Flunarizine protects neurons from death after axotomy or NGF deprivation

Article Abstract:

While death is usually regarded as a pathological phenomenon, cell death is often a normal part of developmental and physiological processes. At certain points of development, cells that are no longer useful seem to die according to a specific program. In the development of some neurons, or nerve cells, a substance known as nerve growth factor plays a role in the intricate process of cell death and development. In an investigation of the factors which determine life and death for individual neural cells, investigators have found that the drug flunarizine helps keep neurons alive. In tissue culture, some neurons degenerate and die when deprived of nerve growth factor; this process can be inhibited by flunarizine. Furthermore, the death of neurons from physiological damage can also be inhibited by the drug. When the long axons which connect neurons to other cells are cut, the neurons often die. However, when axons from the dorsal root ganglia of rats are cut, the administration of flunarizine enhances the survival of neurons. Flunarizine is a calcium channel antagonist that is used in the treatment of vertigo, epilepsy, migraine headaches, and vascular insufficiency. There is some evidence that it protects brain cells during experimental hypoxia (deprivation of oxygen) in rats. However, it seems that the calcium channel action of the drug is not the action responsible for protecting neurons. In culture, the amounts of flunarizine necessary for protection are greater than those necessary for blocking the calcium channels. Furthermore, other drugs which block calcium channels, such as nimodipine, do not show a protective effect. The results indicate the flunarizine is capable of enhancing the survival of neurons, and that this effect is probably the result of some process inside the cell, and not merely calcium channel blocking. (Consumer Summary produced by Reliance Medical Information, Inc.)

Neurons, Nerve growth factor, Calcium channel blockers, Flunarizine

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Erythropoietin retards DNA breakdown and prevents programmed death in erythroid progenitor cells

Article Abstract:

Erythropoietin stimulates the production of red blood cells. Normally produced in the kidney and liver, erythropoietin is used with great success in the treatment of some complications of kidney failure. The mechanism by which erythropoietin stimulates the production of new red blood cells, however, is not known. Experiments have now shown that at least one possible mechanism of action is the suppression of apoptosis, or programmed cell death. Many normal developmental processes make use of normal cell death. Cells which have served their function or are not needed die according to an internal program. This can be observed by feeding the cells radioactive thymidine, which the cells incorporate into their DNA. In healthy cells, the DNA can be recovered in long pieces. During programmed cell death, the DNA is cleaved into smaller fragments. Such fragments can be observed in the progenitors of red blood cells in tissue culture. The process may be experimentally observed in erythroid spleen cells removed from mice infected with an anemia-causing strain of Friend leukemia virus. In culture, DNA fragments accumulate in two to four hours; the cells begin dying by 16 hours. When erythropoietin is added, however, the progenitor cells do not die and differentiate into reticulocytes, or young red blood cells. The results suggest that programmed cell death may play a role in the normal regulation of red blood cell production, and that one possible mechanism of action of erythropoietin is the inhibition of this internal cellular program. (Consumer Summary produced by Reliance Medical Information, Inc.)

Erythropoietin, Erythropoiesis

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Controlling cell death

Article Abstract:

Programmed cell death is an orderly process forming a cascade of cellular events that can be divided into several stages. Research is discovering the agents that interact in the control and execution stage of the cell death cascade.

Cellular control mechanisms, Cell regulation

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