Platinum complexes such as cisplatin [cis-diamminedichloridoplatinum(II)] and its analogues are widely used as very effective chemotherapeutic agents. The cytostatic action of these metal complexes is connected with their binding to the DNA molecule causing structural changes that significantly affect the life of the tumor cells. However, the use of these drugs in clinical practice is limited by a number of side effects and their effectiveness in cancer therapy is limited by the acquired resistance [1, 2]. These limitations are impetus for the development of new platinum compounds with lower toxicity which can be activated by light selectively in the target cancer cells .The Pt(IV) diazido complex trans,trans,trans-[Pt(N3)2(OH)2(pyridine)2] (1) is unreactive in the dark but is cytotoxic when photoactivated by UVA and visible light. We have shown that 1 when photoactivated accumulates in tumor cells and binds strongly to nuclear DNA under conditions in which it is toxic to tumor cells. The nature of the DNA adducts, including conformational alterations, induced by photoactivated 1 are distinctly different from those produced in DNA by conventional cisplatin or transplatin. In addition, the observation that major DNA adducts of photoactivated 1 are able to efficiently stall RNA polymerase II more efficiently than cisplatin suggests that transcription inhibition may contribute to the cytotoxicity levels observed for photoactivated 1. Hence, DNA adducts of 1 could trigger a number of downstream cellular effects different from those triggered in cancer cells by DNA adducts of cisplatin. This might lead to the therapeutic effects that could radically improve chemotherapy by platinum complexes. The findings of the present work help to explain the different cytotoxic effects of photoactivated 1 and conventional cisplatin and thereby provide new insights into mechanisms associated with the antitumor effects of platinum complexes photoactivated by UVA and visible light.