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10.4067/s0716-97602002000200012

http://scihub22266oqcxt.onion/10.4067/s0716-97602002000200012
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12415738!ä!12415738

suck abstract from ncbi


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pmid12415738      Biol+Res 2002 ; 35 (2): 209-14
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  • Ion movements in cell death: from protection to execution #MMPMID12415738
  • Barros LF; Castro J; Bittner CX
  • Biol Res 2002[]; 35 (2): 209-14 PMID12415738show ga
  • Cell death is preceded by severe disruption of inorganic ion homeostasis. Seconds to minutes after an injury, calcium, protons, sodium, potassium and chloride are exchanged between the cell and its environment. Simultaneously, ions are shifted between membrane compartments inside the cell, whereby mitochondria and endoplasmic reticulum play a crucial role. Depending of the type and severity of injury, two mutually exclusive metastable states can be reached, which predict the final outcome. Cells characterized by large increases in cytosolic [Ca2+], [Na+] and [Mg2+] swell and die by necrosis; alternatively, cells characterized by high [H+] and low [K+], with normal [Na+] and normal to moderate [Ca2+] increases die by apoptosis. The levels of these ions represent central determinants in signaling events leading to cell death. Their movements are explained mechanistically by specific modulation of membrane transport proteins including channels, pumps and carriers.
  • |Animals[MESH]
  • |Calcium/metabolism[MESH]
  • |Cell Death/*physiology[MESH]
  • |Humans[MESH]
  • |Ion Channels/*metabolism/physiology[MESH]
  • |Ion Transport[MESH]
  • |Magnesium/metabolism[MESH]
  • |Potassium/metabolism[MESH]
  • |Proto-Oncogene Proteins c-bcl-2/metabolism[MESH]


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