Phospholipid Metabolism in Apoptosis by Volker Lehmann, Vladimir Shatrov (auth.), Peter J. Quinn,

By Volker Lehmann, Vladimir Shatrov (auth.), Peter J. Quinn, Valerian E. Kagan (eds.)

The previous few years have witnessed an explosion of either curiosity and data approximately apoptosis, the method in which a cellphone actively commits suicide. The variety of guides at the subject has elevated from not anything within the early Eighties to greater than 10,000 papers every year this present day. it really is now good well-known that apoptosis is key in lots of features of ordinary improvement and is needed for holding tissue homeostasis. the concept existence calls for loss of life turns out a bit paradoxical, yet telephone suicide is vital for an animal to outlive. for instance, with no selective destruction of “non-self” T cells, an animal may lack immunity. equally, significant neural connections within the mind are whittled from a mass of cells. additional, developmental phone home improvement in the course of tissue maturation contains programmed mobile loss of life because the significant mechanism for practical and structural secure transition of undifferentiated cells to extra really good opposite numbers. Apoptosis study, with roots in biochemistry, developmental and telephone biology, genetics, and immunology, embraces this long-ignored usual legislations. Failure to correctly keep watch over apoptosis could have catastrophic outcomes. melanoma and lots of ailments (AIDS, Alzheimer’s illness, Parkinson’s sickness, center assault, stroke, and so on. ) are proposal to come up from deregulation of apoptosis. As apoptosis emerges as a key organic regulatory mechanism, it has turn into more durable and tougher to maintain with new advancements during this field.

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We concluded, therefore, that the enhanced peroxidation reactions are responsible for geranylgeranoic acid-induced apoptosis. In the literature, most drug-induced apoptosis is well known to require intracellular hyper-production of reactive oxygen species and several antioxidants inhibit apoptotic cell death. While it is clear that peroxidation reactions induce apoptosis, the precise molecular mechanism of how reactive oxygen species convey death-signals is unknown. 1 Peroxidation of cardiolipin We directed our initial attention to the mitochondrion-specific phospholipid, cardiolipin because it is particularly rich in polyunsaturated fatty acids which are vulnerable to oxidative attack.

Spin-labelled analogs have also been used (Seigneuret and Deveaux, 1984). , 1995). The major disadvantage of these analogs is that the reporter group introduces significant changes in lipid conformation and properties and the effect this may have on behaviour is problematic. , 44 Peter J. Quinn 1986). Methods of assessing transmembrane movement of sphingolipids have been reviewed by Sillence et al. (2000). Measurement of transmembrane movement of phospholipids using florescent or other probe methods requires demonstration that incorporation of the phospholipid analogs occurs by a monomeric transfer from an exogenous resevoir into the outer leaflet of the plasma membrane rather than a fusion of bilayer vectors containing the probes with the plasma membrane.

FEBS Lett. , 1993, Mitochondrial cardiolipin in diverse eukaryotes. Comparison of biosynthetic reactions and molecular acyl species. Eur. J. Biochem. , 2000, Protection of mitochondrial integrity from oxidative stress by the triaminopyridine derivative flupirtine. , 1997, Rapid loss in the mitochondrial membrane potential during geranygeranoic acid-induced apoptosis. Biochem. Biophys. Res. Commun. , 1999, Loss of molecular interaction between cytochrome c and cardiolipin due to lipid peroxidation.

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