Juvenile rats do not exhibit elevated sensitivity to acrylamide toxicity after oral administration for 12 weeks

Takami, Shigeaki; Imai, Toshio; Cho, Young‐Man; Ogawa, Kumiko; Hirose, Masao; Nishikawa, Akiyoshi

doi:10.1002/jat.1686

Cited by 6 publications

(2 citation statements)

References 37 publications

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“…Additionally, there is historical evidence of mild testicular tubule atrophies in control male F344 rats (27%) as reported in the 2-year drinking water study of acrylamide by the [19] . It should be noted that in a previous oral exposure study, acrylamide at a high dose of 40 ppm (equivalent to 4.4 mg/kg BW/day) administered for 12 weeks caused testicular toxicity, but no effects were observed at either 10 or 20 ppm [30] . Supporting our data related to the testes, we found no changes in serum testosterone levels between the control and any of the acrylamide-treated groups ( Table 4 ), suggesting no male hormone-specific testicular toxicity at low dose exposure.…”

Section: Resultsmentioning

confidence: 84%

Lack of adverse health effects following 30-weeks of dietary exposure to acrylamide at low doses in male F344 rats

et al. 2016

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Understanding the health hazards following exposure to food-borne acrylamide, especially at low levels typified by human diets, is an ongoing food safety issue. We recently published results from a study that aimed to understand the effects of acrylamide short-term exposure at doses known to cause tumors in rodents, demonstrating that a number of key toxicological end points were altered by acrylamide exposure. Additionally, we reported that at much lower doses for 30 weeks of exposure, dietary acrylamide was ‘not a complete carcinogen’ to the colon in an organ-specific rodent carcinogenesis study but acted as a co-carcinogen along with azoxymethane (AOM, a colon-specific carcinogen). Here, we present toxicological data from a sub-set of this long-term exposure study from animals that received saline (instead of AOM). Briefly, male F344 rats were randomized to receive acrylamide at 0.5, 1.0 and 2.0 mg/kg diet (∼0.02, 0.04, and 0.09 mg/kg BW/day, respectively) or no acrylamide (control), for 30 weeks; all rats were then euthanized and their tissues harvested and processed for toxicological evaluation. We report that at the doses tested, acrylamide did not cause any changes in general well-being, body weight or food intake. Similarly, acrylamide did not cause any biologically relevant change in parameters associated with immunophenotyping, serum biochemistry or hematology. Histopathology assessment of tissues showed no changes except in the testis, where non-specific mild lesions were observed in all the groups, inclusive of the controls. No neuropathological effects of acrylamide were observed in the brain and nerve tissues. Together, these results suggest that acrylamide administered to rats through the diet at low doses for 30 weeks did not cause any toxicologically relevant changes. Given that the doses of acrylamide in the current study are low and are comparable to human dietary exposure, this null-effect study provides data that contribute to the body of scientific evidence relevant to understanding the health effects of acrylamide.

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Section: Resultsmentioning

confidence: 84%

Lack of adverse health effects following 30-weeks of dietary exposure to acrylamide at low doses in male F344 rats

et al. 2016

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“…There are many reports demonstrating various toxic effects of AA in experimental animals (Takami et al 2012), including reproductive toxicity (Park et al 2010), genotoxicity (Li et al 2015 and neurotoxicity (Tyl et al 2000). AA is a substance classified as a probable human carcinogen (Mucii and Wilson 2008).…”

mentioning

confidence: 99%

Acrylamide-Induced Changes in Femoral Bone Microstructure of Mice

Sarocka

Babošová²,

Kováčová³

et al. 2017

Physiol Res

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Acrylamide (AA) is one of the most common toxins in foods. Its effect on bone microstructure has not been investigated. The aim of our study was to analyze the impact of acute exposure to AA on femoral bone microstructure in mice. Adult animals were treated perorally with 2 doses of AA (E1 group, 1 mg/kg b.w.) in a 24-h period and with 3 doses of AA (E2 group, 1 mg/kg b.w.) in a 48-h period. Mice exposed to AA had smaller sizes of primary osteon's vascular canals. Secondary osteons were significantly smaller in mice from E2 group; however their increased number (from 38 % to 77 %) was identified in both E1 and E2 groups. In these groups, a higher number of resorption lacunae (from 100 % to 122 %) was also found. The values for bone volume, trabecular number were increased and that for trabecular separation was decreased in mice administered AA. Significantly higher value of bone surface was observed in mice from E1 group whereas trabecular thickness was increased in E2 group. The effect of AA on microstructure of compact and trabecular bone tissues is different. In our study, one dose of AA was used and acute effects of AA were investigated. Therefore, further studies are needed to study mechanisms by which AA acts on bone.

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Toxicological effects of short-term dietary acrylamide exposure in male F344 rats

Raju

Roberts

Taylor

et al. 2015

Environmental Toxicology and Pharmacology

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Juvenile rats do not exhibit elevated sensitivity to acrylamide toxicity after oral administration for 12 weeks

Cited by 6 publications

References 37 publications

Lack of adverse health effects following 30-weeks of dietary exposure to acrylamide at low doses in male F344 rats

Lack of adverse health effects following 30-weeks of dietary exposure to acrylamide at low doses in male F344 rats

Acrylamide-Induced Changes in Femoral Bone Microstructure of Mice

Toxicological effects of short-term dietary acrylamide exposure in male F344 rats

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