Table 2.

The antioxidant activity of p53 in chemically induced oxidative stress.

Chemical	Cell lines/animals	Assays	Result	Ref.
Acetaminophen	C57BL/6 mice wild type and p53−/−, APAP, 300 mg/kg, i.p., 1, 2, 4, and 24 h. PFTα, 2.2 mg/kg, i.p., nutilin-3a, 10 mg/kg, gavage p53 ASO, 50 mg/kg, i.p.	ROS, NAPQI adducts, Sab, p-JNK, ALT	(i) Sustained JNK activation leading to increased mitochondrial ROS. (ii) p53 inhibition enhanced sustained JNK activation, while the JNK was suppressed with the p53 activator.	[36, 37]
Palmitate	HUVEC and HAEC cells, 0.4 mM PA, 8–16 h. C57BL/6J mice, HFAD-fed, 12 w	ROS, NO, GPX1, aortic lesions	(i) Palmitate-siRNA rescued the inhibition of p53 binding to GPX1 promoter and then blocked PA-induced ROS formation. (ii) HFAD-induced oxidative stress and vascular damage via PTEN nuclear export, p53/GPX1 inhibition.	[58]
Glucose	HUVEC and HAEC cells, 20 mM, 0–48 h	ROS, TAF1	(i) TAF1-mediated p53 phosphorylation at Thr55 and GPX1 suppression plays a critical role in ROS accumulation.	[60]
Nitric oxide	VSMC wild type and p53−/−, DETA/NO, 1 mM, 24 h	ROS, SOD-2, PRx-3, and TRx-2	(i) p53−/− VSMC have increased levels of ROS at baseline and following exposure to NO compared with p53+/+ VSMC. (ii) p53 have antioxidant properties and antiapoptotic functions in VSMC.	[61]
1-Methyl-4-phenylpyridinium	SH-SY5Y, 100 μM, 24–72 h	ROS, 4HNE	(i) Increased expression of sestrin2 induced by MPP+ was abolished by downregulation of p53. (ii) Inhibition of sestrin2 by siRNA significantly promoted increased levels of ROS induced by MPP+.	[57]