Calcium and cell death

Fern R. 1998. Intracellular calcium and cell death during ischemia in neonatal rat white matter astrocytes in situ. J Neurosci 18 7232-7243. 

Decreased cerebral blood flow, resulting from acute arterial occlusion, reduces oxygen and glucose delivery to brain tissue with subsequent lactic acid production, blood-brain barrier breakdown, inflammation, sodium and calcium pump dysfunction, glutamate release, intracellular calcium influx, free-radical generation, and finally membrane and nucleic acid breakdown and cell death. The degree of cerebral blood flow reduction following arterial occlusion is not uniform. Tissue at the... 

Adults require 1-2 mg of copper per day, and eliminate excess copper in bile and feces. Most plasma copper is present in ceruloplasmin. In Wilson s disease, the diminished availability of ceruloplasmin interferes with the function of enzymes that rely on ceruloplasmin as a copper donor (e.g. cytochrome oxidase, tyrosinase and superoxide dismutase). In addition, loss of copper-binding capacity in the serum leads to copper deposition in liver, brain and other organs, resulting in tissue damage. The mechanisms of toxicity are not fully understood, but may involve the formation of hydroxyl radicals via the Fenton reaction, which, in turn initiates a cascade of cellular cytotoxic events, including mitochondrial dysfunction, lipid peroxidation, disruption of calcium ion homeostasis, and cell death. 

In contrast to the reports by Wang et al. (1997) and Grant et al. (1994), (see page 28) it was also reported that H-7 and staurosporine blocked apoptosis following induction by ara-C in HL-60 cells (Kharbanda, et al, 1991). The calcium ionophore A23187 induced apoptosis in immature mouse thymocytes. H-7 inhibited the DNA fragmentation and cell death (Kizaki et al.. 

Trump BF, Berezesky IK. Calcium mediated cell injury and cell death. FASEB J 1995 9 219-228. 

The expression of genes involved in cell proliferation and cell death is regulated by nuclear transcriptional factors. NFAT (Nuclear Factor of Activated T cells) proteins are a family of Ca2+-dependent transcription factors (Crabtree, 2001), whose nuclear translocation and transcriptional activity is regulated by Ca2+/calmodulin-dependent protein phosphatase, calcineurin (Crabtree, 2001). Thus, NFAT proteins can potentially be activated by diverse stimuli that lead to increased intracellular calcium levels. The NF-kB (nuclear factor kappa B) family... 

Hanson C.J., Bootman M.D., and Roderick H.L. 2004 Cell signalling IP3 receptors channel calcium into cell death. Curr Biol 14, R933-935. 

Orrenius S., and Nicotera P. 1994 The calcium ion and cell death. J Neural Transm Suppl 43, 1-11. 

Waring P. 2005 Redox active calcium ion channels and cell death. Arch Biochem Biophys 434, 33—42. 

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