TABLE 1.
Summary of findings related to PFJ consumption and oxidative status1
| Reference | Study design, duration2 | Type of juice | Subjects (healthy unless specified)3 | Results4 |
| Ko et al., 2005 (5) | Single-dose postprandial | Apple, orange, grape, 150 mL | n = 10, ♂, 24 ± 1 y | ↓ DCF at 90 min (apple, orange) and 2 h (grape) |
| Vieira et al., 2012 (6) | Single-dose postprandial | Apple, 300 mL | n = 9, ♀, 21–27 y | ↑ FRAP, ABTS, uric acid, and ascorbic acid at 1 h vs. baseline and water control; ↓ LH and TBARS |
| Godycki-Cwirko et al., 2010 (7) | Single-dose postprandial | Apple, 1 L cloudy; clear; ± polyphenols | n = 12, ♀♂, 32 ± 5 y | All juices ↑ FRAP, DHHP-scavenging, uric acid over 4 h post-intake (P = 0.01) |
| Hyson et al., 2000 (8) | Crossover, 6 wk juice vs. whole apple | Apple, 375 mL/d | n = 25, ♀♂, 40 ± 2 y | Delay LDL oxidation, ↓ conjugated diene production; ↔ fasting lipids |
| Vinson et al., 2008 (9) | Single-dose postprandial | Cranberry, 240 mL/d (27% juice cocktail) | n = 10, ♀♂, 25–28 y | ↑ FRAP vs. control beverage (maintained up to 7 h after consumption) |
| Shidfar et al., 2012 (10) | Double-blind, placebo-controlled, 12 wk | Cranberry, 240 mL/d | n = 10, type 2 diabetic ♂, 55 ± 9 y | ↑ apoA1 and paraoxonase activity, ↓ glucose and apoB vs. baseline and vs. control (P range < 0.0001 to < 0.05). ↔ Lp(a) |
| Stein et al., 1999 (11) | Pre- and post-test, 2 wk; (juice 2 h before post-test) | Grape (Concord), 7.7 mL/kg per day | n = 15, ♀♂, CAD/hypertension, dyslipidemia, 63 ± 13 y | Delay LDL oxidation; ↑ total cholesterol (P = 0.043), ↑ TG (P < 0.001), ↑ insulin (P = 0.004); ↑ FMD (P = 0.003; see Table 2) |
| Vinson et al., 2000 (12) | Pre- and post-test; high or low vitamin C (7 d each), or no vitamin C | Grape (Concord), 2 × 200 mL daily (+76 mg vitamin C vs. juice 6 mg vitamin C) vs. no vitamin C (orange juice similar protocol) | n = 8, ♀♂, 20–55 y, high and low vitamin C; n = 6, ♀♂, 20–34 y in no vitamin C group | Delay LDL oxidation in all groups; not sustained after 7-d washout. ↔ LDL oxidation after orange juice |
| O’Byrne et al., 2002 (13) | Pre- and post-test, 2 wk juice, plus grape vs. α-tocopherol group | Grape (Concord), 10 mL/kg or 400 IU α-tocopherol/d, dietary flavonoids restricted | Grape group, n = 15, ♀♂, 28 ± 3 y vs. α-tocopherol, n = 17, ♀♂, 28 ± 5 y | Grape vs. α-tocopherol ↓ plasma protein carbonyls, ↑ TG; both groups ↑ ORAC (P < 0.001), delayed LDL oxidation rate (P < 0.01), ↑ LDL oxidation lag time (P < 0.001), ↔ endogenous urinary F2-isprostane, ↔ AAPH-induced plasma protein oxidation |
| Yuan et al., 2011 (14) | Pre- and post-test, 2 wk | Grape, 300 mL + apple, 300 mL/d | n = 25, ♀♂, 20–23 y | ↑ Plasma T-AOC (P < 0.01), ↓ plasma MDA, ↔ carbonyls, ↑ erythrocyte CAT and GSH-Px, ↔ SOD, ↔ urinary 8-OHdG, ↔ DNA damage in lymphocytes |
| Gonzáles-Flores et al., 2012 (15) | Pre- and post-test, 5 d | Grape (Tempranillo), 200 mL/d | n = 6/age group, ♀♂, 20 ± 10, 45 ± 10, 75 ± 10 y | ↑ Urinary aMT6s, ↑ ATBS |
| Castilla et al., 2006 (16) | Pre- and post-test, 2 wk | Grape (concentrated Bobal), 100 mL/d | n = 26, hemodialysis, 62 ± 3 y ♀♂ n = 12, no juice, hemodialysis, 59 ± 4 y | Juice ↑ TEAC, ↓ oxidized LDL within week 1, sustained day 14 (P < 0.001) vs. no juice, ↔ TEAC, ↔ oxidized LDL |
| Castilla et al., 2008 (17) | Pre- and post-test, 2 wk | Grape (concentrated Bobal), 100 mL/d ± 800 IU vitamin E, or vitamin E alone vs. placebo control | n = 8 each group, hemodialysis ♀♂, 33–79 y | All but placebo ↓ oxidized LDL (P < 0.01), grape juice only ↑ HDL (P < 0.001), ↑ apoA-1 (P < 0.01), juice ± vitamin E ↓ total and LDL cholesterol, apoB vs. baseline (P < 0.001), juice ↓ plasma MCP-1, ↔ VCAM-1, hsCRP, complement C3 protein |
| Sánchez-Moreno et al., 2003 (18) | Single dose plus pre- and post-test, 2 wk | Orange (fresh), 500 mL single dose; 500 mL/d | n = 12, ♀♂, 20–32 y (subset n = 3 smokers) | Single dose ↑ plasma vitamin C in ♂ (P = 0.001) and ♀ (P = 0.009), ↓ plasma 8-epi-PGF2α, in ♂, greater effects in smokers |
| Johnston et al., 2003 (21) | Crossover × 3, juice vs. vitamin C supplement | Orange, 250 mL, 500 mL, 72 mg vitamin C | n = 11, ♀, 21–39 y | ↑ Plasma vitamin C after 500-mL juice (P = 0.0001) and 72-mg vitamin C (P = 0.001), ↓ TBARS after 250-mL juice and vitamin C (P = 0.01) |
| Deopurkar et al., 2010 (22); Ghanim et al., 2010 (23) | Repeat single-dose tests | Orange, 300 kcal equivalent vs. 300 kcal quantity of cream or glucose | n = 10/group, ♀♂, 20–40 y; n = 12/group, ♀♂, 25–47 y | Juice ↓ ROS generation by mononuclear cells, attenuated rise in plasma endotoxins and mRNA for TLR2, TLR4, and SOD-protein at 1, 3, 5 h vs. glucose or cream beverage, suppressed monocyte p38 MAPK protein, mRNA for/and plasma MMP-9 |
| Codoñer-Franch et al., 2008 (24) | Pre- and post-test, 4 wk | Mandarin, 500 mL/d | n = 48, hypercholesterolemic children, 8–12 y | ↓ Plasma MDA, carbonyl groups (P < 0.01), ↑ reduced glutathione, vitamin C (P < 0.00001), vitamin E (P < 0.001) |
| Guo et al., 2008 (25) | Pre- and post-test, 4 wk | Pomegranate vs. apple, 250 mL/d | n = 26, ♀♂, >60 y | Both juices ↓ plasma MDA (P < 0.01), pomegranate ↓ FRAP, carbonyl content, ↔ oxidation LDL, GSH |
| Shema-Didi et al., 2012 (26) | Double-blind, placebo-controlled, 12 mo | Pomegranate, 100 mL 3 × wk, during first hour of dialysis | n = 66 juice vs. n = 35 placebo, hemodialysis ♀♂, >18 y | ↓ CD11b, myeloperoxidase, oxidized fibrinogen, MDA, IL-6, TNF-α (P < 0.03–0.001), fewer infections juice vs. placebo |
| Rock et al., 2008 (27) | Pre- and post-test, 4 wk | Pomegranate, 50 mL/d concentrate | n = 10 ♂, n = 10 postmenopausal ♀ (age not specified) | ♂ Only↓ TBARS, AAPH-induced serum lipid peroxidation, ↑ FRAP, thiol groups, ↑ paraoxonase free and HDL-related activity (binding, catalytic), ↔ lipids, glucose, Hb A1c |
| Rosenblat et al., 2006 (28) | Pre- and post-test, 12 wk vs. control | Pomegranate, 50 mL fresh diluted 1:5 (v:v) | n = 10, diabetic ♂ vs. 10 ♂, 50 ± 10 y | ↓ Plasma peroxides, C-peptide, ↑ thiols, paraoxonase arylesterase activity vs. control/baseline (P < 0.01) |
1
AAPH, 2,2′-azobis(2-amidinopropane)dihydrochloride; aMT6s, 6-sulfatoxymelatonin; ABTS 2,2′-azino-di-[3-ethylbenthiazoline sulphonate); CAD, coronary artery disease; CAT, catalase; DCF, 2,7-dichlorofluorescin; DHHP, 1,1-diphenyl-2-picrylhydrazyl; FMD, flow-mediated dilation; FRAP, ferric-reducing antioxidant power; GSH-Px, glutathione peroxidase; Hb A1c, glycated hemoglobin; hsCRP, high-sensitivity C-reactive protein; LH, lipid hydroperoxides; Lp(a), lipoprotein (a); MCP-1, monocyte chemoattractant protein; MDA, malondialdehyde; MMP-9, matrix metallopeptidase 9; ORAC, oxygen radical absorbance capacity; PFJ, pure (100%) fruit juice; p38 MAP, mitogen-activated protein kinase; ROS, reactive oxygen species; SOD, superoxide dismutase; T-AOC, total antioxidant capacity; TEAC, Trolox equivalent antioxidant capacity; TLR2, toll-like receptor 2; TLR4, toll-like receptor 4; urinary 8-OHdG, 8 hydroxydeoxyguanosine; VCAM-1, vascular cell adhesion molecule-1; 8-epi-PGF2α, 8-epi-prostaglandin 2α.
2
Study design was randomized unless otherwise indicated.
3
Values are mean age ± SD or range, rounded to nearest whole number.
4
P < 0.05 unless otherwise indicated; ↑, increase; ↓, decrease; ↔, no effect; ♀, women; ♂, men.