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Determination of Hemoglobin Adducts in Humans Occupationally Exposed to Acrylamide

Cited by 195 publications

References 0 publications

Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake, smoking habits and gender

Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake, smoking habits and gender

Associations between estimated acrylamide intakes, and hemoglobin AA adducts in a sample from the Malmö Diet and Cancer cohort

Probing acrylamide alkylation sites in cysteine-free proteins by matrix-assisted laser desorption/ionisation time-of-flight

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