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During the cell division dynamic processes take place, the origin of which are to find in the physical characteristics of cell components. The most important characteristics are the electrical charge and the energy of the moving base components in a viscous cytoplasm. During the emergence of the new hydrogen bonds takes place a competition of the complementary base components which are electrostatically attracted by the codogen matrix. Thus, the base components will be accelerated more and more in the course of replication, and the resulting binding energies become always larger in a monotonous sequence. We call this process “base rivalry”. It is shown that the strength of these new bindings depends on three factors: First it is dependent on the length of a monotonous sequence, second it is dependent on the viscosity of the cytoplasm, and third it is dependent on the replication speed. In the study in detail is stated, how it affects the effectiveness of the DNA repair mechanism, mutation susceptibility, and thus also affects the cancer susceptibility. This is a condition where the DNA repair mechanism fails: Because of the base rivalry, in a monotonous base sequence there is (for a short time) a high binding energy between the complementary bases from a critical sequence length upwards, and the effectiveness of the repair mechanism is strongly decreased. If a tautomeric base pair is behind the end of monotonous sequence, then an extension of the monotonous sequence is provoked so that, for example, the monotonous sequence CCCT irreparably changes itself into CCCC (see section 2.2). The author describes in detail how the base rivalry affects on the evolution and on the mutation of viruses. The probability for the emergence of an irreparable mutation (caused by base rivalry) will be calculated. The result is (for a large number of individuals) a mathematical connection between temperature and the length of monotonous DNA - sequences which are lengthened by base rivalry. In the study, there are preferentially used physical and statistical computations and therefore is to understand as theoretical work. For the examination of this theory, two different computations are necessary: 1. Statistical computation: It is safe to assume that an individual base component exists (for example, dGTP) having a very large fading time in the case of excitation (preferable, owing to rotation energy after it became lumpy). Such a base component is very rarely, so that it appears within a DNA-fragment either not or once at most. This is called the “elitist”. If it appears within the fragment, we can compute the probability for its appearance in a certain position during replication, namely in a monotonous sequence of this fragment. The calculation of the probability must be statistically, because the replication is a distribution on the codogen matrix. 2. Physical computation: If the elitist (accidentially) arrives at a monotonous sequence of the DNA-fragment, it will reach the end of this monotonous sequence because of its high base rivalry energy, and now we can the tunnel probability calculate for the conversion into the tautomeric form which leads to a mutated hydrogen bond at the end of monotonous sequence. This mutated hydrogen bond is irreparabel, if the fading time of the excited elitist higher is than the repair time of the DNA repair mechanism. Both probabilities have to be connected for the computation of the total probability of the irreparable mutation. The result of this connection is an interesting equation between temperature and monotonous sequence length which is irreparably lengthened, and this gives rise to the speculation that this theory as well as the resulting equation may have a certain importance for the theory of evolution, and may have an importance for the dangerous virus mutations. In the case of base rivalry within of a DNA - fragment, there is a connection between the base sequence (especially the monotonous sequence length) and the temperature at which irreparable mutations are be expected (equation [96a]. This work is a revision of the article 'Die Kalkulation irreparabler Mutationen” by the same author. Errors have been corrected in some chapters in the mathematical representation. Chapters 6 and 7 have been re-edited. Corrected excerpts from 'Tumour Physics' [25] and from 'Evolution Physics' [26] are used in this work. In the appendix [28] are supplementary remarks in order to understand the sections better. There is, too, a remark concerning the coherence between tumor development and cell - viscosity. This modified version differs from the previous one, since it (according to the latest considerations) is not realistic, the electrostatic attraction (between codogen basic components and the complementary basic components) attributable to the sum of all partial charges, but attributable to only one. The reason for this is that (in the course of attraction) not all part charges of the matrix and complements will be the same distance from each other, since they are located at different positions. This altered version has consequences in the sections 1, 2, 7, 8, and picture 7.

Bei der Replikation monotoner DNA - Sequenzen tritt theoretisch ein Vorgang auf, den wir als „Basenkonkurrenz“ bezeichnen: Da sich an jeder Replikations-Stelle mehrere Basenbausteine bewerben, aber immer nur einer benötigt wird, bewerben sich die übrig gebliebenen Bausteine an den jeweils nächsten Replikations - Positionen und erlangen wegen der fortwährenden Beschleunigung durch elektrostatische Anziehung immer größere kinetische Energien. Das führt dazu, dass an einer bestimmten Stelle der replizierenden monotonen Sequenz der eine Partner der Wasserstoffbrückenbindung ein hohes Energieniveau erreicht. Es wird berechnet, dass sich dadurch kurzzeitig eine sehr hohe Bindungsenergie zwischen den beiden Partnern der Wasserstoffbrückenbindung einstellt, wodurch der in dieser kurzen Zeitspanne wirkende DNA-Reparaturmechanismus unterdrückt wird. Die Auswirkungen der hohen Basenkonkurrenz – Energien werden berechnet (hohe Bindungsenergien der Wasserstoffbrückenbindungen, Tunnelvorgänge, irreparable Mutationen). Die Folgen dieser Erscheinung sind Tumorbildung, Alterung, Veränderung der DNA – Struktur, Beeinflussung der Evolution, worauf im Einzelnen eingegangen wird. Es zeigt sich, dass die negativen Auswirkungen der Basenkonkurrenz vorwiegend bei zu niedriger Viskosität des Zellplasmas auftreten.

Bei der Replikation monotoner DNA - Sequenzen tritt theoretisch ein Vorgang auf, den wir als „Basenkonkurrenz“ bezeichnen: Da sich an jeder Replikations-Stelle mehrere Basenbausteine bewerben, aber immer nur einer benötigt wird, bewerben sich die übrig gebliebenen Bausteine an den jeweils nächsten Replikations - Positionen und erlangen wegen der fortwährenden Beschleunigung durch elektrostatische Anziehung immer größere kinetische Energien. Das führt dazu, dass an einer bestimmten Stelle der replizierenden monotonen Sequenz der eine Partner der Wasserstoffbrückenbindung ein hohes Energieniveau erreicht. Es wird berechnet, dass sich dadurch kurzzeitig eine sehr hohe Bindungsenergie zwischen den beiden Partnern der Wasserstoffbrückenbindung einstellt, wodurch der in dieser kurzen Zeitspanne wirkende DNA-Reparaturmechanismus unterdrückt wird. Die Auswirkungen der hohen Basenkonkurrenz – Energien werden berechnet (hohe Bindungsenergien der Wasserstoffbrückenbindungen, Tunnelvorgänge, irreparable Mutationen). Die Folgen dieser Erscheinung sind Tumorbildung, Alterung, Veränderung der DNA – Struktur, Beeinflussung der Evolution, worauf im Einzelnen eingegangen wird. Es zeigt sich, dass die negativen Auswirkungen der Basenkonkurrenz vorwiegend bei zu niedriger Viskosität des Zellplasmas auftreten.

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