Cell death passive

To sum up the absence of stimulation by antigens and second signals promotes passive cell death. Maintenance, homeostasis, is only guaranteed when the cell continuously... 

Cell death is widely recognized to play an important role in the development and function of tissues and organs in all multicellular organisms, including fishes. Cell death can be induced by specific developmental cues that promote active, targeted cell removal ( programmed cell death)127 or can be the passive consequence of... 

The recent explosive interest in the study of apoptosis has led to the development and promotion of a generalized dichotomy between active (apoptotic) and passive (necrotic) cell death pathways. Unfortunately, this dichotomy becomes problematic... 

Figure 19.5 Central role of the plasma membrane ATPase in the maintenance of proton homeostasis within the cytoplasm. Protons gain entry into the cytoplasm through passive proton diffusion, which can increase with increasing ethanol from the uptake of protonated acids from symport with amino acids or from metabolism. The cytoplasm and vacuole can buffer proton levels, but the main buffering activity is provided by the action of the ATPase. Saturation of the ATPase can lead to cell death thus metabolic activities are tightly coordinated with ATPase activity.

Infection of cultured cells with many lytic viruses results in a marked decrease in the rate of cellular protein synthesis. Usually, this decrease is accompanied by increasing rates of viral protein synthesis, marked cytopathic effects, and ultimately cell death. In most cases, it is not known whether the shut-off of host cell protein synthesis results from an active process induced by the virus evolved for that (or some other) purpose, or whether it is merely a passive result of another viral function, such as production of large quantities of viral mRNA which compete effectively with their cellular counterparts. In the case of poliovirus, however, three types of studies suggested that the former, active type of mechanism was at work. Kinetic analysis of the rate of protein synthesis in cells synchronously infected with high multiplicities of virus showed that cellular protein synthesis could be virtually completely inhibited prior to the synthesis of significant quantities of viral RNA and protein (Summers et ai, 1965). In addition, infection in the presence of 1-3 mM guanidine, which prevents detectable replication of viral RNA, nevertheless results in viral inhibition of host cell protein synthesis (Holland, 1%4 ... 

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