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   <subfield code="a">Life stage-related differences in susceptibility to acrylamide-induced neural and testicular toxicity</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Miwa Takahashi, Kaoru Inoue, Naoki Koyama, Midori Yoshida, Kaoru Irie, Tomomi Morikawa, Makoto Shibutani, Masamitsu Honma, Akiyoshi Nishikawa]</subfield>
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   <subfield code="a">In order to assess age-dependence of susceptibility to acrylamide (ACR)-induced neural and testicular toxicity, 3- and 7-week-old male SD rats were given ACR at 0, 50, 100, or 200ppm in the drinking water for 4weeks, and the nervous and male reproductive systems were examined histopathologically. Testicular genotoxicity was evaluated with the comet assay and the micronucleus (MN) test. Glutathione S-transferase (GST) activity and glutathione (GSH) content in the liver and testis were also measured. In both young and adult animals, neurotoxicity was evident from 100ppm and increased in proportion to ACR intake per body weight. In the testis, marked degeneration and exfoliation, mainly of spermatids, were observed from 100ppm limited to young animals. The comet assay revealed ACR to significantly induce DNA damage from 100ppm in both life stages, while MNs were found only in young rats from 100ppm. The level of GST activity in the testis of young rats at the end of experiment was significantly lower than that of adult animals, regardless of the ACR treatment. There were no life stage-related differences in GSH contents in the liver and testis. These results suggest that susceptibility to neurotoxicity might not differ between young and adult rats when exposure levels are adjusted for body weight. Regarding testicular toxicity, young animals around puberty proved more susceptible than adult animals, possibly due to their lower level of testicular GST activity than that in adult animals.</subfield>
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   <subfield code="a">Springer-Verlag, 2011</subfield>
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   <subfield code="a">Acrylamide</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Age</subfield>
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   <subfield code="a">Susceptibility</subfield>
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   <subfield code="a">Neurotoxicity</subfield>
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   <subfield code="a">Testicular toxicity</subfield>
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   <subfield code="a">Takahashi</subfield>
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   <subfield code="u">Division of Pathology, National Institute of Health Sciences, 1-18-1 Kamiyoga, 158-8501, Setagaya-ku, Tokyo, Japan</subfield>
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   <subfield code="u">Division of Pathology, National Institute of Health Sciences, 1-18-1 Kamiyoga, 158-8501, Setagaya-ku, Tokyo, Japan</subfield>
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   <subfield code="a">Koyama</subfield>
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   <subfield code="u">Division of Genetics and Mutagenesis, National Institute of Health Sciences, 1-18-1 Kamiyoga, 158-8501, Setagaya-ku, Tokyo, Japan</subfield>
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   <subfield code="a">Yoshida</subfield>
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   <subfield code="u">Division of Pathology, National Institute of Health Sciences, 1-18-1 Kamiyoga, 158-8501, Setagaya-ku, Tokyo, Japan</subfield>
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   <subfield code="g">85/9(2011-09-01), 1109-1120</subfield>
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