The irradiation was used in order that to create a defective structure evenly in all volume of thin specimen. Then we had observed the time-dependent behaviour of internal friction. Dependence internal friction from the irradiation dose (Q⁻¹(D)) is shown on Figure 1. It’s can to divide on three stages: I: first stage where the internal friction essentially not changed with an increase of the radiation absorbed dose (D) from 10 to 10³ rad; II: second stage where the internal friction reached maximum with an increase of the D from 10³ to 5 × 10⁵ rad; IIIthird stage where the internal friction dropped down at D = 10⁶ rad and further it is slowly rising with an increase of the D from 10⁶ to 10⁹ rad.

First value of Q⁻¹ (see Figure 1) depends from dislocation density that initial specimen contains. The more initial dislocation density, the more value Q⁻¹.

Dependence the internal friction from of the radiation absorbed dose Q⁻¹(D) (shown on Figure 1) and time dependence of internal friction Q⁻¹(t) (shown on Figure 2) were observed in the specimens that have density of dislocations ρ ≥ 10³ cm⁻².

Q⁻¹(D) and Q⁻¹(t) dependences didn’t observed in the specimens if they preliminary anneal and then irradiate.

Dependence Q⁻¹(D) obtained as result of irradiate (see Figure 1) correspond to such process of deformation strengthening that observed in the silicon at the temperature around 750˚C [11,12].

We suppose that the generation of the deformation strengthening in the silicon at temperature around 750˚C and a similar process at room temperature in the irradiated specimen of the silicon are connected with a mechanism of formation of the dislocation loops. This dependence Q⁻¹(D) demonstrate that there are three stage of the deformation strengthening in the silicon with an increase of the radiation absorbed dose. As known the internal friction Q⁻¹ is very sensitive to the little changes of the location of the pinning point of dislocations and it is the measure of strengthening of specimens [1,4,5]. Seemingly, anew arising dislocations bring in the dependence Q⁻¹(D) the basic contribution. For example the radiation defects didn’t exert important influence on the Q⁻¹ at the first stage of irradiation (until 10³ rad) but they make a flat slope of the value of internal friction at the dependence (D) that connected with a speed of formation of dislocation loops. We suppose that growth of quantity of unsteady dislocations in the interval of doses from 10³ to 5 × 10⁵ to facilitate progress a new dislocation loops which found up the dislocation band structure (see Figure 1, II: second stage). Whereas size of loops particularly not depends from dose of radiation [13], the second stage II of the curve Q⁻¹(D) (see Figure 1) demonstrate the generation of dislocation cell structure and as result the irradiated specimen have the radiation strengthening. Dose of radiation 5 × 10⁵ rad generate the critical density of dislocation loops that create favourable conditions for forming free from defects channels [2,3] and thereby bring to sequence transition from dislocation structures to annihilation structures. Whereas the radiation doses modify the density of loops in accordance with law [2]: ρ ∞ Dⁿ, where (n = 1/2 – 2/3). The parabolic dependence Q⁻¹(D) at I and II stages of radiation strengthening demonstrate that in this interval of dose: Q⁻¹ ∞ ρ^2/3.

However the behavior of radiation strengthening corresponds to similarly process in the single crystal of metal at III stage.

Decreasing of the value of the internal friction is shown in Figure 1 at the radiation doses over 5 × 10⁵ rad as result of the strengthening of the specimen. Such drop of the value Q⁻¹ is connected with an increase quantity loops that have density ρ ~ 10⁹ - 10¹⁰ cm⁻² [2,14] at dose over 5 × 10⁵ rad.

The plastic deformation of irradiated crystals has a feature that connected not only with a strengthening influence of radiation defects but and with an unstable nature of behavior of plastic deformation [2].

As known, the energy of dislocation have approximately value ~ 10 × 10⁻¹⁹ joule (or around 6 eV) at the distance between atoms along of the dislocation line (~2.5 Å). For single crystal silicon the amount of energy of such dislocation is 19 eV [12]. There is a strong probability that such high energy will increase the annihilation of the dislocations. Also, it has been reported [2], the generation of cell structure is connected with an action of a few systems of glides at second and third stage of deformation strengthening during the process of plastic deformation.

Two competitive process are developing at the interval of doses over 5 × 10⁵ rad: on the one hand with generation of dislocation cell structure, on the other hand the annihilation of dislocation loops that create boundaries of extensive formations (channels without dislocation) [2].

Though both of the processes are developing at the irradiation but their equilibrium state depend from dose of radiation and temperature.

Probably process of annihilation of dislocation loops prevail over process of formation of cell structure and internal friction Q⁻¹ has moderate growth into interval of dose from 10⁶ to 10⁹ rad.

When the radiation absorbed dose of the initial specimen had a value in the range of doses from 10⁶ rad up to 10⁹ rad, the internal friction increased till its maximum value during 1.5 - 2 hours after stopping of the irradiation (see Figure 2).

It was as result probably of the intensive progress of process of annihilation of dislocation loops, which has

cooperative nature of the evolution.

It should be noted that value of internal friction was changing through 7 - 8 hours and even through twentyfour hours from starting point of observation.

The process of annihilation has the further development in a random way as result of a sequential activation of dislocation kinks within a boundary microstructure by fields of internal tensions and process of annihilation steadily tend to its equilibrium value. Such long process of annihilation is connected probably with more late a diffusion of delayed defects to dislocations and to boundaries of cells.