Table 2.
Summary of studies on bioavailability and action of polyphenols, vitamins and carotenoids using animal models or clinical trials.
| Compound | Study Design | Bioavailability | Assays | Results | Related Antioxidant Activity |
Reference |
|---|---|---|---|---|---|---|
| Guaraná powdered seed (Paullinia cupana) | Humans (healthy overweight adults) n = 12 | Detected 1 h after intake and remained after plasma clearance (plasma HPLC) | ORAC | ↑ORAC | Guaraná is a rich source of bioavailable catechins and contributes to reducing the oxidative stress parameters of clinically health overweight individuals by direct antioxidant action and up-regulation of antioxidant enzymes. | Yonekura et al. (2016) [178] |
| Single dose (3 g/90 mg catechins and 60 mg epicatechins equivalent) daily for 15 days | SOD/CAT/GPx activities | ↑CAT/GPx ↔SOD |
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| Blood samples: overnight-fasting and 1 h after intake | Ex vivo LDL oxidation/H2O2 induced DNA damage in lymphocytes (Comet Assay) | ↓LDL oxidation (only in the first day of study) ↓DNA damage (only after 1 h intake) |
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| Green (GT) and Black Tea (BT) (commercially acquired) | Male Wistar rats (n = 18) | Not evaluated | Drug metabolizing enzymes activity (hepatic and pulmonary) | ↑P450 (CYP) 1A1 (hep) ↑UDP-glucoronosyltransferase (hep/pulm) ↑CYP 1A2 (hep) ↓CYP 2C (hep) ↓CYP 2E1 (hep) ↓CYP 3A (hep) |
Feeding both tea drinks to rats modulated drug metabolizing enzymes at a transcriptional level and reduced oxidative stress in the liver and lungs, but green tea was more effective in reducing oxidative stress. Their possible interactions with drugs or toxic compounds should be taken into account. | Yao et al. (2014) [179] |
| Ad libitum with food and as water replacement for 5 weeks | GSH, GSSG and GSH/GSSG ratio | ↓[GSH] (hep/pulm) ↓Lipid peroxide (pulm/GT) |
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| Blood and tissue (liver and lungs) samples after being euthanized | GPx and GSR TBARS and ROS |
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| DNA-binding activity of nuclear factors | ||||||
| Coffee (caffeic and ferulic acids) | Humans (n = 20) | Detected 1 h after intake (plasma HPLC) | ORAC | ↑ORAC | Lara-Guzmán et al. (2016) [180] | |
| FRAP/TRAP | ↑FRAP/↔TRAP | The experiments on plasma with caffeic and ferulic acids showed a significant increase in the antioxidant activity as well as delay of LDL oxidation. | ||||
| After acute consumption (1 h/400 mL) | Ex vivo LDL oxidation | ↓LDL oxidation | ||||
| Vitamin C supplementation | Male Sprague Dawley rats (n = 6–7 per group) | Detected in plasma and cerebral tissue (spectrophotometry) | Histopathology | Diabetic state: ↑infarct volume and edema Vit. C: ↓damage |
Daily intake of ascorbic acid attenuates the exacerbation of cerebral ischemic injury in a diabetic state, which may be attributed to anti-apoptotic and anti-inflammatory effects via the improvement of augmented oxidative stress in the brain. Ascorbic acid supplementation may protect endothelial function against the exacerbated ischemic oxidative injury and improve its transport through SVCT2 in the cortex. | Iwata et al. (2014) [184] |
| Streptozotocin-induced type 1 diabetes | IHC (SVCT2, GLUT-1, cleaved caspase-3, TNF-α, IL-1β | ↓cleaved caspase-3 ↓inflammatory cytokines (TNF-α and IL-1β) |
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| 100 mg/kg of ascorbic acid (gavage) for 2 weeks before cerebral ischemia-reperfusion protocol | PCR (SVCT2 and GLUT1) | ↑SVCT2 (neurons and endothelial cells) ↑GLUT1 (endothelial cells) |
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| Cerebral ischemia-reperfusion (infarct induction) | Superoxide production | ↓superoxide radical | ||||
| Multivitamin supplementation (vit. C + vit. E + sodium selenite + β-carotene) | Female Sprague Dawley rats (n = 40) | Not evaluated | Histopathology | ↓honeycomb-like injury ↓edema ↔inflammatory infiltrate |
The antioxidant combination protected lung tissue against damage by enhancing biochemical parameters and pulmonary edema, while no significant effect on protection of pulmonary inflammation was observed. The antioxidant vitamin supplementation with selenium can be used in the prevention of acute lung injury. | Bayrak et al. (2016) [185] |
| Vitamin C (100 mg/kg/day), vitamin E (100 mg/kg/day), sodium selenite (0.2 mg/kg/day and β-carotene (15 mg/kg/day) via gavage for 3 days before the injury protocol | ||||||
| D-galactosamine-induced (DGaIN) acute lung injury | GSH/GPx/PON TF/LDH/CAT/SOD/MPO/XO / |
↑GSH/GPx/PON ↓TF/LDH/CAT/SOD/MPO/XO/Na+/K+ ATPase |
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| LPO (MDA) | ↓LPO | |||||
| Multivitamin supplementation (vit. C + vit. E + sodium selenite + β-carotene) | Female Sprague Dawley rats (n = 40) |
Not evaluated | Histopathology | ↓edema ↓necrosis ↓inflammatory infiltrate |
The combination of antioxidants suppressed histopathological changes in the liver and biochemical parameters in D-GaIN-induced hepatotoxicity rats. The antioxidant vitamin supplementation with selenium can be used in the prevention of acute hepatotoxicity. | Catal et al. (2017) [186] |
| Vitamin C (100 mg/kg/day), vitamin E (100 mg/kg/day), sodium selenite (0.2 mg/kg/day and β-carotene (15 mg/kg/day) via gavage for 3 days before the injury protocol | Blood GSH/CAT Blood AST/ALT/ALP/GGT/LDH Blood sialic and uric acid Hepatic CAT/SOD/GSH/GPx Hepatic GST |
↑blood GSH and CAT ↓blood AST/ALT/ALP/GGT/LDH ↓blood sialic and uric acid ↑hepatic CAT/SOD/GSH/GPx ↔hepatic GST |
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| D-galactosamine-induced (DGaIN) acute liver injury | LPO (MDA) | ↓hepatic LPO | ||||
| Histopathology | ||||||
| Carotenoids derived from microalgal biomass (Spirulina platensis, Haematococcus pluvialis and Botryococcus braunii) | Male Wistar rats (n = 25) | Detected in plasma after 2 h, in the liver after 4 h and in the eyes after 6 h (HPLC/LC-MS) Carotenoid’s accumulation: liver > eyes > plasmaAstaxanthin from H. pluvialis had better bioavailability and accumulation than other groups. |
Plasma and hepatic SOD, CAT, peroxidase and lipid peroxidation (TBARS) | ↑plasma and hepatic SOD, CAT and peroxidase ↓Lipid peroxidation |
Rao et al. (2013) [194] | |
| Sigle dose of microalgal biomass (200 µM equivalent of β-carotene, astaxanthin and lutein) via gavage for 15 days | These results indicate that the astaxanthin from H. pluvialis has better bioavailability and better antioxidant properties compared to other carotenoids. Microalgae biomass is capable of preventing lipid peroxidation through scavenging free radicals and hydroxyl radicals in living cells and also restoring antioxidant enzyme activity. | |||||
| Fucoxanthin (FUCO) solubilized in glycolipid (GL) and absorbed from chitosan nanogels (NG) | Rat model Groups: control, FUCO, FUCO+NG-GL, FUCO+NG+GL |
Plasma FUCO (HPLC). After single dose: ↑ 227.5% After repeated doses: ↑ 292.4% (compared to control and -GL groups). |
CAT/GST/SODLipid peroxidation (TBARS) | ↑CAT/GST/SOD (+GL > ☐GL > controls) ↓Lipid peroxidation (controls > ☐GL > +GL) |
The advantage of CS-NGs + GL for improved FUCO bioavailability via passive and active transport through PPARc mediated SRB1 activation was demonstrated. Elevated plasma and tissue levels of FUCO in these groups could be the reason for a higher activity of antioxidant enzymes and lower lipid peroxides. | Ravi and Baskaram (2017) [195] |
| Single dose study: 48 h Repeated dose study: 14 days Dietary feeding study: 1 month |
Plasma FUCO (HPLC) after dietary feeding: ↑ 57.5% (compared to ☐GL) ↑ 400% (compared to seaweed) ↑ 287% (compared to control) |
PPARγ/SRB1 | ↑PPARγ/SRB1(FUCO and GL had an agonist action) | |||
| Lycopene | Murine emphysema model (n = 40) | Not evaluated | Histopathology | Inhibited emphysema-like features when treated with LY | Lycopene acts as an antioxidant and anti-inflammatory through the neutralization of reactive species production in vitro and in vivo, the restoration of the GSH/GSSG ratio, decreasing oxidative damage, decreasing pro-inflammatory cytokines through decreased cell influx and the direct suppression of cytokine production. | Campos et al. (2017) [196] |
| Cigarette smoke exposure 3 times a day for 60 days | SOD/CAT/GPxGSH/GSSG ratio | ↔SOD/↓CAT/↑GPx ↑GSH/GSSG ratio |
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| Treatment with lycopene (LY) diluted in sunflower oil (25 and 50 mg/kg/day) | TBARS | ↓TBARS | ||||
| IFN-γ/TNF-α/IL-10 (bronchoalveolar fluid) | ↓ IFN-γ/TNF-α/IL-10 | |||||
| Leukocyte influx (bronchoalveolar fluid) | ↓ Leukocyte influx |