Mineura K, Sasajima T, Kuwahara N, Kowada M, Murakami M, Uemura K
Neurosurgical Service, Akita University Hospital, Japan.
J Neurooncol. 1993 Mar;15(3):229-33. doi: 10.1007/BF01050068.
Autoradiographic study of (14C-methyl)-L-methionine with brain tumor bearing rats aimed at an elucidation of the mechanism of tracer accumulation in the protein synthesis of tumor. Twice as much tracer accumulated in the tumors compared as in the contralateral gray matter (nontumor region) at 90 min post intravenous injection. The protein-bound fraction of the tumors, expressed as acid-insoluble fraction (AIF), was 1.7 +/- 0.6 (mean +/- standard deviation, n = 6), significantly higher than that (0.8 +/- 0.2) of the nontumor region (p < 0.05 by the Mann-Whitney test). The tumor AIF comprised 82.3 +/- 9.2% of the total amount of the tracers accumulated in the tumors. The protein synthesis inhibitor cycloheximide reduced the tracer uptake and the AIF of the tumors to an almost same level as the nontumor region. These findings indicate that metabolic acceleration of protein synthesis may be a main reason for the high accumulation of (14C-methyl)-L-methionine in tumor.
对荷脑肿瘤大鼠进行（14C-甲基）-L-蛋氨酸的放射自显影研究，旨在阐明示踪剂在肿瘤蛋白质合成中蓄积的机制。静脉注射后90分钟，肿瘤中蓄积的示踪剂是对侧灰质（非肿瘤区域）的两倍。以酸不溶性部分（AIF）表示的肿瘤蛋白质结合部分为1.7±0.6（平均值±标准差，n = 6），显著高于非肿瘤区域的（0.8±0.2）（曼-惠特尼检验 p < 0.05）。肿瘤AIF占肿瘤中蓄积的示踪剂总量的82.3±9.2%。蛋白质合成抑制剂环己酰亚胺将肿瘤的示踪剂摄取和AIF降低到与非肿瘤区域几乎相同的水平。这些发现表明，蛋白质合成代谢加速可能是（14C-甲基）-L-蛋氨酸在肿瘤中高蓄积的主要原因。
