Alcohol-induced Oxidative Injury Research Articles

Amelioration activity of the high bioaccessible chrysanthemum (Gongju) phenolics on alcohol-induced oxidative injury in AML-12 cells

The main bioavailable phenolics from of Gongju (GJ) and their mechanism for hepato-protection remain unclear. To select the GJ phenolics with high bioavailability, chrysanthemum digestion and Caco-2 cells were used and their hepato-protective potential were examined by using AML-12 cells. The digestive recovery and small intestinal transit rate of the main phenolic compounds ranged from 28.52 to 69.53% and 6.57% ∼ 15.50%, respectively. Among them, chlorogenic acid, 3,5-dicaffeoylquinic acid, and 1,5-dicaffeoylquinic acid, showed higher small intestinal transit rates and digestive recoveries. Furthermore, we found that by increasing intracellular Catalase (CAT) and Superoxide dismutase (SOD) viability and lowering Malondialdehyde (MDA) level (P < 0.05), 3,5-dicaffeoylquinic acid significantly mitigated the oxidative damage of AML-12 liver cells more than the other two phenolics. Our results demonstrated that 3,5-dicaffeoylquninic acid was the primary phenolic compounds in GJ that effectively reduced liver damage, providing a theoretical basis for the development of GJ as a potentially useful resource for hepatoprotective diet.

Sucrose-induced abiotic stress improves the phytochemical profiles and bioactivities of mung bean sprouts

This study aimed to examine the impact of sucrose treatment on the growth conditions, dietary nutritional quality, and biological activities of mung bean sprouts. Mung bean seeds were sprouted with solutions containing different sucrose concentrations (10, 20, and 30 g/L). The application of exogenous sucrose significantly decreased the height and fresh weight of mung bean sprouts. However, the sucrose-treated sprouts contained more polyphenols, flavonoids, γ-aminobutyric acid, phytosterols, and vitamins. The antioxidant capacities were also significantly higher in the sucrose-treated sprouts than in the control sprouts. The sprouts treated with 2–3 % sucrose showed markedly improved FFA-induced insulin resistance and alcohol-induced oxidative injury in HepG2 cells. Taken together, the elicitor application of sucrose at 3 % during mung bean sprouting could be an effective strategy to improve the dietary phytochemical composition and provide potential health benefits.

Jujube (Ziziphus jujuba Mill.) Protects Hepatocytes against Alcohol-Induced Damage through Nrf2 Activation.

This study aimed at evaluating the cytoprotective activity of jujube water extract (JWE) against alcohol-induced oxidative stress via the activation of the Nrf2 pathway in HepG2 cells. JWE had various phenolic compounds, and the vanillic acid content was the highest in the extract. To determine the cytoprotective effect of JWE against alcohol-induced damage, hepatocytes were treated with JWE and 3% ethanol. JWE (100 μg/mL) markedly increased cell viability by approximately 100% in a dose-dependent manner. Moreover, JWE attenuated the production of malondialdehyde, reactive oxygen species, aspartate, and alanine aminotransferase and the depletion of glutathione. Moreover, JWE enhanced the expression of antioxidant defense enzymes including heme oxygenase-1, NADPH quinone oxidoreductase 1, and γ-glutamate-cysteine ligase catalytic against alcohol-induced oxidative damage in hepatocytes via the activation of Nrf2. Taken together, JWE possesses the protective effect against alcohol-induced oxidative injury in hepatocytes through the upregulation of the Nrf2 signaling pathway. Therefore, jujube fruit might have the potential to improve alcohol-related liver problems.

Antioxidant activity and hepatoprotective effect of Schizandra chinensis Baill. Extracts containing active components in alcohol-induced HepG2 cells

The antioxidant activities and hepatoprotective effects of Schizandra chinensis Baill. extracts (SCE) were evaluated. The contents of the active components schisandrin, schisandrin C, gomisin A, and gomisin N in SCE were 8.802±1.390, 1.011±0.203, 0.954±0.191, and 3.351±0.829 mg/g, respectively. The antioxidant activity of SCE was measured based on the DPPH free radical scavenging activity and the superoxide dismutase (SOD)-like activity. The IC50 values for the DPPH radical scavenging activity and SOD-like activity were 18.1 and 44.2mg/mL, respectively. The protective effect of SCE against alcohol-induced oxidative injury in HepG2 cells was investigated. Cells pretreated with SCE (100–400 μg/mL) showed an increased resistance to oxidative stress in a dose-dependent manner. Expressions of Bcl-2 and pro-caspase-3 proteins were induced by SCE in HepG2 cells. SCE can be useful for management of antioxidant and hepatoprotective effects.

Studies onIn VivoFunction of Peroxiredoxins in Knockout Mice

appearance and fertile, however showed several pathophysiological disorders. Using the mice, we found that Prx II is an essential antioxidant enzyme that prevents oxidative stress in erythropoiesis, protects against endotoxin-induced lethal shock, regulates platelet-derived growth factor signaling and angiogenesis, inhibits cellular senescence, preserves cognitive function against age-linked hippocampal oxidative damage and exacerbates tumorigenesis in a liver cancer mouse model. The Prx I-/- mice were also healthy in appearance and fertile like Prx II -/- mice. With the mice, we found that Prx I suppresses K-ras-driven lung tumorigenesis by opposing the redox-sensitive extracellular-signal-regulated kinase/ cyclin D1 pathway and plays concerted action with sulfiredoxin in preventing against al cohol-induced oxidative injury in the mouse liver. The results obtained suggest that Prx I and II are essential antioxidant enzymes for maintaining redox homeostasis in mice.

Depression by a Green Tea Extract of Alcohol-Induced Oxidative Stress and Lipogenesis in Rat Liver

We determined the effects of a green tea extract with 36% alcohol on the blood alcohol content, oxidative stress, lipogenesis, inflammation and liver function of female Wistar rats. Tea alcohol significantly decreased the O₂⁻, H₂O₂ and HOCl amounts via catechins and not caffeine. Thirty days of alcohol gavage improved the level of reactive oxygen species (ROS) in the liver, bile and blood, increased the 4-hydroxynonenal-protein adducts, Kupffer cell infiltration and lipid accumulation in the liver, and elevated the plasma alanine aminotransferase level. A western blot analysis showed reduced expression of the oxidative enzymes (CYP2E1 and NADPH oxidase p47phox protein) and lipogenic enzymes (SREBP-1c and fatty acid synthase) in the alcohol-treated liver. Tea alcohol significantly attenuated these elevated parameters. We conclude that the green tea extract in alcohol efficiently reduced the amounts of O₂⁻, H₂O₂ and HOCl primarily due to the catechin content, and not caffeine. The developed tea liquor attenuated alcohol-induced oxidative injury and lipogenesis in the liver by the synergetic action of catechins and caffeine.

Concerted Action of Sulfiredoxin and Peroxiredoxin I Protects Against Alcohol-Induced Oxidative Injury in Mouse Liver σ

Peroxiredoxins (Prxs) are peroxidases that catalyze the reduction of reactive oxygen species (ROS). The active site cysteine residue of members of the 2-Cys Prx subgroup (Prx I to IV) of Prxs is hyperoxidized to cysteine sulfinic acid (Cys-SO(2) ) during catalysis with concomitant loss of peroxidase activity. Reactivation of the hyperoxidized Prx is catalyzed by sulfiredoxin (Srx). Ethanol consumption induces the accumulation of cytochrome P450 2E1 (CYP2E1), a major contributor to ethanol-induced ROS production in the liver. We now show that chronic ethanol feeding markedly increased the expression of Srx in the liver of mice in a largely Nrf2-dependent manner. Among Prx I to IV, only Prx I was found to be hyperoxidized in the liver of ethanol-fed wildtype mice, and the level of Prx I-SO(2) increased to ≈30% to 50% of total Prx I in the liver of ethanol-fed Srx(-/-) mice. This result suggests that Prx I is the most active 2-Cys Prx in elimination of ROS from the liver of ethanol-fed mice and that, despite the up-regulation of Srx expression by ethanol, the capacity of Srx is not sufficient to counteract the hyperoxidation of Prx I that occurs during ROS reduction. A protease protection assay revealed that a large fraction of Prx I is located together with CYP2E1 at the cytosolic side of the endoplasmic reticulum membrane. The selective role of Prx I in ROS removal is thus likely attributable to the proximity of Prx I and CYP2E1. The pivotal functions of Srx and Prx I in protection of the liver in ethanol-fed mice was evident from the severe oxidative damage observed in mice lacking either Srx or Prx I.

Antioxidant nutrients and alcohol

Alcohol is a constituent of the diet that is generally taken in on a voluntary basis. The amount and type of alcohol consumed along with the frequency of alcohol consumption can vary tremendously and can have divergent effects on an organism. Animal models have been developed to investigate the mechanisms by which both acute alcohol administration and chronic alcohol consumption affect the various organ systems of the body. The deleterious effects of alcohol, at least partly involve alcohol induced oxidative injury that has been documented by measurement of oxidant radicals, alterations in oxidant/antioxidant balance and oxidant induced changes in cellular proteins and lipids. In addition, evidence for alcohol-induced oxidant injury comes from studies in which pretreatment with antioxidants such as vitamin E, vitamin C, and agents that enhance antioxidant capacity attenuate alcohol induced effects. The susceptibility of tissues to alcohol-induced injury is related to their function and the method by which they are exposed to alcohol. For example, the stomach and liver are exposed to the highest concentrations upon ingestion and absorption of alcohol. The liver is also the major organ for metabolism, and with chronic alcohol use, P450 2E1 is induced. This enzyme activity however, adds additional oxidative stress to the liver. Although antioxidants can attenuate alcohol-induced injury, there is no one antioxidant that protects all organs during all modes of exposure. In addition, more studies are needed to determine if administration of antioxidants after alcohol exposure can reverse alcohol induce tissue damage. This review will summarize results from experiments in which alcohol has been delivered for a short time (acute) or prolonged period (chronic); in vivo or in vitro; at physiologic doses or at supraphysiologic doses. The effects of alcohol on various tissues will be presented and finally, the contribution of oxidant injury to alcohol induced tissue damage will be discussed.

INTERACTION OF EXERCISE TRAINING WITH ETHANOL AND THEOPHYLLINE ON CARDIAC ANTIOXIDANT DEFENSE SYSTEM IN RATS

Earlier studies from our laboratory have shown that exercise training for 6.5 to 10 weeks up-regulated the cardiac antioxidant system and attenuated alcohol-induced oxidative injury in rat heart. Since many individuals perform regular exercise and also consume alcoholic and/or methylxanthine containing beverages, therefore, the objective of this study was to investigate the effects of exercise training (Ex) and its interaction with chronic low dose ethanol (Et) and theophylline (Th) administration on cardiac antioxidant defense system in rats. Male Fisher-344 rats were divided into five different groups and treated as follows: (1) Sedentary Control; (2) Exercise; (3) Ex + Et (1g/kg, p.o.); (4) Ex + Th (1.7x10–6 moles/kg, i.p.); and (5) Ex + Et + Th. The animals were treated with the drugs and exercised on a treadmill for 6.5 weeks, and physiological parameters such as respiratory exchange ratio (RER), time to reach maximal oxygen consumption (VO2max time), heart rate and blood pressure were recorded every week. The rats were sacrificed 24 hours after the last treatments and hearts were isolated. The results showed a significant effect over time, including a significant linear trend for RER, VO2max time and blood pressure. Total SOD and GSH-Px activities significantly increased (119% and 132% of control) in the heart of Ex plus Et group. Theophylline blocked cardiac SOD and GSH-Px activities induced by Ex and Et. The ratio of GSH-Px/SOD significantly decreased (64% of control) in Ex plus Et plus Th group. It is concluded that theophylline modified the cardiac antioxidant system induced by ethanol and exercise training, which in turn influenced the physiological parameters in rats. Supported by AHA-IL Affiliate 9708751 A

Influence of Sex Hormonal Status on Alcohol-Induced Oxidative Injury in Male and Female Rat Liver

Influence of Sex Hormonal Status on Alcohol-Induced Oxidative Injury in Male and Female Rat Liver

Influence of Sex Hormonal Status on Alcohol‐Induced Oxidative Injury in Male and Female Rat Liver

Oxidative stress contributes to the development of liver injury after chronic alcohol intake. Women exhibit greater sensitivity to alcohol-induced liver disease than do men. The aim of the study was to determine the relationship between the sex hormone status of male and female rats and the degree of alcohol-induced oxidative stress in the liver. Male and female rats were pair-fed a liquid diet that contained 36% of their total daily calories as ethanol (EtOH group) or maltose (control group). Blood and liver samples were collected at the end of 8 weeks of diet. Male EtOH rats experienced a reduction in plasma testosterone (T) and an increase in estradiol (E2) levels, with an increase in their calculated E2/T ratio with respect to their controls. Malonaldehyde (MDA) levels, an index of lipid peroxidation, and protein carbonyl content, an index of protein oxidation, in the liver were greater among the EtOH groups in females than in males. In males, an inverse correlation was found between hepatic MDA and circulating T levels, and a direct correlation was disclosed between MDA and estradiol levels. In addition, the hepatic histopathological score correlated inversely with the plasma T levels and directly with the calculated E2/T ratio, an index of feminization. Alcohol-induced oxidative injury, which contributes to hepatic injury in both male and female rats, is enhanced in females compared with males. A role for plasma T levels in protecting male rat liver from ethanol-induced oxidative injury can be hypothesized.