[Processes of cell necrosis--apoptosis--and their modification by toxic substances].
Apoptosis--a programme physiological necrosis of cells is a synonym of a complex multistage process of cell reduction described during the 1970s. It occurs during metamorphosis on insects and amphibians as well as during embryogenesis, intrauterine and extra-fetal life of mammals. It regulates the atrophy of completely developed organs, e.g. thymus, and the hormonal restructuring of adrenal glands, mammary and prostate glands, ovaries and others. It is a reverse of proliferation and it guarantees homeostasis of the number, structure and biochemical activity of tissues and organs. It is developed by apoptosis substances and factors represented by protein hormones, peptides, steroid hormones, cytokines and metabolites of vitamin A, antimetabolites, drugs, toxic substances, ionizing radiation, antigens. On the other hand, the development of apoptosis is arrested by so called "survival factors"--erythropoietin, CSF, NGF, IL-1 and 2, certain hormones, phenobarbital, cyproterone. The process of a programmed necrosis is associated with spectacular "events" of morphological, biochemical and macromolecular nature. Steering is provided by a group of genes, partly recognized, particularly in the Nematode of Caenorhabditis elegans. They are among others killer genes which remove the remnants of decaying cells and genes which hinder the expression of death genes. Transduction of the signal from the receptor to the nuclear chromatin releasing a programmed necrosis of cells is also discussed.
Kamiński
M
M
II Katedry i Zakładu Histologii i Embriologii, Slaskiej Akademii Medycznej, Katowicach.
D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000235:genetics / Q000502:physiology; D005786:Gene Expression Regulation; D006801:Humans; D009154:Mutation; D015398:Signal Transduction; D014118:Toxins, Biological / Q000494:pharmacology*
D014118:Toxins, Biological
Procesy obumierania komórek--apoptoza--i ich modyfikacja przez substancje toksyczne.