State 1-State 2 transitions in the cyanobacterium Synechococcus 6301 are controlled by the redox state of electron carriers between Photosystems I and II

1990 ◽  
Vol 23 (3) ◽  
pp. 297-311 ◽  
Author(s):  
Conrad W. Mullineaux ◽  
John F. Allen
Keyword(s):  
Redox State ◽  
Photosystems I And Ii ◽  
Synechococcus 6301 ◽  
Electron Carriers ◽  
State 1

scholarly journals Effects of photobiomodulation on the redox state of healthy and cancer cells

2020 ◽  
Author(s):  
Clara Maria Gonçalves de Faria ◽  
Heloisa Ciol ◽  
Vanderlei Salvador Bagnato ◽  
Sebastião Pratavieira
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Redox State ◽  
Mitochondrial Metabolism ◽  
Atp Production ◽  
Distinct Cell ◽  
Irradiation Cell ◽  
Oxidase Enzyme ◽  
Oral Cancer Cells ◽  
Electron Carriers

Photobiomodulation (PBM) uses light to stimulate cells. The molecular basis of the effects of PBM is being unveiled, but it is stated that the cytochrome-c oxidase enzyme in mitochondria, a photon acceptor of PBM, contributes to an increase in ATP production and modulates the reduction and oxidation of electron carriers NADH and FAD. As it can stimulate cells, PBM is not used on tumors. Thus, it is interesting to investigate if its effects correlate to mitochondrial metabolism and if so, how it could be linked to the optical redox ratio (ORR). To that end, fibroblasts and oral cancer cells were irradiated with a light source of 780 nm and a total dose of 5 J/cm2, and imaged by optical microscopy. PBM down-regulated the SCC-25 ORR by 10%. Furthermore, PBM led to an increase in ROS and ATP production in cancer cells after 4 h, while fibroblasts only had a modest ATP increase 6 h after irradiation. Cell lines did not show distinct cell cycle profiles, as both had an increase in G2/M cells. This study indicates that PBM shifts the redox state of oral cancer cells towards glycolysis and affects normal and tumor cells through distinct pathways. To our knowledge, this is the first study that investigated the effects of PBM on mitochondrial metabolism from the initiation of the cascade to DNA replication. This is an essential step in the investigation of the mechanism of action of PBM in an effort to avoid misinterpretations of a variety of combined protocols.

scholarly journals Photoacoustic Study of Changes in the Energy Storage of Photosystems I and II during State 1-State 2 Transitions

1991 ◽  
Vol 97 (1) ◽  
pp. 330-334 ◽  
Author(s):  
Konka Veeranjaneyulu ◽  
Marc Charland ◽  
Denis Charlebois ◽  
Roger M. Leblanc
Keyword(s):  
Energy Storage ◽  
Photosystems I And Ii ◽  
State 1

Dynamics of NAD-metabolism: everything but constant

2015 ◽  
Vol 43 (6) ◽  
pp. 1127-1132 ◽  
Author(s):  
Christiane A. Opitz ◽  
Ines Heiland
Keyword(s):  
Redox State ◽  
Complex Dynamic ◽  
Metabolic Pathway Analysis ◽  
Dynamic Changes ◽  
Nad Metabolism ◽  
Phosphorylated Form ◽  
Cyclic Adp Ribose ◽  
Messenger Molecules ◽  
Concentration Changes ◽  
Electron Carriers

NAD, as well as its phosphorylated form, NADP, are best known as electron carriers and co-substrates of various redox reactions. As such they participate in approximately one quarter of all reactions listed in the reaction database KEGG. In metabolic pathway analysis, the total amount of NAD is usually assumed to be constant. That means that changes in the redox state might be considered, but concentration changes of the NAD moiety are usually neglected. However, a growing number of NAD-consuming reactions have been identified, showing that this assumption does not hold true in general. NAD-consuming reactions are common characteristics of NAD+-dependent signalling pathways and include mono- and poly-ADP-ribosylation of proteins, NAD+-dependent deacetylation by sirtuins and the formation of messenger molecules such as cyclic ADP-ribose (cADPR) and nicotinic acid (NA)-ADP (NAADP). NAD-consuming reactions are thus involved in major signalling and gene regulation pathways such as DNA-repair or regulation of enzymes central in metabolism. All known NAD+-dependent signalling processes include the release of nicotinamide (Nam). Thus cellular NAD pools need to be constantly replenished, mostly by recycling Nam to NAD+. This process is, among others, regulated by the circadian clock, causing complex dynamic changes in NAD concentration. As disturbances in NAD homoeostasis are associated with a large number of diseases ranging from cancer to diabetes, it is important to better understand the dynamics of NAD metabolism to develop efficient pharmacological invention strategies to target this pathway.

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