癌变·畸变·突变 ›› 2000, Vol. 12 ›› Issue (1): 8-011.doi: 10.3969/j.issn.1004-616x.2000.01.003

• 论著 • 上一篇    下一篇

d2筒箭毒碱对V79 细胞和小鼠骨髓细胞有丝分裂的影响

和智君,汪 旭   

  1. 云南师范大学生命科学系,云南昆明 650092
  • 收稿日期:1999-05-30 修回日期:1999-07-29 出版日期:2000-01-30 发布日期:2000-01-30

STUDY OF MITOTIC EFFECTS OF d2TUBOCURARINE IN V79 CHINESE HAMSTER CELLS AND IN MOUSE BONE MARROW CELLS

HE Zhi-jun , WAN G Xu   

  1. Department of Life Sciences, Yunnan Normal University, Kunming  650092, China
  • Received:1999-05-30 Revised:1999-07-29 Online:2000-01-30 Published:2000-01-30

摘要: 目的:探讨烟碱型乙酰胆碱受体阻断剂d2筒箭毒碱对V79细胞和小鼠骨髓细胞有丝分裂的影响。方法:在离体情况下以受试物处理中国仓鼠V79细胞,通过分析V79细胞晚末期和早G1 期细胞核与细胞质构型、双核细胞频率,探讨受试物对细胞质质裂的影响;研究同时探讨了活体情况下,该化合物对小鼠骨髓细胞的C2有丝分裂(C ———M) 效应,分析其对哺乳动物体细胞有丝分裂的影响。结果:d2筒箭毒碱能使V79细胞的晚末期—早G1 期细胞核和细胞质分裂构型发生显著变化( P < 0. 001)双核细胞的频率显著提高( P < 0. 001) 。在小鼠骨髓细胞C ———M 效应分析中,该化合物除在低剂量组导致较明显的C —有丝分裂细胞增加外( P < 0. 05) ,其他未见异常。结论:研究提示受试物可通过N 型胆碱受体阻断过程对哺乳动物细胞质裂的真实性产生影响;同时,该化合物还具有影响染色体正常分离的潜在能力。对胆碱受体功能的研究将有助于探索非整倍体产生的各种机制。

关键词: 中国仓鼠V79 细胞, d-筒箭毒碱, 有丝分裂, 非整倍体

Abstract: Purpose : The mitotic effects of d-tubocurarine in V79 cells and mouse bone marrow cells was investigated in this study. d2t ubocurarine is a antagonist to cholinergic receptors and inhibitor of nicotinic receptor. Methods : V79 Chinese hamster cells were t reated in vit ro by d2tubocurarine. The alteration of late telophaseearly G1 configuration induced by this chemical was determined by analyzing of presence or lack of a cleavage furrow in late telophase and very early G1 cells , the abnormal cytokinesis was investigated for the f requencies of binuclear cells in interphase cells. Simultaneously , we investigated the C2M effect s of d2t ubocurarine in mouse bone marrow cells. Results : The tested chemical disturbed mitotic coordination and significantly induced high frequency of binuclear cells in V79 cell line ( P < 0. 001) . There is no other distinguished abnormality in mouse bone marrow cells but significant enhance of C2M cells at low dose group. Conclusion : The result s indicated that d-tubocurarine is able to inhibit mammal mitosis by blocking the function of nicotinic receptor. The malfunction of cholinergic and nicotinic receptors may be a mechanism of aneuploid induction.

Key words: V79 hamster cell, mitosis, aneuploidy

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