Controlled Necrosis

Some necrosis mechanisms are considered. Although traditionally necrosis is considered as an uncontrolled and catastrophic cell death caused by intense damaging impacts, last data have shown that necrosis may occur in some physiological processes. Moreover, necrosis may be controlled by the intracellular signaling processes. For example, experiments with photodynamic treatment of neurons and surrounding glial cells have shown that increase in plasma membrane permeability leading to necrosis is controlled by neurotrophins, Ca²⁺-, cAMP-, and cGMP-dependent signaling pathways. An assortment of signaling proteins involved in these responses are different in neurons and glial cells. Thus, necrosis is uncontrolled under very strong impacts. However, necrotic processes induced by moderate impacts may be controlled by the cellular signaling system. Moreover, in some physiological situations necrosis may be performed according to the predetermined program.     

Noradrenaline Metabolism in Neocortex and Hippocampus Following Transient Forebrain Ischemia in Rats: Relation to Development of Selective Neuronal Necrosis

Noradrenaline (NA) metabolism in the neocortex and hippocampus was examined in rats at 1, 24, and 48 h following 15 min of reversible forebrain ischemia. As assessed by the ratio of accumulated 3,4-dihydroxyphenylalanine (DOPA) to the tissue NA level after inhibition of DOPA decarboxylase, the NA turnover rates were markedly increased (120-148% above the control) at 1 h postischemia in both the neocortex and hippocampal formation (CA1 and CA3 plus dentate gyrus). The DOPA:NA ratio went back to control levels after longer postischemic survival times. The ratio between levels of the deaminated NA metabolite, 3,4-dihydroxyphenylethyleneglycol (DOPEG), and NA, which gives another measure of NA turnover rate, showed similar changes. In the neocortex and the CA3 plus dentate gyrus, the DOPEG:NA ratio was markedly increased (89-118%) 1 h after the ischemia, but this change had disappeared at 24 and 48 h. Thus, both the DOPA accumulation experiments and the NA and DOPEG measurements indicate that following transient forebrain ischemia, there is an increased NA turnover in the hippocampus and cortex only in the early recirculation period and not after longer postischemic survival times. The degree of neuronal necrosis in the CA1 region was examined light microscopically on celestine blue-acid fuchsin-stained sections at 24, 48, and 96 h following the ischemic insult. The neuronal damage in CA1 was sparse after 24 h of recovery, had increased markedly after 48 h, and was very pronounced at 96 h.(ABSTRACT TRUNCATED AT 250 WORDS)     

Necrosis in yeast

Necrosis was long regarded as an accidental cell death process resulting from overwhelming cellular injury such as chemical or physical disruption of the plasma membrane. Such a definition, however, proved to be inapplicable to many necrotic scenarios. The discovery that genetic manipulation of several proteins either protected or enhanced necrotic cell death argued in favor of a regulated and hence programmed process, as it is the case for apoptosis. For more than a decade, yeast has served as a model for apoptosis research; recently, evidence accumulated that it also harbors a necrotic program. Here, we summarize the current knowledge about factors that control necrotic cell death in yeast. Mitochondria, aging and a low pH are positive regulators of this process while cellular polyamines (e.g. spermidine) and endonuclease G as well as homeostatic organelles like the vacuole or peroxisomes are potent inhibitors of necrosis. Physiological necrosis may stimulate intercellular signaling via the release of necrotic factors that promote viability of healthy cells and, thus, assure survival of the clone. Together, the data obtained in yeast argue for the existence of a necrotic program, which controls longevity and whose physiological function may thus be aging.     

Renal Tubular Necrosis and Papillary Necrosis after Gastroenteritis in Infants

Three young infants who had severe gastroenteritis developed radiological and histological features of renal tubular necrosis. Characteristically the excretion urogram showed renal enlargement with prolonged and heavy opacification of the renal parenchyma and a pronounced increase in density of the pyramids. Subsequent radiological studies showed extensive papillary necrosis. Though these infants are now apparently fit, renal damage has occurred and this may eventually give rise to features indistinguishable from chronic pyelonephritis.