Objective — to determine the morphological parameters of mitochondrial dysfunction of peripheral placental cytotrophoblast in preeclampsia of varying severity and to clarify risk factors for adverse perinatal outcomes in this complication of pregnancy. Subject and methods. The courses of pregnancy, labor, and the status of newborn infants born to 107 patients with moderate preeclampsia (Group 1), to 90 patients with severe preeclampsia (Group 2), and to 105 patients with uncomplicated pregnancy were analyzed. Organometry and plain histological and immunohistochemical examinations of 30 placentae from patients with moderate preeclampsia, 30 placentae from those with severe preeclampsia, and 30 ones from control patients were performed using goat polyclonal primary antibodies to mitochondrial transcription factor A (TFAM). Results. Perinatal pathology was diagnosed in 86.8% of the babies born to mothers with preeclampsia, which is a risk factor for adverse perinatal outcomes. The structure of neonatal morbidity in preeclamptic mothers was dominated by fetal growth restriction, perinatal CNS lesions, and congenital pneumonia. The morphological features of placentae from the patients with preeclampsia were characterized by stage II and III hypoplasia, marginal cord insertion, and mitochondrial dysfunction of the peripheral cytotrophoblast. The placentas from Group 1 patients, unlike those from the control group, displayed a decrease in the TFAM expression index (EI) from 0.41 to 0.32 arbitrary units. The minimum TFAM EI of 0.31±0.02 arbitrary units was found in the cytotrophoblast of the placental basal plate in severe preeclampsia. Thus, the neonatal outcomes were worse in Group 2 patients with severe preeclampsia than in those with moderate preeclampsia, which were due to the earlier terms of delivery and concomitant fetal growth restriction. Conclusion. The found changes in the TFAM EI can be used as an additional immunohistochemical marker for the severity of preeclampsia.