The aim of this paper is to elucidate the role of oxidative and nitrosative stress as well as the tryptophan catabolites pathway in the development of depression and the mechanism of action of antidepressant drugs, based on the available literature. According to the World Health Organization (WHO), an estimated 350 million people worldwide suffer from depression. The pathogenesis of depressive disorders has not been fully explained yet and several causes of this disease have been suggested. There is evidence for the involvement of several interconnected biochemical pathways, including oxidative and nitrosative stress as well as the tryptophan catabolites pathway. Studies to date indicate that patients with depression have lower levels of enzymatic and non-enzymatic elements of an antioxidant response and, at the same time, they display an increased amount of oxidative stress markers, when compared to healthy individuals. The development of depression is also associated with excessive activity of nitric oxide synthase. Furthermore, decreased levels of tryptophan and increased levels of its harmful catabolites, i.e. kynurenine and quinolinic acid, may lead to progression of the disease. Changes in these biochemical pathways can be used as risk factors for the development of depression and, in the future, they could be utilized as diagnostic biomarkers. Moreover, regulation of biochemical processes may contribute to the development of a new, effective and personalized antidepressant therapy.