Acrylamide, acrylic acid, or 2‐acrylamido‐2‐methyl‐1‐propanesulfonic acid induced cytotoxic in Photobacterium phosphoreum, PC12, and SK‐N‐SH cells.

In enhancing oil recovery, more and more new water‐soluble polymers are developed to replace the high toxicity and low stability acrylamide (ACR) monomer. The common replacement monomer is acrylic acid (AA) and 2‐acrylamido‐2‐methylamido‐2‐methyl‐1‐propanesulfonic acid (AMPS), which are considered safe and efficient. In this study, AA, ACR and AMPS caused remarkable cytotoxicity in Photobacterium phosphoreum, the rat pheochromocytoma cells (PC12) and the Human neuroblastoma cells (SK‐N‐SH). ACR is much more lethal than AA and AMPS in PC12 and SK‐N‐SH cells, meanwhile, the toxicity of AA and AMPS decreases with the decrease of acid. Furthermore, similar to ACR, AA, and AMPS can induce severe DNA double‐strand breakage in PC12 and SK‐N‐SH cells. Both AA and ACR can cause cell cycle arrest in the G0/G1 phase in PC12 and SK‐N‐SH cells. In addition, like ACR, AA, and AMPS can generate reactive oxygen species (ROS) accumulation, mitochondrial dysfunction and mitochondrial‐dependent apoptosis in both PC12 and SK‐N‐SH cells. The acute toxicity of AA and AMPS is lower than ACR, however, the decline in acute toxicity in monomers does not mean toxic‐free. We should focus on the toxicity of AA and ACR and reduce occupational contact to protect employee occupational health. [ABSTRACT FROM AUTHOR]