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. Author manuscript; available in PMC: 2024 Jul 15.
Published in final edited form as: Toxicol Lett. 2019 Dec 26;322:1–11. doi: 10.1016/j.toxlet.2019.12.023

Fig. 3. NAC pre-treatment ameliorated CP-induced changes in markers related to DNA damage, apoptotic cell death and oxidative stress, and MAPK phosphorylation.

Fig. 3.

HCE cells. HCE cells were either exposed to CP (50μM) or pre-treated with NAC (5 mM NAC for 1 h) and then exposed to 50 μM CP for 24 h. After 24 h, cell lysates were prepared and western immunoblotting for H2A.X and p53 phosphorylation, p53 accumulation, and cleaved-PARP (A), JNK1/2 phosphorylation and accumulation (B), and HO-1 expression (C) was carried out as detailed under Materials and Methods section. Protein loading was checked by stripping and re-probing the membranes for beta-actin. The results obtained were quantified by densitometric analyses of the immunoblots and fold change compared to control was calculated. C, control; CP, chloropicrin; NAC, N-Acetyl-L-Cysteine.

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