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Presumably Common Trigger Mechanism of Action of Diametrically Different Carcinogens on Target Cells

机译:推测完全相同的致癌物对靶细胞的作用的共同触发机制

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A large number of carcinogens and the wide spectrum of their actions may indicate their ability to trigger a common, general mechanism inside the normal biological program of somatic cells, which can lead to the development of the carcinogenic transformation of the normal cell. Numerous carcinogenic substances and factors of different natures probably can signify that these carcinogens must start up some common mechanism of normal cells transition into transformed states. Influence of physical, chemical, and biological carcinogenic agents on cells probably are adequate. By our opinion the common mechanism of action of diametrically different carcinogens on target-cells is the destruction of the plasmatic membrane. After influence of different carcinogens, cells’ fusion originates as a result of cytoplasmic membranes perforations (or modifications), i.e. formation in plasma membranes pores, what induces alteration of summary superficial charge of cells’ surface. Because of these, cells acquire ability to approach each other (adhesion), what in many cases may be a premise for fusion process. Thus, the initial target of carcinogenic agents is cells’ plasma membrane, but not the genetic apparatus of cells.
机译:大量的致癌物及其作用的广泛范围可能表明它们有能力触发体细胞正常生物学程序内部的通用机制,从而导致正常细胞发生致癌转化。许多致癌物质和不同性质的因子可能表明这些致癌物必须启动正常细胞转变为转化状态的某些共同机制。物理,化学和生物致癌剂对细胞的影响可能是足够的。我们认为,完全不同的致癌物作用于靶细胞的共同机制是质膜的破坏。在受到不同致癌物的影响后,细胞融合是由于细胞质膜穿孔(或修饰),即在质膜孔中形成,导致细胞表面的表面总电荷发生变化而引起的。由于这些原因,细胞获得了彼此接近(粘附)的能力,这在许多情况下可能是融合过程的前提。因此,致癌剂的最初目标是细胞的质膜,而不是细胞的遗传装置。

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