Serum Activity of Proteolytic Enzyme Trypsin in Rats under Conditions of Water and Food Deprivation.

Trypsin is mainly regarded as a digestive enzyme, but there is evidence that activation of protease-activated receptor-2 (PAR-2) leads to behavioral changes. There are no data on trypsin activity in the serum of animals under conditions of thirst and starvation in the available literature. In our experiments, water deprivation led to a significant (p⩽0.05) increase in trypsin activity in rats, and food deprivation led to its decrease in comparison with controls (free access to water and food). After deprived rats received water and food, a decrease in trypsin activity was observed in both experimental groups. Changes in trypsin activity under conditions of water or food deprivation and after satiation were accompanied by shifts in some biochemical parameters of the bloods. Under conditions of metabolic stress (starvation and thirst), opposite changes in trypsin activity seem to indicate its participation in the mechanisms of adequate restructuring of metabolism and maintenance of vital processes in the body.

Interphase chromosome locus displacement induced by low-doses of radiation.

The most important stage in the making of mutations is a reparation of different DNA damage, including the more deleterious double-strand DNA breaks (DSB). The first stage of adaptive response--fundamental antimutagenic cell reaction, purposeful to reparation for induced DSB repair--is investigated in present work. Non-radioactive in situ hybridization of biotin-labeled DNA probe was used to mark chromosome 1 pericentromeric regions (PR) in G0 human lymphocytes. It was shown that under 3-10 cGy (X-radiation, 160 kV) PR become displaced from a nucleus periphery to inner territory of a nucleus. The moving process realizes during several hours after an irradiation. As far as some non-specific gene repressors are co-localized with chromosome centromeric regions it is possible hypothesizes that the displacement cause changing expression of some genes. It is possible to propose that an absence of radiation induced chromosome locus displacement may be one of causes DSB repair disturbance. This hypothesis was tested by the model. It is assumed that one consequence of the underlying defect may be inappropriate involvement of cell's recombination machinery in the repair of DSB. We studied lymphocytes of patients with hereditary BRCA2 mutation. It is thought that this gene takes part in DSB repair. The significant differences of the PR moving between control samples and the cases were revealed under 10 cGy. Similar results were observed on lymphocytes of patients with Fanconi syndrome. Thus, abnormal moving of interphase nucleus chromosomes conditioned by low-dose irradiation may suggest on imperfect machinery of DSB repair, i.e. genetic risk. We realize that further investigations are needed for definitive conclusion.