This monograph presents the results of comprehensive studies performed in in vivo experiments on animals with CCl4 (fatty hepatosis) and heliotrine (protein dystrophy) acute toxic hepatitis. For the first time, it was found that high inhibition of calmodulin-dependent eNOS activity and stimulation of calmodulin-independent iNOS, further initiates NO formation and increases ONO2-. In-depth study of the relationship between oxidative stress, nitrergic system and apoptosis development factors can clarify the biochemical basis of the accelerated collagen synthesis, develop early diagnostic criteria, create an algorithm for differential diagnosis of liver lesions of various genesis. Results of researches allow to develop the tactics of management of such patients and to improve pharmacotherapy, that essentially reduces progression of fibrosis and improves quality of life of patients. The study of eNOS gene polymorphism in patients with liver pathology of different genesis and elucidation of specific genetic markers allow to predict cirrhotic outcome of liver lesions.