Atrazine induces apoptosis of SH-SY5Y human neuroblastoma cells via the regulation of Bax/Bcl-2 ratio and caspase-3-dependent pathway

• Atrazine is a common environmental contaminant.
• We study the cytotoxicity of atrazine in the human neuroblastoma SH-SY5Y cells.
• Atrazine induces apoptosis by increasing Bax/Bcl-2 ratio and ROS levels.
• Cell death was caspase-3 dependent.
• The study showed the potential neurotoxic effects of atrazine.

Atrazine (ATZ) is a well known herbicide that is frequently detected in ground and surface water at significant levels. Our objective was to study the toxic effect of ATZ on the human neuroblastoma (SH-SY5Y) cells, and the degree of cytotoxicity and morphological changes were followed during the cell death. Application of cytotoxicity bioassays indicates that ATZ (5–50 µg/mL) decreases cell viability in a dose- and time-dependent manner. The evidence of apoptosis was confirmed by an increase in caspase-3 activity, and cell death was blocked when caspase-3 activity was inhibited. Typical apoptotic phenotype that includes nuclear fragmentation, micro nuclei formation, DNA fragmentation and increase in the expressions apoptosis-associated markers Bax, p53 and p21 and decreased expression of Bcl-2 were observed in treated cells. We also observed dose-dependent increase in reactive oxygen species (ROS) levels in ATZ-treated cells. These results suggest that ATZ-induces apoptosis and ROS levels in SH-SY5Y cells, and could be implicated in human neurodegenerative disorder.

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