Glöckner R, Klinger W
Exp Pathol. 1981;20(4):215-20. doi: 10.1016/s0232-1513(81)80025-4.
In vitro induction of aminoketone synthesis (AKS) by allylisopropylacetamide (AIA) in liver slices from 30 day-old male rats was reversibly inhibited by puromycin (50 micrograms/ml incubation mixture). Normal AKS was initially stimulated and thereafter blocked. Chloramphenicol (350 micrograms/ml) inhibited AIA mediated induction of AKS only partially and only when added 1 h before AIA to the incubation mixture. In vivo puromycin (3 i.p. injections of 15 mg/kg in 1 h intervals) did not influence AKS or AIA mediated AKS induction in newborn rats, whereas chloramphenicol (500 mg/kg s.c. 30 min prior to AIA) inhibited AIA mediated AKS induction in newborn rats. In 40 day-old rats pretreatment with chloramphenicol completely inhibited AKS induction by 200 mg/kg AIA.
在30日龄雄性大鼠肝脏切片中，嘌呤霉素（50微克/毫升孵育混合物）可可逆性抑制烯丙基异丙基乙酰胺（AIA）对氨基酮合成（AKS）的体外诱导。正常的AKS起初受到刺激，随后被阻断。氯霉素（350微克/毫升）仅在孵育混合物中于AIA加入前1小时添加时，才对AIA介导的AKS诱导有部分抑制作用。在新生大鼠体内，嘌呤霉素（1小时内腹腔注射3次，每次15毫克/千克）不影响AKS或AIA介导的AKS诱导，而氯霉素（在AIA前30分钟皮下注射500毫克/千克）可抑制新生大鼠中AIA介导的AKS诱导。在40日龄大鼠中，用氯霉素预处理可完全抑制200毫克/千克AIA对AKS的诱导。
