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Loguercio, C. Drinking habits and risk of altered liver enzymes in the general population of a rural area in Southern Italy. Liver Dis. Download references. We thank the people who participated in the study, the study-site personnel, and members of the Rafsanjan cohort study and Rafsanjan University of Medical Sciences.
The Iranian Ministry of Health and Medical Education has contributed to the funding used in the PERSIAN Cohort through Grant No. The context of this article are the views of the authors and the funder had no role in design of the study and collection, analysis, and interpretation of data, decision to publish and writing the manuscript.
Clinical Research Development Unit CRDU , Ali-Ibn Abi-Talib Hospital, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Department of Pathology, Medical School, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Immunology of Infectious Diseases Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Student Research Committee, Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Social Determinants of Health Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Department of Epidemiology, School of Public Health, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Non-Communicable Diseases Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Neurology Department, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Clinical Research Development Unit CRDU , Moradi Hospital, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Clinical Research Development Unit CRDU , Niknafs Hospital, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
You can also search for this author in PubMed Google Scholar. and M. designed the study and supervised the project. collected the data. prepared Tables 1 , 2 , 3 and 4. performed the statistical analysis.
wrote the main manuscript text. All the authors read and approved the final manuscript. Correspondence to Zahra Jamali. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Open Access This article is licensed under a Creative Commons Attribution 4.
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nature scientific reports articles article. Download PDF. Subjects Diseases Gastroenterology. Abstract Oxidative stress has been considered the main contributor to liver injury.
Introduction As one of the most important organs in the body, the liver plays a key role in carbohydrate, protein, and fat metabolism 1. Materials and methods Study design and participant selection This cross-sectional study was conducted using the RCS data as a population-based prospective cohort, a part of the Prospective Epidemiological Research Studies in IrAN PERSIAN Data collection Through a standardized interview and validated questionnaire, data on socio-economic status, smoking habits, opium use, alcohol consumption, disease history, diet, and physical activity were collected.
Dietary intake assessment The participants completed a semi-quantitative FFQ with items which asked about dietary intake over the past year by trained nutritionists. Laboratory assessment Blood samples were taken from all subjects between and a.
Definition of terms The laboratory's reference range in the Cohort center was used to define elevated ALT, AST, GGT, and ALP. Statistical analyses Baseline characteristics of individuals, including demographic characteristics, personal habits, and medical and laboratory characteristics, were compared across the groups of the present study elevated liver enzymes using chi-square χ 2 for categorical and t-test for continuous variables.
Ethics approval and consent to participate The ethics committee of Rafsanjan University of Medical Sciences approved this study Ethical codes: ID: IR. Results In the present study, participants from the baseline phase of the Rafsanjan adult cohort study, who had completed data on serum liver enzymes, were included.
Full size table. Table 4 Association of the dietary antioxidants and odds of elevated liver enzymes in study participants using the crude and adjusted models. Discussion In the present study, we assessed the association of some dietary antioxidant intakes, including vitamin A, vitamin C, vitamin E, selenium, and carotenoids α-carotene, β-carotene, lycopene, and β-cryptoxanthin with odds of elevated liver enzymes in a large population of Iranian adults.
Conclusion Subjects with higher consumption of Se, Vit A, Vit E, and provitamin A carotenoids β-carotene, α-carotene, β-cryptoxanthin showed decreased odds of elevated ALP. Data availability The datasets used during the current study are available on the Persian Adult Cohort Study Center, Rafsanjan University of Medical Sciences, Iran.
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Funding The Iranian Ministry of Health and Medical Education has contributed to the funding used in the PERSIAN Cohort through Grant No. View author publications. Ethics declarations Competing interests The authors declare no competing interests.
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Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med. Sharifi N, Amani R, Hajiani E, Cheraghian B. Does vitamin D improve liver enzymes, oxidative stress, and inflammatory biomarkers in adults with non-alcoholic fatty liver disease?
A randomized clinical trial.
Select your Antioxidant and liver health of interest to Antioxidqnt the aand content in your interested language. Oxidants Anttioxidant Antioxidant and liver health in Medical Science received citations as per google scholar report. Trest Allen, Department of Chemical Engineering, University of Tehran, Tehran, Iran, Email: trtesalenl gmail. Received: May, Manuscript No. EJMOAMS; Editor assigned: May, Pre QC No.Open access peer-reviewed chapter. Submitted: 20 September Hhealth 11 December Published: 24 June com customercare cbspd.
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Molecular mechanisms explaining the hepatoprotective effect of food bioactives. In the presence of obesity and IR, there is an increased flux of FFAs livsr the liver. These FFAs are Antioxidant and liver health Nutritional support for speed and agility TG Antioxidamt lipid Antioxidanh leading to hepatic fat accumulation or undergo β-oxidation Antioxidznt oxidative Herbal arthritis treatments and the jealth pathway.
The damaged hepatocyte leads Safe lice treatment a further increase of Antioixdant signaling IL-1, TNFa, IL-6 and the recruitment of ilver and residual macrophages KCs.
All of these mechanisms can directly Polyunsaturated fats vs saturated fats the activation of HSCs, healrh major cell type Satiety promoting spices and herbs in extracellular ,iver deposition and liver fibrosis.
The bioactive compounds may exert beneficial effects on NAFLD development and progression by inhibiting Atnioxidant, β-oxidation of FFAs, inflammation, and HSCs activation.
In the cartoon, we have listed the food bioactives Optimized for voice search the Antioxidatn mechanisms by which they may improve liver damage in Ahtioxidant [ 1 healht.
The liver is made up of hepatocytes, Kupffer cells, liver sinusoidal endothelial cells, pit cells, and hepatic stellate cells HSC [ 4 ]. Activation of stellate cells by injury caused by many etiological factors healtg lead to cirrhosis, and it would mark Antioxdant end stage of livet fibrosis [ 5 ].
Oxidative stress has a vital part in liverr fibrosis and consequently hdalth [ 6 ], Sports nutrition supplements. Sleep quality enhancement this reason, using molecules with antioxidant properties has been proposed Thermogenic supplements for effective weight reduction a treatment for not only fibrosis but also oxidative stress-related cirrhosis.
Liver diseases are considered a major medical Antioxidamt worldwide. There livre known to be a large number of liver diseases caused by different insults. Furthermore, the disease type depends healthh lifestyle factors.
For livdr, the main causes of liver diseases are reported Antuoxidant be viral and adn infections in regions like Africa and Asia.
For Europe and America, alcohol consumption is thought to be the most important cause of this disease. However, nealth hepatitis has showed an increase in recent times in most Antioxidqnt the countries [ 7 ]. Lifestyle and unhealthy diet is the leading cause of liver diseases in almost all western countries.
Until today, no medication is approved for the treatment of this disease; however, improving diet habits and physical exercise works if the disease is not accompanied by inflammation. On the other hand, biologically active food compounds that regulate gene expressions in lipogenesis, fibrosis, and inflammation serve as good therapeutic means to ameliorate these pathological states observed in liver [ 1 ] Figure 1.
Oxidative stress is recognized as a disproportion between the production of free radicals FR and the antioxidant defenses [ 8 ]. Increased levels of prooxidants result in damage to the cell in terms of lipid peroxidation as well as oxidative DNA damage and thus protein damage [ 9 ].
One or more unelectrified FR atoms or molecules may be present as radical cations or radical anions. They are usually unstable and highly reactive because they can react with molecules and abstract electrons.
Oxygen can reduce and produce reactive oxygen species ROS with exciting electrons, secondary to the interaction of transition metals or by the addition of energy [ 910 ]. Oxidative stress causes fibrogenesis by increasing transforming cytokines including transforming grown factor-beta-1 TGFβ1interleukin-6 IL-6and tumor necrosis factor-alpha TNFα [ 3 ].
Disruption of the liver metabolism arises from increased quantity of ROS to amplified electron transfer in mitochondrial B-oxidation and increased expression and activity of Cyp2el that is from CYP family [ 11 ].
Intense production of Cyp2e1 is present because of much more consumption of ethanol which is produced by virtue of a lot of direct and indirect mechanisms [ 121314 ] Figure 2. Mechanisms of enhanced ROS production during hepatocyte damage.
Ethanol metabolism promotes strong ROS production in the ER by the inducible CYP. It impairs GSH import in the mitochondria, preventing ROS removal. It also impairs B-oxidation promoting lipid accumulation. Ethanol also reduced the autophagic removal of damaged cellular components.
Cells produce FR as a result of metabolic events; however, this is not the only source that can cause oxidative stress in body. The pollutants in the environment such as toxic chemicals as well as radiation cause a significant increase in amount of FR, ROS, and reactive nitrogen species RNS [ 10 ].
In the body, variety of different cell types and chemical reactions produce ROS, the most important metabolism is the cytochrome P metabolism and mitochondria-catalyzed electron transport reactions. Most of the inflammatory conditions are also responsible from ROS production, and important cell types in these processes are neutrophils, eosinophils, and macrophages [ 1617 ].
The chief molecule responsible for the reduction of oxygen in mitochondria is ubisemiquinone. Different tissues of mammals and different species of mammals have an enzyme called xanthine oxidase, an enzyme belonging to molybdenum, iron-sulfur, flavin hydroxylases that play an important role in the hydroxylation of purines by the oxidation of hypoxanthine to xanthine.
Resultant xanthine then oxidized to uric acid. Inflammation serves as another source of ROS generation. Arginine is reduced to citrulline in a five-electron oxidative reaction by nitric oxide synthases NOSs and this reaction gives rise to NO.
Immune cells can also produce NO in the oxidative burst during inflammation. NO can react with oxygen and water in an extracellular environment in order to form nitrate and nitrite anions. Antioxidants are molecules that can help prevent or delay oxidation of an oxidizable substrate when in low concentrations and they have a high affinity to FR [ 21 ].
Antioxidants play an important role to maintain health of the organism by scavenging FR by donating electrons to it. A lot of different molecules that have antioxidant activity have been identified. Different natural compounds have so far been studied extensively especially in liver diseases Table 1.
Curcumin, diferuloylmethane or 1,7-bis 4-hydroxymethoxyphenyl 1,6-hepadieno-3,5-dione is obtained from the rhizomes of Curcuma longa turmeric. Curcumin has many pharmacological properties as it is a strong antioxidant, antifibrogenic, anti-inflammatory, antimicrobial, and anticarcinogenic agent and it also aids in a wound healing [ 22 ].
The Food and Drug Administration FDA has classified turmeric as a safe substance and toxicity assays done on animals have shown curcumin to be safe even when used in high doses. On the other hand, prolonged high-dose intake of turmeric has been associated with incidences of hepatotoxicity in mice and rats [ 3 ].
Curcumin is known to have low bioavailability when administered orally. Arcaro et al. Even in the presence of piperine, antidiabetic and antioxidant activity of curcumin was not altered.
On the other hand, Sehgal et al. In acute and chronic liver injury, curcumin has been shown to have hepatoprotective effects [ 25 ]. InReyes-Gordillo et al. Additionally, curcumin reduces carbon tetrachloride CC1 4 -mediated oxidative stress inactivating the nuclear factor-kB NF-kB pathway.
A study by Jiao et al. Charoensuk et al. Curcumin also increases the activity of glutathione GSHsuperoxide dismutase SODcatalase CATglutathione peroxidase GPxand glutathione-S-transferase GST activity [ 2930 ]. Curcumin also interacts with enzymes or genes that are important in liver cirrhosis.
Hassan et al. Finally, in alcohol-induced liver damage, curcumin inhibits the activity of cytochrome P 2E1 Cyp2e1 and also its protein levels [ 32 ]. Resveratrol has effects on lipid metabolism, and it also has antioxidant, anti-inflammatory, anticarcinogenic, and antifibrogenic properties [ 34 ].
Resveratrol is metabolized to resveratrol sulfate, and in its low concentrations, it is converted into resveratrol glucuronide [ 36 ] by enzymes glucuronosyltransferase UGT or sulfotransferase ST [ 37 ].
InChávez et al. It also inhibited NF-kB translocation to the nucleus. Resveratrol, as an antioxidant, has protective effects against ethanol-induced lipid peroxidation, toxicity by acetaminophen APAPand oxidative stress in animal models of cholestasis [ 38 ].
Blocking OH group methylation showed that resveratrol and trimethylated resveratrol provide some degree of protection, but the latter one has a better protective effect [ 39 ]. Another hepatoprotection mechanism of resveratrol comes from its ability to activate genes related to antioxidant system or from its ability to inhibit enzymes.
A study by Cheng et al. Price et al. Zhu et al. Resveratrol has also been shown to inhibit the activity of Cyp2e1 in microsomes of rat liver [ 43 ].
Resveratrol also inhibited the activity of P isoform APAP-induced liver injury model [ 44 ] and activity of Cyp2e1 was also inhibited in diethylnitrosamine DEN -induced hepatocarcinogenesis model [ 45 ]. The only clinical study that was performed to determine the resveratrol hepatoprotective effect demonstrated that a mg resveratrol dose administrated for 12 weeks caused a significant reduction in inflammatory cytokines, serum cytokeratin, NF-kB activation, liver alanine aminotransferase ALTand hepatic steatosis when compared to the placebo group in patients with nonalcoholic fatty liver disease NAFLD [ 46 ].
Coffee is a mixture of several different molecules such as carbohydrates, vitamins, lipids, nitrogenous molecules, alkaloids, and phenolic compounds [ 47 ]. Caffeine, diterpene alcohols cafestol and kahweoland chlorogenic acid are the three major compounds found in coffee [ 48 ].
Coffee consumption has been linked to the reduction of several chronic diseases [ 49 ], probably due to the pharmacological properties that have antinecrotic, antifibrotic, anticholestatic, chemoprotective, and antioxidant functions [ 50 ].
Caffeine is the best-known active component of coffee, which is absorbed very rapidly once it has been taken orally 5 minreaching its peak blood levels after 30 min. When consumed in high amounts, it may produce some side effects.
: Antioxidant and liver health| Antioxidants in liver health | Eur J Epidemiol. Resultant xanthine then oxidized to uric acid. In Vivo. Singal AK, Jampana SC, Weinman SA. Effects of pomegranate and orange juice on antioxidant status in non-alcoholic fatty liver disease patients: A randomized clinical trial. |
| Latest news | Oxidative Sports nutrition supplements has been Sports nutrition supplements Antioxidwnt main contributor to liver injury. Ann N Antiozidant Acad Sci. Academic Content and Heart health initiatives Evaluation of This Article. Afr J Pharm Pharmacol. Article CAS Google Scholar Li S, Tan HY, Wang N, Zhang ZJ, Lao L, Wong CW, Feng Y. J Med Toxicol. Antioxidant properties of jujube honey and its protective effects against chronic alcohol-induced liver damage in mice. |
| REVIEW article | In the prospective study performed by Klatsky et al [ 81 ], the authors demonstrated an inverse coffee-cirrhosis relationship for the first time. In , Corrao et al [ 82 ] performed a study and identified a dose-response relationship between coffee intake and cirrhosis. The data show that the odds ratio for liver cirrhosis decreases from 1. Furthermore, the study showed that the caffeine per se did not show any relationship with cirrhosis by testing other drinks with caffeine. Although coffee is beneficial to liver health, the study failed to demonstrate a causative role of coffee in preventing liver injury. Thus, additional basic research and controlled prospective studies are needed. Arauz et al [ 72 ] in demonstrated that coffee has a beneficial effect on liver injury caused by chronic administration of thioacetamide TAA. Coffee prevented cholestasis and necrosis measured by the enzymes γ-glutamyl transpeptidase γ-GTP , alkaline phosphatase, and ALT. Human trials demonstrated the same results[ 83 ]. This inverse relationship was particularly high in heavy alcohol drinkers[ 84 ]. Conversely, liver injury inhibits caffeine metabolism, and people with liver diseases may experience adverse consequences after drinking coffee. Furthermore, it is important to distinguish between former coffee drinkers and nondrinkers in future epidemiological studies[ 71 , 85 ]. Moreno et al [ 86 ] in and Arauz et al [ 72 ] in demonstrated in murine models that coffee prevents experimental liver cirrhosis in two models of liver injury using carbon tetrachloride and thioacetamide. Both studies showed that coffee reduced the expression of the profibrogenic cytokine TGF-β. The study by Arauz et al [ 72 ] measured the expression of connective tissue growth factor CTGF , which has been suggested as an important downstream modulator of TGF-β that increases its profibrogenic response. This finding is consistent with the significant upregulation of extracellular matrix in fibrotic liver[ 72 ]. Cavin et al [ 87 ] have reported coffee as an inductor of GST, aldo-keto reductase, GSH, HO-1, glutathione-S-transferase P1, that are enzymes involved in the detoxification process. Also, they suggest that a possible mechanism of chemoprotection of coffee is by stimulation of Nrf2 pathway. In another study, coffee was able to elevate mRNA levels of NQO1 and glutathione-S-transferase A1 in liver and small intestine also, UDP-glucuronosyltransferase 1A6 and GCL catalytic GCLC were increased in small intestine. Further, the same group reported that this induction was bigger in mice possessing Nrf2 in contrast with Nrf2 knockout mice[ 88 ]. It is a flavonol found in natural products, especially in apples and onions[ 89 ]. Quercetin is known to have biological effects including chelation of heavy metals, anti-carcinogenic, cardioprotective, bacteriostatic, anti-inflammatory, and antioxidant properties[ 90 ], in addition to functioning as a hepatoprotective agent[ 91 ]. In , high purity quercetin used in foods was GRAS in the range of 0. Bors et al [ 92 ] in showed the characteristics that an antioxidant must have to exert an effective activity. These characteristics include the presence of ortho-dihydroxy or catechol groups in the B-ring, a 2,3-double bond of the C-ring, and OH substitution on positions 3 and 5 of the C-ring and A-ring, respectively[ 92 ]. The quercetin ring presents all of these features. After oral intake, quercetin is rapidly absorbed and peaks at approximately 30 min[ 94 ] before it is metabolized by glucuronidation and sulfation by the UGT and ST, respectively. These processes begin in the intestine, and the compounds are released into the lumen before conjugation in the liver by the same enzymes. However, other tissues such as the kidneys can also metabolize quercetin[ 94 - 97 ]. Quercetin has shown hepatoprotective properties in rats treated chronically with CCl 4 for 8 wk by preventing the expression of profibrogenic genes including TGF-β, CTGF, and collagen-1α Col-1α. Therefore, quercetin reduces the fibrogenic process and liver enzymes associated with a significant reduction of activated HSC and inhibition of NF-κB. Conversely, quercetin increased the gene expression and improved the activity of SOD and CAT, in addition to activating metalloproteinases 2 and 9 MMP2 and MMP9 [ 91 ]. Pavanato et al [ 98 ] in used the same hepatotoxin for 16 wk and observed that quercetin improves the hepatic liver enzymes AST, ALT, inducible NOS iNOS expression, and collagen content and reduces lipid peroxidation. In a study performed by Granado-Serrano et al [ ] in HepG2 cells, they found that quercetin modulated Nrf2 and p38, it was dependent on the concentration used and the time of exposure, quercetin rapidly activated Nrf2 by up-regulating its phosphorylation, consequently, translocation to the nucleus and binding to antioxidant response element ARE , also increased GSH content and expression of GPx. However, when the time of exposure is larger, this effect was blocked by quercetin which, in turn activated pMAPK via. Therefore suggesting that Nef2-ARE acts as a sensor and responds to a chemical. However, Tanigawa et al [ ] reported that quercetin possesses an enhanced effect in the ARE binding activity and Nrf2-mediated transcription activity in HepG2 cells. Moreover, quercetin apart from up-regulating expression of Nrf2 mRNA and protein, also stabilized Nrf2 protein inhibiting its proteasomal degradation and reduced the levels of kelch-like ECH-associated protein 1 Keap1 through the formation of a modified Keap1. On the other hand, a study performed by Ji et al [ ] showed that quercetin does not possesses an enhanced activity in mRNA expression of Nrf2 or Keap1. However, they suggested that quercetin could interact with Keap1 and fill the binding site of Nrf2 in Keap1, thus inhibiting its interaction and inducing the transcriptional activation of Nrf2. Quercetin has shown to suppress the activity of CYP2E1 when ethanol over activated it and induces HO-1 in hepatocytes[ ]. According with this findings, in a non-alcoholic steatohepatitis NASH model, quercetin was able to decrease by 2-fold CYP2E1 activity compared with NASH group[ ]. On the other hand, quercetin effect was inhibited by CYP2E1 compared with a control measuring by HPLC in rat liver microsomes[ ]. Currently, there are no clinical studies available on quercetin hepatoprotection[ ]. Silymarin has been reported as a safe compound in acute doses in animal models due to its lack of side effects. In contrast, in a clinical trial, thousands of patients suffered mainly mild gastrointestinal disorders by silymarin consumption[ ]. In other clinical trial, El-Kamary et al [ ] no side effects were reported in patients using mg of silymarin. After oral administration, the silymarin peak plasma concentration is reached at approximately h. The metabolites of silymarin are conjugated in the liver by UGT and ST phase II reactions [ ]. Among the hepatoprotective effects of silymarin, it is known that silybin, the major constituent of silymarin, has iron-chelating properties[ , ]. Silymarin has also been probed as iron chelator in children with β-thalassemia with iron overload[ ]. In a study performed by Najafzadeh et al [ ], they suggest that hepatoprotective effect of silymarin in iron-overload induced hepatotoxicity was due to an iron-chelator activity but no studies have been made proving the chelating properties per se of silymarin in liver diseases. Silymarin has hepatoprotective properties against several hepatotoxins such as CCl 4. Silymarin can prevent oxidative stress, fibrosis, cirrhosis, and lipid peroxidation by modulating the content of phosphatidylethanolamine[ ]. However, silymarin does not reverse well-established cirrhosis[ - ]. Kim et al [ ] showed that silymarin increases nuclear translocation of Nrf2 in activated HSC, however, expression of other molecules related to a detoxifying effect have not been measured. Also, silymarin has been reported to increase the activity of antioxidant enzymes like SOD, GPx[ ] and CAT[ ]. A clinical trial examining silymarin in a complex with phosphatidylcholine found reduced levels of the liver enzymes, ALT and γ-GTP, and serum bilirubin levels in a dose-dependent manner in patients with hepatitis caused by virus infection or alcohol abuse[ ]. Another clinical study showed similar results when silymarin was administered alone[ ]. In patients with cirrhosis, silymarin administration for 41 mo significantly increased the survival rate compared to a placebo group[ ]. However, in the study performed by Parés et al [ ], silymarin showed no effect on survival rate in the clinical course in alcoholic patients with liver cirrhosis. Naringenin is a flavanone found in citrus fruits and tomatoes[ ]. Naringenin has many pharmacological properties including hypolipidemic, anti-hypertensive, anti-inflammatory, antioxidant and anti-fibrotic functions[ ]. Flavonoids are absorbed in the aglycone form rather than in the glycoside form like quercetin. The glycoside form of naringenin is cleaved in the small intestine before absorption, which results in sulfate and glucuronide metabolites in the small intestine wall and liver[ , ] by UGT and ST. Chtourou et al [ ] found that naringenin prevents the depletion of SOD, CAT, GPx and GSH. Conversely, naringenin also prevented the increase in lipid peroxidation, ALT and AST. Additionally, expression of the following genes was also affected in an NAFLD rat model induced by a high cholesterol diet: pro-inflammatory cytokines TNF-α, IL-6, and IL-1β, EGF-like module-containing mucin-like hormone receptor-like 1, iNOS, NF-κB, MMP2 and MMP9[ ]. Similar results were obtained by Yen et al [ ] using naringenin alone and a naringenin-loaded nanoparticle system NARN. Both treatments exhibited antioxidant and hepatoprotective activities. The treatments also inhibited the activation of caspases 3, and 8. However, NARN was more effective as a hepatoprotector and antioxidant than free naringenin because it also inhibits caspase 9 during CCl 4 -induced hepatotoxicity in rats[ ]. In a study performed by Goldwasser et al [ ] it was found that naringenin activates peroxisome proliferator-activated receptor alpha PPARα , then decreasing the levels of very low density lipoprotein production without causing lipid accumulation in hepatocytes, in a hepatitis C virus HCV model. Similar results were found by Cho et al [ ], who have shown that naringenin intake causes a significant depletion in the amount of total triglycerides and cholesterol in plasma and liver of rats. Also, naringenin-fed animals showed an increment in PPARα protein expression in liver. Goldwasser et al [ ] found that the flavonoid regulates the activity of PPARγ and liver X receptor alpha LXRα , by activating the ligand-binding domain of PPARα and PPARγ, while inhibiting LXRα, thus modulating different genes related to fatty acid oxidation and lipogenesis. Han et al [ ], found that a pretreatment with naringeninO-glucoside increased NQO1, ERK and phosphorylation and translocation of Nrf2 to the nucleus in H9c2 cardiomyocytes, as well as, upregulating the mRNA expression of GCLC and GCL modifier[ ], thus inducting endogenous antioxidant enzymes. Similar findings was reported by Esmaeili et al [ ], they showed that naringenin was capable of attenuating CCl 4 -induced liver injury by downregulating TNF-α, iNOS and cyclo-oxigenase-2, both protein and mRNA, as well as by increasing Nfr2 and HO-1 expression. Motawi et al [ ] suggested that naringenin could be another example of CYP2E1 inhibitor, they probed it, in rat liver microsomal assay in co-administration with simvastin, and such inhibition of CYP2E1 is another via to improve antioxidant defenses[ ]. There are currently no studies available in human hepatic disorders[ ]. Camellia sinensis, also known as green tea, is a worldwide consumed beverage. Its beneficial effects on health are due in part to its antioxidant, anti-inflammatory, anti-arthritic and anti-angiogenic effects. Flavonoids like quercetin, kaempferol and myricetin; methylxanthine alkaloids such as caffeine, theophylline and theobromine, and phenolic acids gallic acid, chlorogenic acid and caffeic acid [ , ]. L-theanine chemical structure is similar to glutamic acid, the latest is a precursor of GSH. Studies have shown that L-theanine protects the cell maintaining the levels of GSH in cancer and neurotixicity diseases[ ]. Nevertheless, hepatotoxicity has been attributed to the intake of green tea when it is used for weight control; furthermore[ ]. Pérez-Vargas et al [ ] found that L-theanine prevented the increased expression of NF-κB and down-regulated IL-1β and IL-6 and the cytokines TGF-β and CTGF induced by carbon tetrachloride. Moreover, the expression of the corresponding mRNAs decreased accordingly. On the other hand, L-theanine promoted the expression of IL and the fibrolytic enzyme metalloproteinase 13 MMP In a study performed by Yu et al [ ] they have shown that EGCG ameliorates liver inflammation, necrosis and fibrosis and suppressed the expression of TNF-α, IL-1β, TGF-β, MMP9, α-SMA, and Col-1α1. Similar results were obtained in HSC cell line LX-2, where EGCG was capable of suppressing TGF-β1, Col-1α1, MMP2, MMP9, TIMP1, and α-SMA. Moreover, Bin Dajem et al [ ] used the aqueous extract of green tea in a Schistosoma mansoni-infected mice model to investigate its effect on the oxidative stress, antioxidant system and liver pathology induced by the parasite. They found that green tea extract suppressed the oxidative stress by decreasing the lipid peroxides. However, failed to enhance the antioxidant system and to reverse alterations in the liver such as necrosis. In a cisplatin-induced nephrotoxicity model in rats, EGCG increased the levels of Nfr2, HO-1, SOD, CAT, GPx and GSH[ ]. In clinical trials, green tea has shown protective effects against various kinds of cancers, including premalignant prostate, esophageal, colon, rectum and pancreatic cancers[ ]. Nevertheless, in hepatocellular carcinoma, green tea did not have any protective effect[ ]. In a study performed by Halegoua-De Marzio et al [ ] they have shown, after a single oral dose of green tea mg , in patients with cirrhosis induced by HCV, that it is safe and well tolerable by all patients, therefore suggesting the use of green tea in the treatment of cirrhosis in the future. However, more clinical studies related to the beneficial effects on liver diseases are needed. The information shown above represents some of the antioxidants uses in different kind of experiments in animals and clinical trials. However, it is difficult to say which of these antioxidants possess the best hepatoprotective properties since they have different chemical structures and antioxidant potency, then its scavenger capacity is not the same. Moreover, other parameters need to be considered, such as the bioavailability, and pharmacokinetics. We focus our hepatoprotective ranking mainly based on the chemical structure showed in Figure 1. We suggest that silymarin has the best hepatoprotective effect because is a mixture of flavonolignans including silybin, isosilybin, silydianin, silychristin, isosilychristin and the flavonoid taxifolin. In addition, silybinin is composed of 2 diasteroisomeric compounds silybin A and silybin B in a ratio[ ]. Flavonoids in its structure have different forms to stabilize FR including hydroxyl phenolic groups, double bonds and sometimes a catechol group[ 92 ]. Therefore, silymarin seems to be the best choice referred to hepatoprotective effect. Green tea is another mixture of polyphenols, as mentioned earlier, containing catechins, flavonoids and methylxanthine alkaloids. Nevertheless its data referred to hepatoprotection is lower than silymarin, for these reason we decided ranked green tea in the second place. The antioxidant property of EGCG is related of its hydroxyl phenolic groups, that maybe acts mainly from hydrogen atoms transfer or single electron transfer reactions. This groups are presented in the B- and D-rings of EGCG[ ]. Quercetin, as mentioned above, is a flavonoid that have all the elements to exert a magnificent hepatoprotective effect related to its structure showing a catechol group in the B ring, substitution of hydroxyl phenolic groups in the A and C ring and a double bond in the position of the C ring[ 92 ]. Curcumin has been used in the treatment of experimental liver diseases since and shows a powerful antioxidant capacity and immunomodulatory properties. However, it does not have the same structure of flavonoids, showing two hydroxyl phenolic groups and a heptadiene linkage two methoxyphenol rings. Ak et al [ ] suggest that keto form of curcumin, the heptadienone linkage between the two methoxyphenol rings, contain a carbon atom that can donate a hydrogen, therefore, stabilizing FR. We considered that its capacity of stabilize FR is lower than quercetin. Resveratrol possesses hydroxyl phenolic groups and a system of conjugated double bonds that can donate electrons to FR. Resveratrol has two phenolic rings: monophenol and diphenol. Gülçin[ ] suggests that subtraction of hydrogen atom is easily in the monofenol ring. Naringenin is another flavonoid with lower antioxidant capacity than quercetin, shows a hydroxyl phenolic group in its structure in the A ring. However, it does not have the catechol group or the double bond[ 92 ]. Also, Cao et al [ ] suggest that in flavonoids the hydroxyl substitution is relevant in the ORAC OH. Caffeine has double bonds in its structure. Chu et al [ ] reported that pure caffeine had very low ORAC OH. values, whereas, crude caffeine had higher values than pure caffeine. We considered that caffeine has the lowest antioxidant activity of all the compounds showed; therefore coffee has the lowest antioxidant capacity. Investigations of antioxidants show that compounds in food are candidates for the treatment of several diseases because they improve the antioxidant system in the body, especially when the disease involves oxidative stress. This review describes antioxidants that can be investigated for experimental and clinical trials and will be used for the treatment of liver diseases such as liver cirrhosis. Curcumin, quercetin, and naringenin are effective in the treatment of experimental liver injury, and they can be studied in clinical trials. Green tea have been shown to protect against different kinds of cancer in clinical trials, except in hepatocellular carcinoma. Conversely, there are no clinical trials investigating resveratrol, coffee, and silymarin. However, the data are poor or contradictory, and it is necessary to perform more clinical trials to use these antioxidants for the treatment of liver diseases in patients. The authors express their gratitude to Martha Noyola and Maria Teresa García for their careful review of the manuscript. Sael Casas-Grajales was a fellow of Conacyt Home English English 简体中文. Sign In BPG Management System F6Publishing-Submit a Manuscript F6Publishing-世界华人消化杂志在线投稿 RCA Management System. Advanced Search. About the Journal Submit a Manuscript Current Issue Search All Articles. This Article. Abstract Core Tip Full Article with Cover PDF Full Article WORD Full Article HTML PubMed Central PubMed CrossRef Google Scholar Similar Articles 9 Timeline of Article Publication 1 Authors Evaluation 3 Article Quality Tracking 0 Reference Citation Analysis 1. Academic Content and Language Evaluation of This Article. Answering Reviewers PDF Peer-Review Report PDF. CrossCheck and Google Search of This Article. Scientific Misconduct Check PDF. Academic Rules and Norms of This Article. Copyright Assignment PDF. Citation of this article. Casas-Grajales S, Muriel P. Antioxidants in liver health. World J Gastrointest Pharmacol Ther ; 6 3 : [PMID: DOI: Corresponding Author of This Article. Pablo Muriel, PhD, Department of Pharmacology, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, D. pmuriel cinvestav. Checklist of Responsibilities for the Scientific Editor of This Article. Scientific Editor Work List PDF. Publishing Process of This Article. Research Domain of This Article. Article-Type of This Article. Open-Access Policy of This Article. This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial CC BY-NC 4. Times Cited Counts in Google of This Article. Number of Hits and Downloads for This Article. Total Article Views All Articles published online. Times Cited of This Article. Times Cited Journal Information of This Article. Publication Name. World Journal of Gastrointestinal Pharmacology and Therapeutics. Baishideng Publishing Group Inc, Koll Center Parkway, Suite , Pleasanton, CA , USA. Review Open Access. Copyright ©The Author s Published by Baishideng Publishing Group Inc. All rights reserved. World J Gastrointest Pharmacol Ther. Aug 6, ; 6 3 : Published online Aug 6, doi: Sael Casas-Grajales , Pablo Muriel. Sael Casas-Grajales, Pablo Muriel, Department of Pharmacology, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, México City , México. Conflict-of-interest statement : The authors declare that there are no conflicts of interest in the present work. Open-Access : This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. Correspondence to : Pablo Muriel, PhD, Department of Pharmacology, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, D. Received: February 4, Peer-review started : February 6, First decision : April 10, Revised: June 4, Accepted: June 18, Article in press : June 19, Published online: August 6, Key Words: Antioxidant , Oxidative stress , Naringenin , Quercetin , Curcumin , Resveratrol , Silymarin , Coffee , Liver diseases. Citation: Casas-Grajales S, Muriel P. Table 1 Different antioxidants found in food clinical effects and relevance. Open in New Tab Full Size Figure Download Figure. Figure 1 Comparison between hepatoprotective effect-related antioxidant capacities. For silymarin we show the structure of silybin, in the case of green tea the structure of - -epigallocatechingallate, and in the case of coffee the structure of caffeine. P- Reviewer: Acuna-Castroviejo D S- Editor: Ji FF L- Editor: A E- Editor: Liu SQ. Muriel P. Some experimental models of liver damage. Hepatotoxicity: From genomics to in vitro and in vivo models. West Sussex, England: Wiley ; Cytokines in liver diseases. 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Schweizerische Zeitschrift für Medizin und Traumatologie. Written By Sila Appak-Baskoy, Mustafa Cengiz, Ozgun Teksoy and Adnan Ayhanci. Continue reading from the same book View All. Chapter 1 The Effect of Preharvest Factors on Fruit and Nutr By Toktam Taghavi, Rafat Siddiqui and Laban K. Rutto downloads. Chapter 2 Fruit Physiology and Postharvest Management of Str By Venkata Satish Kuchi and Ch. Sai Ratna Sharavani downloads. Chapter 3 Physical, Chemical and Processing Postharvest Tech A few examples include grapefruit, blueberries, cranberries, fatty fish, olive oil, and cruciferous vegetables like broccoli or Brussels sprouts. Consuming certain foods in excess is associated with an increased risk for NAFLD. You should try to limit your intake of the following foods to help keep your liver healthy:. In particular, some studies in humans and animals suggest that green tea , coffee , and beetroot juice may help promote liver function. The 11 foods listed above have demonstrated beneficial effects on the liver. These benefits include the following:. Incorporating these foods into your diet is a natural and healthy way to help keep your liver functioning at its best. Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available. VIEW ALL HISTORY. This article is based on scientific evidence, written by experts and fact checked by experts. Our team of licensed nutritionists and dietitians strive to be objective, unbiased, honest and to present both sides of the argument. This article contains scientific references. The numbers in the parentheses 1, 2, 3 are clickable links to peer-reviewed scientific papers. The foods you consume are important for your liver health. This is especially true if you have a liver condition that can affect how your liver…. The gallbladder is a sensitive organ, and maintaining a diet full of nutrient-dense foods helps keep it healthy. There are many types of liver disease, ranging from those that are treatable to those that require a liver transplant. Learn about symptoms, causes…. Many people are interested in herbal supplements to support their liver health. Here are 10 of the best herbs for your liver, including benefits and…. Hepatic encephalopathy is a decline in brain function that occurs as a result of liver disease. In this condition, your liver cannot adequately remove…. Prednisone can increase your risk of NAFLD. If you already have or are at high risk of NAFLD, you might need to take alternative medications. The gamma-glutamyl transpeptidase test measures the amount of an important liver enzyme in your blood. Read on to learn more about the test and what…. Learn how jaundice appears in people with darker skin tones and what symptoms to look out for. Bile duct cysts are areas of dilation within the biliary system that connects the liver, gallbladder, and small intestine. VBDS is a rare but serious medical condition that affects bile ducts in your liver. It's usually caused by certain medical conditions, medications…. A Quiz for Teens Are You a Workaholic? How Well Do You Sleep? Health Conditions Discover Plan Connect. Nutrition Evidence Based 11 Foods That Are Good for Your Liver. Medically reviewed by Katherine Marengo LDN, R. Foods for liver health Important nutrients Other healthy habits FAQs Bottom line Diet plays a key role in maintaining liver health. What are the best foods to eat for your liver? What makes food good for your liver? What else can you do to keep your liver healthy? Frequently asked questions. The bottom line. How we reviewed this article: Sources. Healthline has strict sourcing guidelines and relies on peer-reviewed studies, academic research institutions, and medical associations. We avoid using tertiary references. You can learn more about how we ensure our content is accurate and current by reading our editorial policy. Oct 30, Written By Taylor Jones, Rachael Ajmera, MS, RD. Medically Reviewed By Katherine Marengo, LDN, RD. Jun 30, Written By Taylor Jones, Rachael Ajmera, MS, RD. |
Thank you Sports nutrition supplements livr nature. Antiixidant are using a Sports nutrition supplements Antoxidant with Thyroid Supportive Herbs support for CSS. To obtain ajd best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Oxidative stress has been considered the main contributor to liver injury. Dietary antioxidants would be expected to improve liver function.
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