Lumpkin C K, Taylor J M, Tarpley M D, Hayden J B, Badger T M, McClung J K
Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock 72205.
Alcohol. 1992 May-Jun;9(3):279-82. doi: 10.1016/0741-8329(92)90066-j.
In order to elucidate the effects of acute ethanol on compensatory liver growth (regeneration), the steady state c-myc mRNA levels were studied following two-thirds partial hepatectomy. After surgery, control rat livers exhibited two peaks of c-myc transcripts, at 0.5-2 h and at 8-10 h. Sham surgery did not induce c-myc mRNA expression. Ethanol (3 g/kg), administered by gavage at 1 hour prehepatectomy, had no effect on the initial peak of c-myc mRNA; however, the second peak was eliminated. Control gavage of isocaloric glucose prior to partial hepatectomy had no effects on either of the subsequent c-myc mRNA peaks. Blood alcohol levels were found to be elevated throughout the prereplicative phase. These results suggest that ethanol may disrupt proto-oncogene expression near the restriction point at the G1/S boundary of the cell cycle in hepatocytes.
为了阐明急性乙醇对肝脏代偿性生长(再生)的影响,在三分之二肝部分切除术后研究了稳态c-myc mRNA水平。手术后,对照大鼠肝脏在0.5 - 2小时和8 - 10小时出现两个c-myc转录本峰值。假手术未诱导c-myc mRNA表达。在肝切除术前1小时经口灌胃给予乙醇(3 g/kg),对c-myc mRNA的初始峰值无影响;然而,第二个峰值消失了。在部分肝切除术前对等量葡萄糖进行对照灌胃,对随后的两个c-myc mRNA峰值均无影响。发现在整个复制前期血醇水平均升高。这些结果表明,乙醇可能在肝细胞细胞周期的G1/S边界的限制点附近破坏原癌基因的表达。