**6. Abbreviations:**

198 Apoptosis and Medicine

treatment with colchicines.

**5. Conclusions** 

Drug concentrations – 0.1 µМ for *К562/2-DQO* cells, 0.001 µМ for *K562* cells, 0.001 µМ for *К562/4-NQO* cells. X-axis: cytotoxic index ratio of effector cells with treated cell lines to control cell lines without treatment, % (cytotoxic index

**Figure 13.** The *К562* cell line sensitivity to cytotoxic lysis by human peripheral blood white cells after

Thus, treatment of tumor cells with chemical compounds may simultaneously induce cell apoptosis and modulate their susceptibility to the cytotoxic lysis of blood leukocytes. In these treatment conditions the expression and/or activity of intracellular apoptosis regulators, namely caspases, changes, and this change may tell on the effectiveness of the leukocyte lysis effect, which is based on induction of target cell apoptosis. It is essential that the susceptibility of tumor cells to the lysis of leukocytes containing NK cells changed in those variants where the expression and activity of caspases-3, -6, -9 were promoted (cultures treated with *4-NQO, 2-NSQO*, and *4-NSQO*)*.* On the other hand, the equivocal nature of the results proves that the process involves extra intracellular factors. One can therefore assume that similar patterns of the response of tumor cells to treatment with chemical compounds can occur *in vivo* in humans and animals treated with the anticancer drugs stimulating cell apoptosis. This effect can persist when nontoxic or low-toxicity doses are applied, and caspases, being a cell's major apoptosis inducing factor, can be viewed as

Over 40 years have passed since the first publication devoted to apoptosis. Since then, the problem of apoptosis regulation mechanisms has become central to pharmacology, genetics,

value of control cells is 100 %). Effector cells to target cells ratio is 50:1. Incubation time – 48 h; \* p<0.05.

potential targets for pharmacologically active agents.

Quinoline – *Q*, 2-methylquinoline – *2-MeQ*, quinoline-1-oxide – *QO*, 2-methylquinoline-1 oxide – *2-MeQO*, 4-nitroquinoline-1-oxide – *4-NQO,* 2-methyl-4-nitroquinoline-1-oxide – *2-Me-4-NQO*, 2-(4'-dimethylaminostyryl)quinoline-1-oxide *– 2-DQO,* 4-(4'-dimethylaminostyryl) quinoline-1-oxide – *4-DQO,* 2-(4'-nitrostyryl)quinoline-1-oxide – *2-NSQO,* 4-(4'-nitrostyryl) quinoline-1-oxide – *4-NSQO*, and 4-(4' -dimethylaminostyryl)pyridine-1-oxide – *4-DPyO*; death effector domain – DED, caspase recruitment domain – CARD, death inducing domain – DID, р53-induced protein with a death domain – PIDD, death-inducing signalling complex – DISC, DNA fragmentation factor – DFF, caspase-activated DNase – CAD, permeability transition роrе – РТР, apoptosis inducing factor – AIF, tumor necrosis factor receptor – TNFR, death domain – DD, death receptor – DR, Fas-associated DD-protein – FADD, TNFR1-associated DD-protein – TRADD.
