Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: "Mitochondrial concept of leukemogenesis: key role of oxygen-peroxide effects | Theoretical Biology and Medical Modelling BioMed Central Open Access Mitochondrial concept of leukemogenesis key role of oxygen-peroxide effects Boris N Lyu Sanzhar B Ismailov Bolat Ismailov and Marina B Lyu Address Scientific Center for Anti-Infectious Drugs Almaty Kazakhstan Email Boris N Lyu - mlyu@ Sanzhar B Ismailov - sanzhar73@ Bolat Ismailov-sanzhar73@ Marina B Lyu - mlyu@ Corresponding author Published II November 2008 Received 2 October 2008 T _J .J. -mno I lozinn r T Accepted 11 November 2008 Theoretical Biology and Medical Modelling 2008 5 23 doi 1742-4682-5-23 This article is available from http content 5 1 23 2008 Lyu et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background and hypothesis The high sensitivity of hematopoietic cells especially stem cells to radiation and to prooxidative and other leukemogenic agents is related to certain of their morphological and metabolic features. It is attributable to the low minimal number of active mitochondria and the consequently slow utilization of O2 entering the cell. This results in an increased intracellular partial pressure of O2 pO2 and increased levels of reactive oxygen ROS and nitrogen RNS species and a A PO - AO imbalance between the pro-oxidative PO and antioxidative AO constituents. Proposed mechanism Because excessive O2 is toxic we suggest that hematopoietic cells exist in a kind of unstable dynamic balance. This suggestion is based on the idea that mitochondria not only consume O2 in the process of ATP production but also constitute the main anti-oxygenic stage in the cell s protective antioxidative system. Variations in the mitochondrial base capacity quantity .
