Apoptosis is the biologically regulated suicide program used by irreparably damaged, genetically modified or obsolete cells for their safe self-removal, the malfunctioning of which has severe implications for human health.

The factors involved in the execution of this program are well understood but the cellular signalling events that trigger execution are not yet fully resolved. Scientists in the School of Chemistry at UEA have used unique equipment which allows simultaneous optical and electrochemical measurements to be carried out in large magnetic fields to show that molecular oxygen either in place of, or in addition to reactive oxygen species, may initiate the cell death process.Their suggestion arises from studies of the interaction between cytochrome c, a small protein known for many years to be involved in electron transport, and the lipid cardiolipin. Both molecules are present in the mitochondrial compartment of eukaryotic cells. Cytochrome c and cardiolipin are usually separated but on coming together they form a complex capable of the selective oxidation of cardiolipin which then acts as a trigger for the leakage of molecules out of the mitochondria and the onset of cell death. This complex will encounter both molecular oxygen and reactive oxygen species leading to two possible routes to cardiolipin oxidation as described in the Journal of the American Chemical Society, vol. 133 (2011), pages 19676-19679. This research was led by Prof. Julea Butt and Dr Myles Cheesman from the Centre for Molecular and Structural Biochemistry, School of Chemistry and School of Biological Sciences at the University of East Anglia.