Table 3. Literature compiled on oxidative stress imposed through various dietary modifications.

Publication information (Ref#)	Research model	Age at start (weeks)	Stress intensity	Length of stress	p53 expression (residue modification)	p53 cellular localization	Regulation of signaling pathways with stress		Signaling pathway(s) activated	Path model
							mRNA	Protein
Diet modification
Nakahara et al., Am J Physiol Endocrinol Metab, 2003 [62]	Wistar rats n = 8–10	6–7	(1) Chronic alcohol (35% total dietary energy) + restriction (2) Acute alcohol (75 mmol/kg) + starvation	(1) 6–7 weeks alcohol (2) 24–48 h starvation + 2.5 h alcohol	1) n/a 2) ↓ p53 mRNA (starvation)	n/a	(1) ↑ c-myc (F + alcohol), (2)↑ c-myc (alcohol and/or starvation)	n/a	Proto-oncogenic activation, pre-apoptotic effect	Chronic alcohol exposure
Yokoyama et al., Cell Rep, 2014 [56]	C57BL/6 Tie2-Cre w/ p53, p53 + eNOS, Mdm4 mice n= 5–10	4	HF/HS	8 weeks	↑ p53 protein	n/a	↑Cdh5, ↑ Kdr, ↓ mtDNA content	↑ Insulin-induced p-Akt @ ser473, ↓p-eNOS @ser1177, ↓ PGC-1α, ↓ Akt, ↑PHLDA3, ↓GLUT1	Endothelial cell expression, glucose metabolism, mitochondrial biogenesis	Insulin resistance + obesity
Dietary restriction
Edwards et al., BMC Genomics, 2007 [44]	C57BL/6NHsd mice n = 5	6–7	26% <normal diet (∼98 kcal/week)	130 weeks	↓ p53 mRNA	n/a	↓ MYOD1, ↓PLAGL1, ↓p21, ↓IGF-BP3, ↓Krt15 mcII, ↓ PERP, ↓sestrin 1, ↓PTEN, ↓ PEG3, ↓ RB1, ↑Bcl6 B cell leukemia, ↑ cyclin G1, ↑ mdm2, ↓ bbc3/puma, ↓ pmaip1/noxa, ↓tnfrsf10b/ killer/dr5, ↓bok	↓ p21, ↓ Gadd45a	cellular senescence, apoptosis *77% prevention by CR on p53-related genes	n/a
Assaily et al., Mol Cell, 2011 [49]	C2C12 myoblasts w/Lpin1, p53 KO	n/a	1 or 0 mM glucose + 24 h fasting	2 h	↑p53 and p-p53 @ ser18	↑53BP1 nuclear	↑ Lpin1	↑ p-AMPK @ Thr172, ↑ p-ACC @ ser79, ↑p-ATM @ ser1987, ↑ p-H2AX	Glycolysis, pentose phosphate pathway, fatty acid oxidation	n/a
Fasting/complete food withdrawal
Schupp et al., BMC Genomics, 2013 [38]	C57B1/6J mice n = 25	10–12	`Withdrawn food	Timecourse: 0, 3, 6, 12, 24, 48 h	↑ p53 mRNA	n/a	↑ Pkc1 (3–48 h), ↑ G6P (3–20 h), ↑ Pcx (48 h), ↑Gyk (12–24 h), ↑Hmgcs2 (12–48 h), ↑ Fgf21 (24 h), ↑ Ppargc1a (24–48 h), ↑Ppara (3 + 24 h), ↑ Cdkn1a, ↑Ses1 + 2, ↑ Lpin1, ↓ Srebf1 + 2, ↓ Acss2, ↓ Acaca, ↓ Fasn, ↓ Scd1 + 2, ↑ Ddit4 (12–48 h) * review study for full list	↑ AMPK, ↓ mTORC1, ↓ Ppargc1a	Fatty acid oxidation, cholesterol biosynthesis	n/a
Aquilano et al., Antioxid Redox Signal, 2013 [48]	C57/BL/6J and CDI mice n = 4	5	Withdrawn food	24 h	↑ p53 protein	↑ p53 nuclear + ↑ binding PGC-1α @ −2317	↑ PGC-1α, ↑ SOD2	↓ GSH, ↑ PGC-1α, ↑SOD2	Antioxidant	n/a

Notes: Literature (six studies) was grouped by diet modification (two studies), dietary restriction (two studies), or fasting/complete food withdrawal (two studies). Arrows indicate whether markers regulated by this form of stress increased (↑) or decreased (↓) in expression and/or activation. If a WT vs. KO model is employed, only the results from the WT group are indicated. Various time measurements are indicated for the length of imposed stress. KO: knockout; Cre: creatine; HF/HS: high fat/high sucrose; F: fasting; CR: caloric restriction.