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本文报告 N-甲对 P~(32)参入正常及肿瘤组织(或细胞)中核酸的影响。N-甲在治疗剂量下对 P~(32)参入大鼠吉田肉瘤(腹水及实体型)及小鼠艾氏癌腹水型的肿瘤细胞(或组织)核酸有明显抑制作用,且以对参入 DNA 的影响最强。N-甲对 P~(32)参入小鼠艾氏癌实体型肿瘤组织核酸无影响;在小剂量下对 P~(32)参入小鼠网织细胞肉瘤组织核酸亦无明显影响。N-甲对 P~(32)参入正常及肿瘤动物脾脏核酸有明显抑制作用。N-甲与溶肉瘤素对 P~(32)参入正常及肿瘤组织核酸的影响类似,但在等毒性剂量下其作用较溶肉瘤素稍弱。
This article reports the effect of N-methyl on the incorporation of P ~ (32) into normal and tumor tissues (or cells). N-A at the therapeutic doses of P ~ (32) into the Yoshida sarcoma (ascites and solid type) and mouse Ehrlich ascites tumor cells (or tissue) nucleic acid significantly inhibited, and to participate in the DNA The strongest impact. N-A had no effect on the incorporation of P ~ (32) into the nucleic acid of mouse Ehrlich carcinoma solid tumors, and had no significant effect on the incorporation of P ~ (32) into the reticulocyte sarcoma of mice in low dose. N-methyl P ~ (32) into the normal and tumor animal spleen nucleic acid was significantly inhibited. The effect of N-methionine and lysostautin on P ~ (32) incorporation into normal and tumor tissues was similar, but its effect was slightly weaker than that of lysogenic sarcoma at equal dose.