Molecular factors regulating mitochondrial biogenic response following septic infection

This paper had been presented for promotion at the University of Khartoum. To get the full text please contact the other at abumalaz2002@gmail.comIt was well-established that sepsis affects the mitochondrial functions in mammalian cells resulting in multiple organ failure, This study aimed at identify some molecular factors regulating the mitochondria! biogenesis during .E coil sepsis_ The changes in cellular mediators following sepsis and the underlying effects on mitochondria] biogenesis in wild type and inducible nitric oxide knockout (INOST) mice were investigated. Both mRNA and protein expressions were determined. The results obtained indicated obvious adverse effects on cells leading to mitochondria] damage, loss of function and over-expression of cytoplasm signaling molecules, The original results emerged is the recognition of nitric oxide that sepecilically generated by the inducible nitric oxide synthase ON OS) is responsible for the recruiting of the nuclear-encoded mitochondrial proteins namely mitochondrial transcription factor A (Tiara) and superoxide dismutase (SOD2) from the cytoplasm to the mitochondria_ iNOS was also proved as a potent factor in increasing the mitoch.ondrial DNA (mt-DNA) expression namely the cytochronie B gene. Generally, an increase in the nuclear and mitochondrial transcripts and proteins expression in murine liver cells was detected following induced sepsis_ it is therefore, suggested that the clinical usefulness derived from this study, is to maintain a standard levels for the iNOS in the body during sepsis which will help to restore the mitochondrial functions and recover the apoptotic effects expected in the cells