Transplacental transfer of acrylamide and glycidamide are comparable to that of antipyrine in perfused human placenta

Annola, Kirsi; Karttunen, Vesa; Keski‐Rahkonen, Pekka; Myllynen, Päivi; Segerbäck, Dan; Heinonen, Seppo; Vähäkangas, Kirsi

doi:10.1016/j.toxlet.2008.08.006

Cited by 68 publications

(37 citation statements)

References 61 publications

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“…AA and GA crossed the placenta from the maternal to the fetal side with similar kinetics as antipyrine, and the concentrations of AA and GA in the maternal and fetal circulation equilibrated within two hours. No metabolism of AA to GA was detected during an incubation time of 4 hours, nor was a DNA adduct of GA found by HPLC-32 P-postlabelling in the placental tissue perfused with AA or GA (Annola et al, 2008b). …”

Section: Placental Transfermentioning

confidence: 88%

“…The authors perfused the maternal side of three post-partum human placentas with AA at a concentration of about 1 µg/mL without recirculation of the perfusate and found concentrations of about 0.2 µg/mL in the fetal perfusate after 5 to 30 minutes of perfusion. In a later in vitro study, a dual recirculating human placental perfusion was used and the transfer rate of AA (at maternal concentrations of 5 and 10 µg/mL) and GA (5 µg/mL) through the placenta determined (Annola et al, 2008b). Antipyrine (100 µg/mL), which is known to pass through human placenta mainly by passive diffusion, was used as positive control, and all three compounds were determined by HPLC-MS/MS.…”

Section: Placental Transfermentioning

confidence: 99%

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Scientific Opinion on acrylamide in food

Publication¹

2015

EFS2

341

170

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EFSA was asked to deliver a scientific opinion on acrylamide (AA) in food. AA has widespread uses as an industrial chemical. It is also formed when certain foods are prepared at temperatures above 120 °C and low moisture, especially in foods containing asparagine and reducing sugars. The CONTAM Panel evaluated 43 419 analytical results from food commodities. AA was found at the highest levels in solid coffee substitutes and coffee, and in potato fried products. Mean and 95th percentile dietary AA exposures across surveys and age groups were estimated at 0.4 to 1.9 µg/kg body weight (b.w.) per day and 0.6 to 3.4 µg/kg b.w. per day, respectively. The main contributor to total dietary exposure was generally the category 'Potato fried products (except potato crisps and snacks)'. Preferences in home-cooking can have a substantial impact on human dietary AA exposure. Upon oral intake, AA is absorbed from the gastrointestinal tract and distributed to all organs. AA is extensively metabolised, mostly by conjugation with glutathione but also by epoxidation to glycidamide (GA). Formation of GA is considered to represent the route underlying the genotoxicity and carcinogenicity of AA. Neurotoxicity, adverse effects on male reproduction, developmental toxicity and carcinogenicity were identified as possible critical endpoints for AA toxicity from experimental animal studies. The data from human studies were inadequate for dose-response assessment. The CONTAM Panel selected BMDL 10 values of 0.43 mg/kg b.w. per day for peripheral neuropathy in rats and of 0.17 mg/kg b.w. per day for neoplastic effects in mice. The Panel concluded that the current levels of dietary exposure to AA are not of concern with respect to non-neoplastic effects. However, although the epidemiological associations have not demonstrated AA to be a human carcinogen, the margins of exposure (MOEs) indicate a concern for neoplastic effects based on animal evidence. © European Food SUMMARYFollowing a request from the European Commission, the Panel on Contaminants in the Food Chain (CONTAM Panel) was asked to deliver a scientific opinion on acrylamide (AA) in food. The Panel developed the draft scientific opinion which underwent a public consultation from 1 July 2014 to 15 September 2014. The comments received and how they were taken into account when finalising the scientific opinion were published in an EFSA Technical Report (EFSA, 2015).AA is a low molecular weight, highly water soluble, organic compound. It is used inter alia as an industrial chemical and in the production of polyacrylamides. Heightened concerns about exposure to AA arose in 2002 when it was discovered that it forms when certain foods are prepared at temperatures usually above 120 °C and low moisture. It forms, at least in part, due to a Maillard reaction between certain amino acids, such as asparagine, and reducing sugars. However, several other pathways and precursors have also been proposed to contribute to AA formation. AA forms in numerous baked or fried carbohydrate-rich f...

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Section: Placental Transfermentioning

confidence: 88%

Section: Placental Transfermentioning

confidence: 99%

Scientific Opinion on acrylamide in food

Publication¹

2015

EFS2

341

170

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“…Furthermore, some studies suggested that conjugation with GSH is one of the possible mechanisms for the detoxification of acrylamide exposure (Pernice et al, 2009). The neurotoxic metabolite of acrylamide, that is, glycidamide (2,3-epoxy-1-propanamide), is also identified to conjugate and induce the depletion of reduced GSH (Annola et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Pharmacological evaluation of methanolic leaf extract of Swietenia mahagoni on acrylamide-induced neuropathic pain in rats

et al. 2013

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The present study was designed to investigate the antinociceptive effects of methanolic leaf extract of Swietenia mahagoni (MESM) on acrylamide-induced painful neuropathy in rats. The intraperitoneal administration of acrylamide (30 mg/kg; for 24 consecutive days) has been employed for the induction of painful neuropathy. Acrylamide induced nociceptive pain sensitive changes, which have been assessed by hot plate, Von Frey Hair, and tail immersion tests at different time intervals, that is, 0, 6, 12, 18, and 24th day. Furthermore, the biochemical changes, that is, thiobarbituric acid-reactive substances, reduced glutathione, and total calcium levels have been estimated in sciatic nerve tissue on 24th day and histopathological changes have been observed in sciatic nerve tissue sample. MESM and pregabalin have been administered for 14 consecutive days before 1 h of the each acrylamide injection. Administration of acrylamide resulted in significant changes in behavioral and biochemical parameters. Pretreatment of MESM ameliorated acrylamide-induced behavioral, biochemical, and histopathological changes in a dose-dependent manner, which is similar to that of pregabalin-pretreated group. These findings suggested that the neuroprotective effect of S. mahagoni may be due to its potential of antioxidative, calcium channel modulatory, and neuroprotective action.

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“…Acrylamide is known to cross the placenta81 with nonsignificant amounts transferring to the infant through breast milk 82. Rodent models have demonstrated that prenatal and perinatal acrylamide exposures result in low birth weight offspring that develop signs of liver toxicity and lipid accumulation in postnatal life 83,84.…”

Section: Food Processingmentioning

confidence: 99%

Early-life chemical exposures and risk of metabolic syndrome

Long

Holloway

2017

DMSO

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The global prevalence of obesity has been increasing at a staggering pace, with few indications of any decline, and is now one of the major public health challenges worldwide. While obesity and metabolic syndrome (MetS) have historically thought to be largely driven by increased caloric intake and lack of exercise, this is insufficient to account for the observed changes in disease trends. There is now increasing evidence to suggest that exposure to synthetic chemicals in our environment may also play a key role in the etiology and pathophysiology of metabolic diseases. Importantly, exposures occurring in early life (in utero and early childhood) may have a more profound effect on life-long risk of obesity and MetS. This narrative review explores the evidence linking early-life exposure to a suite of chemicals that are common contaminants associated with food production (pesticides; imidacloprid, chlorpyrifos, and glyphosate) and processing (acrylamide), in addition to chemicals ubiquitously found in our household goods (brominated flame retardants) and drinking water (heavy metals) and changes in key pathways important for the development of MetS and obesity.

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Transplacental transfer of acrylamide and glycidamide are comparable to that of antipyrine in perfused human placenta

Cited by 68 publications

References 61 publications

Scientific Opinion on acrylamide in food

Scientific Opinion on acrylamide in food

Pharmacological evaluation of methanolic leaf extract of Swietenia mahagoni on acrylamide-induced neuropathic pain in rats

Early-life chemical exposures and risk of metabolic syndrome

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