Our research suggests that acrylamide causes cytotoxic, anti-proliferative, and apoptotic effects on A549 cells at 4.6 mM IC dose in 24 h.

In conclusion, our results suggested that the IC of acrylamide against NIH/3T3 cells for 24 h was 6.73 mM and that acrylamide exerted its cytotoxic and anti-proliferative effects on these cells mainly via apoptosis.

IntroductionSphingolipids such as ceramide, ceramide-1-phosphate, sphingosine (SPH), and sphingosine-1-phosphate (S1P) offer structural integrity to cell membranes and also assist in the signalling of cellular processes. These cellular processes, including proliferation, apoptosis, inflammation, and cell cycle arrest, play a key role in the evaluation of the antitumour effects of different agents (Beckham et al., 2010). Ceramide and S1P are consequential second messengers derived from sphingolipid metabolites. They exert opposing effects on cell survival. Ceramide induces apoptosis (termed proapoptotic), whereas S1P supports cell survival (termed antiapoptotic) (Oskouian and Saba, 2010). As a result of these opposing effects, the balance between ceramide and S1P is considered a decisive factor in the final metabolic response of a cell (Proksch et al., 2011).As a result of its growth inhibition effects, ceramide is the sphingolipid most commonly investigated in cancer studies and is often termed the 'tumour suppressor lipid' (Taha et al., 2006). The cellular actions of ceramide include modulation of cell apoptosis by inhibiting prosurvival kinases, activation of stress-activated kinases and phosphatases, modification of mitochondrial transmembrane potential, translocation of cytochrome c and apoptosis-inducing factor from mitochondria to cytoplasm, and activation of caspase-3 (Chen et al., 2008). Cancer chemotherapeutic agents such as etoposide, vincristine, daunorubicin, doxorubicin, fludarabine, paclitaxel, and irinotecan all exacerbate suppression of cellular growth by increasing levels of ceramide (Senchenkow et al., 2001;Reynolds et al., 2004).Despite the significant body of work already completed to evaluate the relationship between ceramide metabolic activity and cell death, the precise molecular mechanisms of ceramide-mediated apoptotic signalling are not fully understood. Ceramidases decompose ceramide to SPH, which immediately generates S1P. S1P is the final product of sphingolipid catabolism and is generated under the influence of sphingosine kinase (SK)