Silymarin has been so far widely studied as a hepatoprotective agent stabilizing cell membranes. As his effect is caused by alerted lipid composition of membranes, in addition to inhabitation of lipid peroxidation, the data related to the metabolism of liver lipids and plasma lipoprotein remained summarized in order to assess, whether silymarin deserves to be studied as   hypocholesteolaemic drug. Present study highlights the anticlastogenic activity of the drug silymarin. Four doses of the drug i.e., 2, 4, 8, and 20 mg/ kg. b. wt. were administrated to  mice.  Five genotoxic bioassays were performed: estimation of cell proliferation, analysis of chromosomal abnormalities in mice bone marrow cells,in vivo induction of sister chromatid exchanges (SCEs) in mice, micronucleus test and analysis of primary spermatocytes. Cyclophosphamide (Indoxan) was used as a positive control. Present data prove that the drug silymarin was capable of causing significant increases in cell proliferation (estimated as mitotic index) of mice bone marrow cells; decreasing in total aberrant metaphases as well as SCEs in vivo. Micronucleated polychromatic erythrocytes and aberrant diakinesis were significantly decreased; giving an evidence that silymarin has a strong anticlastogenic activity upon mice genome in somatic as well as germinal cells.