Hayashi M, Tanii H, Hashimoto K
Department of Hygiene, School of Medicine, Kanazawa University, 13-1, Takara-machi, Kanazawa 920, Japan.
Toxicol In Vitro. 1988;2(2):69-74. doi: 10.1016/0887-2333(88)90016-1.
Cerebellar astrocyte cultures derived from 7-day-old rats were exposed to acrylamide. Acrylamide dose-dependently inhibited the proliferation of astrocytes, 50% inhibition occurring at about 0.52 mm. Acrylamide reduced [(3)H]thymidine incorporation into DNA, but did not affect it when cytosine arabinoside was present. The main cause of the inhibition of astrocyte proliferation may be the suppression of mitosis. Interleukin-1, one of the factors that produce astrocyte proliferation after brain injury, increased [(3)H]thymidine incorporation into DNA in astrocyte cultures. Acrylamide was found to abolish this proliferative effect of interleukin-1 completely. It is suggested that acrylamide may influence the astrocytic response to brain injury and the regenerative process.