Cell Death and Apoptosis

摘要: Toxicants cause cell death via apoptosis, necrosis and apocrosis. The last decade of the twentieth century first new millennium witnessed over one million reports exploring occurrence its mechanisms, therapeutic implications. Cooperative efforts every compartment cell, as well various micro macromolecules, orchestrate this form death. Apoptosis has captured attention scientists because retrospective analyses mechanisms human disease show that apoptotic factors either contribute to development or, in large measure, account for it. Although apoptosis been viewed diametrically opposed necrotic death, they share a number key features common. can be versatile even malleable, whereas other forms are not; signaling pathways sharply defined but others not. This chapter discusses overall mechanistic frameworks come under influence drugs, chemicals, stressors, initiation progression during organ toxicity, an up-to-date morphological, biochemical, genetic molecular events characterize apoptosis. Emphasis placed upon insights from both vivo vitro models. is intended serve resource presents current fundamentals scientific bases significant rapidly evolving field. Keywords: acetaminophen; antioxidant responsive element; apoptosis; ASK1; necrosis; Bcl-2; Bcl-xL; Bad; Bax; Bim; Bid; Bak; tBid; FADD; CARD; PUMA; NEMO; JNK; apoptosome; TNF superfamily; TNFR; TRAF2; DISC; drug-induced apoptosis; chemical-induced apoptosis; genetic regulation apoptosis; death domain; apoptosis vivo; apoptosis vitro; signalosome; inflammasome; apoptosis pathways; intrinsic pathway; extrinsic pathway; mitochondria; PKC; IKK; NFκB; oxidative stress; cell death; caspase; paracetamol; dimethylnitrosamine; p53; c-Myc; phagocytosis; apocrosis; DNA fragmentation; apoptotic bodies