Uryvaeva I V
Tsitologiia. 1979 Dec;21(12):1427-37.
The ontogenetic polyploidization of hepatocytes is regarded, within which normal mitoses are changed to polyploidizing mitoses, and diploid hepatocytes transform into polyploid mono- and binuclear cells. A new hypothesis is put forward of the biological significance of the liver cell polyploidy. The hypothesis takes into account a high level of spontaneous chromosomal aberrations in mitotic hepatocytes. The chromosome structural changes interfere with mitosis resulting in the chromosomal imbalance. Polyploidy bestows for hepatocytes a tolerance towards a chromosomal imbalance. Some implications of the hypothesis are discussed: unbalanced genome of hepatocytes after the treatment with mutagens and mitotic stimulators; the reasons of liver cell polyploidy differences in mammalian species; mechanisms of radioresistance of hepatocytes. Chromosomal imbalance of polyploid hepatocytes is assumed to be the basis for wome chronic liver diseases in man.
肝细胞的个体发育多倍体化被认为是正常有丝分裂转变为多倍体有丝分裂,二倍体肝细胞转变为多倍体单核和双核细胞。提出了关于肝细胞多倍体生物学意义的新假说。该假说考虑到有丝分裂肝细胞中自发染色体畸变的高水平。染色体结构变化干扰有丝分裂,导致染色体不平衡。多倍体赋予肝细胞对染色体不平衡的耐受性。讨论了该假说的一些影响:用诱变剂和有丝分裂刺激剂处理后肝细胞基因组的不平衡;哺乳动物物种中肝细胞多倍体差异的原因;肝细胞抗辐射机制。多倍体肝细胞的染色体不平衡被认为是人类某些慢性肝病的基础。