http://www.authorstream.com/Presentation/Pravez-9296-genetic-recombina

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Death by injury Cells that are damaged by injury, such as by mechanical damage exposure to toxic chemicals undergo a characteristic series of changes: They (and their organelles like mitochondria) swell (because the ability of the plasma membrane to control the passage of ions and water is disrupted). The cell contents leak out, leading to inflammation of surrounding tissues. Death by suicide Cells that are induced to commit suicide: shrink; develop bubble-like blebs on their surface; have the chromatin (DNA and protein) in their nucleus degraded; have their mitochondria break down with the release of cytochrome c; break into small, membrane-wrapped, fragments; release (at least in mammalian cells) ATP and UTP. These nucleotides bind to receptors on wandering phagocytic cells like macrophages and dendritic cells and attract them to the dying cells (a "find-me" signal"). The phospholipid phosphatidylserine, which is normally hidden within the plasma membrane, is exposed on the surface. This "eat me" signal is bound by other receptors on the phagocytes which then engulf the cell fragments. The phagocytic cells secrete cytokines that inhibit inflammation (e.g., IL-10 and TGF-β) The pattern of events in death by suicide is so orderly that the process is often called programmed cell death or PCD. The cellular machinery of programmed cell death turns out to be as intrinsic to the cell