Heating of food and haemoglobin adducts from carcinogens: possible precursor role of glycidol

Landin, Helena Hindsø; Tareke, Eden; Rydberg, Per; Olsson, Ulf; Törnqvist, Margareta

doi:10.1016/s0278-6915(00)00093-4

Cited by 33 publications

(16 citation statements)

References 30 publications

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“…The same authors found background levels of diHOPrVal (1-2 pmol/g Hb) in blood of persons without known exposure and suggested that this background levels could originate from glycidol or related compounds found in heat-processed foods (Hindsø Landin et al, 1997). Indeed, increased levels of diHOPrVal were found in Sprague-Dawley rats fed heat-processed (fried) diet (Hindsø Landin et al, 2000). Appel et al (2013) monitored the levels of diHOPrVal adducts in blood of rats administered equimolar doses of glycidyl palmitate or glycidol to address the question of relative bioavailability of glycidol from glycidol esters in vivo.…”

Section: Protein/dna Adductsmentioning

confidence: 95%

“…The same authors found background levels of diHOPrVal (1–2 pmol/g Hb) in blood of persons without known exposure and suggested that this background levels could originate from glycidol or related compounds found in heat‐processed foods (Hindsø Landin et al., ). Indeed, increased levels of diHOPrVal were found in Sprague‐Dawley rats fed heat‐processed (fried) diet (Hindsø Landin et al., ).…”

Section: Assessmentmentioning

confidence: 99%

See 1 more Smart Citation

Risks for human health related to the presence of 3‐ and 2‐monochloropropanediol (MCPD), and their fatty acid esters, and glycidyl fatty acid esters in food

Wallace¹,

Alexander²,

Barregård³

et al. 2016

EFS2

129

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EFSA was asked to deliver a scientific opinion on free and esterified 3-and 2-monochloropropane-1, 2-diol (MCPD) and glycidyl esters in food. Esters of 3-and 2-MCPD and glycidol are contaminants of processed vegetable oils; free MCPDs are formed in some processed foods. The Panel on Contaminants in the Food Chain (CONTAM Panel) evaluated 7,175 occurrence data. Esters of 3-and 2-MCPD and glycidyl esters were found at the highest levels in palm oil/fat, but most vegetable oil/fats contain substantial quantities. Mean middle bound (MB) dietary exposure values to total 3-MCPD, 2-MCPD and glycidol, respectively, across surveys and age groups in µg/kg body weight (bw) per day were 0.2-1.5, 0.1-0.7 and 0.1-0.9; high exposure (P95) values were 0.3-2.6, 0.2-1.2 and 0.2-2.1. Animal studies show extensive hydrolysis of esterified 3-MCPD and glycidol following oral administration; esterified and free forms were assumed to contribute equally to internal exposures. Nephrotoxicity was consistently observed in rats treated with 3-MCPD. Data on 2-MCPD toxicity were insufficient for dose-response assessments. Chronic treatment with glycidol increased the incidence of tumours in several tissues of rats and mice, likely via a genotoxic mode of action. The Panel selected a BMDL 10 value for 3-MCPD of 0.077 mg/kg bw per day for induction of renal tubular hyperplasia in rats and derived a tolerable daily intake (TDI) of 0.8 µg/kg bw per day. The mean exposure to 3-MCPD was above the TDI for 'Infants', 'Toddlers' and 'Other children'. For glycidol, the Panel selected a T25 value of 10.2 mg/kg bw per day for neoplastic effects in rats. The margins of exposure (MoEs) were 11,300-102,000 and 4,900-51,000 across surveys and age groups at mean and P95 exposures, respectively. An exposure scenario for infants receiving formula only resulted in MoEs of 5,500 (mean) and 2,100 (P95). MoEs of 25,000 or higher were considered of low health concern. Amendment: A few editorial amendments were carried out that do not materially affect the contents of the outcome of this scientific output: on pages 5 and 91 'chorine' has been replaced with 'chlorine'; on page 52 the word 'it' has been replaced by 'its' in the first paragraph after Figure 7; on page 54 in the Repeated dose section the reference to MCPD has been replaced with 3-MCPD; on page 54 the 429.5 mg/kg bw day dose has been replaced with 29.5 mg/kg bw day; on page 55 in the first paragraph of the Hematology section the reference 'mg/kg per day' has been replaced with 'mg/kg bw per day; on page 55 the year for the reference Marchesini et al. has been changed from 1989 to 1986; on page 59, in the first paragraph of the Developmental toxicity section the word 'days' has been cancelled; on page 65 the reference 'Onami et al., 2014a,b' has been replaced with 'Onami et al., 2014b'; on page 85 first paragraph, reference to the lowest T25 of 10 has been replaced to 10.2. To avoid confusion, the older version has been removed from the EFSA Journal, but is available on request, as is a version sho...

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Section: Protein/dna Adductsmentioning

confidence: 95%

Section: Assessmentmentioning

confidence: 99%

Risks for human health related to the presence of 3‐ and 2‐monochloropropanediol (MCPD), and their fatty acid esters, and glycidyl fatty acid esters in food

Wallace¹,

Alexander²,

Barregård³

et al. 2016

EFS2

129

View full text Add to dashboard Cite

show abstract

“…In this case, both the quantitative extraction of the derivatives from the reaction mixture and their gas-chromatographic separation are hampered by the presence of these polar functions (Kautiainen et al, 2000). To overcome this difficulty, derivatization of the hydroxyl groups was mainly pursued by acetylation (Hindso Landin et al, 2000) and silylation (Ahn & Shin, 2006;Shin & Ahn, 2006), although recently cyclization of a glycidamide-modified valine derivative into the acetonide derivative was also reported (Paulsson et al, 2003). As an alternative, also LC-ESI-MS-MS of the underivatized phenylthiohydantoin has been recently pursued (Chevolleau et al, 2007).…”

Section: Measurement Of Modified Amino Acidsmentioning

confidence: 99%

Toward an “omic” physiopathology of reactive chemicals: Thirty years of mass spectrometric study of the protein adducts with endogenous and xenobiotic compounds

Rubino

Pitton

Fabio

et al. 2009

Mass Spectrometry Reviews

109

170

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Cancer and degenerative diseases are major causes of morbidity and death, derived from the permanent modification of key biopolymers such as DNA and regulatory proteins by usually smaller, reactive molecules, present in the environment or generated from endogenous and xenobiotic components by the body's own biochemical mechanisms (molecular adducts). In particular, protein adducts with organic electrophiles have been studied for more than 30 [see, e.g., Calleman et al., 1978] years essentially for three purposes: (a) as passive monitors of the mean level of individual exposure to specific chemicals, either endogenously present in the human body or to which the subject is exposed through food or environmental contamination; (b) as quantitative indicators of the mean extent of the individual metabolic processing which converts a non-reactive chemical substance into its toxic products able to damage DNA (en route to cancer induction through genotoxic mechanisms) or key proteins (as in the case of several drugs, pesticides or otherwise biologically active substances); (c) to relate the extent of protein modification to that of biological function impairment (such as enzyme inhibition) finally causing the specific health damage. This review describes the role that contemporary mass spectrometry-based approaches employed in the qualitative and quantitative study of protein-electrophile adducts play in the discovery of the (bio)chemical mechanisms of toxic substances and highlights the future directions of research in this field. A particular emphasis is given to the measurement of often high levels of the protein adducts of several industrial and environmental pollutants in unexposed human populations, a phenomenon which highlights the possibility that a number of small organic molecules are generated in the human organism through minor metabolic processes, the imbalance of which may be the cause of "spontaneous" cases of cancer and of other degenerative diseases of still uncharacterized etiology. With all this in mind, it is foreseen that a holistic description of cellular functions will take advantage of new analytical methods based on time-integrated metabolomic measurements of a new biological compartment, the "adductome," aimed at better understanding integrated organism response to environmental and endogenous stressors.

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“…3-MCPD would however give a very small contribution, as 3-MCPD has more than 1000 times lower rate constant for formation of the adduct to the N-terminal in Hb compared to glycidol [28]. The food-related compounds allyl alcohol, found in garlic, or anhydro sugars from carbohydrates, can also theoretically be precursors to the adduct [29,30]. The formation of glycidol from allyl alcohol could be assumed to be possible via a metabolic oxidation.…”

Section: Discussionmentioning

confidence: 99%

Internal Doses of Glycidol in Children and Estimation of Associated Cancer Risk

Aasa

Vryonidis

Abramsson‐Zetterberg

et al. 2019

Toxics

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The general population is exposed to the genotoxic carcinogen glycidol via food containing refined edible oils where glycidol is present in the form of fatty acid esters. In this study, internal (in vivo) doses of glycidol were determined in a cohort of 50 children and in a reference group of 12 adults (non-smokers and smokers). The lifetime in vivo doses and intakes of glycidol were calculated from the levels of the hemoglobin (Hb) adduct N-(2,3-dihydroxypropyl)valine in blood samples from the subjects, demonstrating a fivefold variation between the children. The estimated mean intake (1.4 μg/kg/day) was about two times higher, compared to the estimated intake for children by the European Food Safety Authority. The data from adults indicate that the non-smoking and smoking subjects are exposed to about the same or higher levels compared to the children, respectively. The estimated lifetime cancer risk (200/105) was calculated by a multiplicative risk model from the lifetime in vivo doses of glycidol in the children, and exceeds what is considered to be an acceptable cancer risk. The results emphasize the importance to further clarify exposure to glycidol and other possible precursors that could give a contribution to the observed adduct levels.

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Heating of food and haemoglobin adducts from carcinogens: possible precursor role of glycidol

Cited by 33 publications

References 30 publications

Risks for human health related to the presence of 3‐ and 2‐monochloropropanediol (MCPD), and their fatty acid esters, and glycidyl fatty acid esters in food

Risks for human health related to the presence of 3‐ and 2‐monochloropropanediol (MCPD), and their fatty acid esters, and glycidyl fatty acid esters in food

Toward an “omic” physiopathology of reactive chemicals: Thirty years of mass spectrometric study of the protein adducts with endogenous and xenobiotic compounds

Internal Doses of Glycidol in Children and Estimation of Associated Cancer Risk

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