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Xenobiotics and their influence on the apoptosis in animal cells

Apoptosis or programmed cell death is a set of ordered events that enables the selective removal of cells from tissue and is essential for homeostasis and proper function of multicellular organisms. This process is tightly regulated through multiple independent signaling pathways. Mitochondria also provide a major switch for the initiation of apoptosis. The mitochondrial inner membrane space contains a number of cell-death-promoting factors, including Cyto-c, apoptosis-inducing factor and latent forms of proteases called caspases. Inappropriate apoptosis is of importance in many common chronic diseases such as cancer, cardiovascular disease, autoimmune disease and neurodegenerative disease and may be triggered by environmental contaminants and toxins. Xenobiotics (i.e. chemical and natural toxins) can either kill cells or interfere with their death programmes. Drugs that trigger cell death to eliminate unwanted cells (like cancer cells) or prevent their death in toxic and disease states are under current development. Understanding cell death mechanisms is therefore important in toxicology and also at early stages of drug design. Research in our team is concentrated on understanding influence of the cell environment within the bioreactor or within the organ on the apoptosis. When considering the same toxicant, injury amplitude (dose) is a primary determinant of whether cell die via active cell death (apoptosis) or failure of homeostasis (necrosis) remains valid. Tissue selectivity of toxicants can stem from the apoptotic or necrotic thresholds at which different cells die, as well as targeting factors such as toxic kinetics, receptor recognition. bioactivation, and cell specific lesions.

animal cells; apoptosis; xenobiotics

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