Cell death is one of the key events by which chemicals cause adverse effects. Of course, the relevance of cell death for in vivo toxicity is organ and tissue dependent. For example, hepatotoxic chemicals often reach cytotoxic levels in vivo; adverse effects, such as fibrosis (Godoy et al. 2013; Nussler et al. 2014), are usually observed after cell killing. On the other hand, adverse effects in other organs, e.g., the central nervous system, may be caused by non-cytotoxic concentrations by compromising connectivity of neurons, receptor expression, or neurotransmitter metabolism (van Thriel et al. 2012; Weng et al. 2014; Balmer et al. 2014; Sisnaiske et al. 2014; Waldmann et al. 2014; Krug et al. 2013). Although it is clear that adverse effects can also occur without cell killing by disturbed cell functions, chemicals always have to be considered as critical when close to cytotoxic concentrations are reached in vivo. Therefore, it is not surprising that cell death research and research on factors modifying susceptibility to cell death represent cutting edge topics in toxicology (Indran et al. 2011; Jazirehi et al. 2011; Jiang et al. 1999; Galán et al. 2001; Ambrosio et al. 1993; Aoki et al. 2002; Ashkenazi and Dixit 1998; Barnhart et al. 2003). The most intensively studied and perhaps also most relevant cell death mechanism is apoptosis (Alster et al. 2014; Lopez et al. 2014; Bezler et al. 2012; Ilowski et al. 2011; Godoy et al. 2009). Its morphological features have already been described by Fleming in 1885 as a series of events that include chromatin condensation, membrane surface blebbing, and the breakdown of the cell into apoptotic bodies (Matés et al. 2012; D’Emilio et al. 2010). This strictly defined sequence of events guaranties that cells die in an orderly way in contrast to the chaotic cell death of necrosis (Matés et al. 2008, 2012; Wyllie 2010; Yoo et al. 2009; Hammad et al. 2014; Gabai et al. 2000). This process allows the removal of cells from tissues without inflammation. It plays an important role in embryonic development of organisms and in tissue homeostasis (Morita et al. 2001). When chemicals interfere with the control mechanisms of apoptosis, they may cause cell death at very low concentrations. Therefore, the control mechanisms of pro- and anti-apoptotic factors and their disturbance by chemicals traditionally represent an intensively studied field in toxicology. To give our readers an overview, we summarize key messages from articles about cell death mechanisms published since 2012 (Table 1).

Table 1 Key messages of publications in the field of cell death mechanisms published in Archives of Toxicology since 2012
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