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Liposomal Antioxidants for Protection against Oxidant-Induced Damage  [PDF]
Zacharias E. Suntres
Journal of Toxicology , 2011, DOI: 10.1155/2011/152474
Abstract: Reactive oxygen species (ROS), including superoxide anion, hydrogen peroxide, and hydroxyl radical, can be formed as normal products of aerobic metabolism and can be produced at elevated rates under pathophysiological conditions. Overproduction and/or insufficient removal of ROS result in significant damage to cell structure and functions. In vitro studies showed that antioxidants, when applied directly and at relatively high concentrations to cellular systems, are effective in conferring protection against the damaging actions of ROS, but results from animal and human studies showed that several antioxidants provide only modest benefit and even possible harm. Antioxidants have yet to be rendered into reliable and safe therapies because of their poor solubility, inability to cross membrane barriers, extensive first-pass metabolism, and rapid clearance from cells. There is considerable interest towards the development of drug-delivery systems that would result in the selective delivery of antioxidants to tissues in sufficient concentrations to ameliorate oxidant-induced tissue injuries. Liposomes are biocompatible, biodegradable, and nontoxic artificial phospholipid vesicles that offer the possibility of carrying hydrophilic, hydrophobic, and amphiphilic molecules. This paper focus on the use of liposomes for the delivery of antioxidants in the prevention or treatment of pathological conditions related to oxidative stress. 1. Introduction Oxidative stress (OS) is defined as an imbalance between the production of reactive oxygen species and antioxidant defenses that can lead to cellular and tissue damage [1–8]. A potential pharmacological strategy in preventing or treating oxidant-induced cellular and tissue damage involves the use of appropriate antioxidants. Antioxidants are substances which are able to prevent, delay, or remove oxidative damage to a molecule [4, 9–11]. Yet, their efficacy is hindered with challenges such as poor solubility, inability to cross cell-membrane barriers, extensive first-pass metabolism, and rapid clearance of antioxidants from cells [12, 13]. To improve the pharmacological and pharmacokinetic properties of antioxidants, diverse systems such as antioxidant chemical modifications and coupling to affinity carriers, micelles, and liposomes are being developed [4, 13–18]. This paper focus on the use of liposomes for the delivery of antioxidants in the prevention or treatment of several pathological conditions linked to oxidative stress. Liposomes are artificial vesicles consisting of an aqueous core enclosed in one or more
Butyrate and Propionate Protect against Diet-Induced Obesity and Regulate Gut Hormones via Free Fatty Acid Receptor 3-Independent Mechanisms  [PDF]
Hua V. Lin, Andrea Frassetto, Edward J. Kowalik Jr, Andrea R. Nawrocki, Mofei M. Lu, Jennifer R. Kosinski, James A. Hubert, Daphne Szeto, Xiaorui Yao, Gail Forrest, Donald J. Marsh
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035240
Abstract: Short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate, are metabolites formed by gut microbiota from complex dietary carbohydrates. Butyrate and acetate were reported to protect against diet-induced obesity without causing hypophagia, while propionate was shown to reduce food intake. However, the underlying mechanisms for these effects are unclear. It was suggested that SCFAs may regulate gut hormones via their endogenous receptors Free fatty acid receptors 2 (FFAR2) and 3 (FFAR3), but direct evidence is lacking. We examined the effects of SCFA administration in mice, and show that butyrate, propionate, and acetate all protected against diet-induced obesity and insulin resistance. Butyrate and propionate, but not acetate, induce gut hormones and reduce food intake. As FFAR3 is the common receptor activated by butyrate and propionate, we examined these effects in FFAR3-deficient mice. The effects of butyrate and propionate on body weight and food intake are independent of FFAR3. In addition, FFAR3 plays a minor role in butyrate stimulation of Glucagon-like peptide-1, and is not required for butyrate- and propionate-dependent induction of Glucose-dependent insulinotropic peptide. Finally, FFAR3-deficient mice show normal body weight and glucose homeostasis. Stimulation of gut hormones and food intake inhibition by butyrate and propionate may represent a novel mechanism by which gut microbiota regulates host metabolism. These effects are largely intact in FFAR3-deficient mice, indicating additional mediators are required for these beneficial effects.
Antioxidants Keep the Potentially Probiotic but Highly Oxygen-Sensitive Human Gut Bacterium Faecalibacterium prausnitzii Alive at Ambient Air  [PDF]
M. Tanweer Khan, Jan Maarten van Dijl, Hermie J. M. Harmsen
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0096097
Abstract: The beneficial human gut microbe Faecalibacterium prausnitzii is a ‘probiotic of the future’ since it produces high amounts of butyrate and anti-inflammatory compounds. However, this bacterium is highly oxygen-senstive, making it notoriously difficult to cultivate and preserve. This has so far precluded its clinical application in the treatment of patients with inflammatory bowel diseases. The present studies were therefore aimed at developing a strategy to keep F. prausnitzii alive at ambient air. Our previous research showed that F. prausnitzii can survive in moderately oxygenized environments like the gut mucosa by transfer of electrons to oxygen. For this purpose, the bacterium exploits extracellular antioxidants, such as riboflavin and cysteine, that are abundantly present in the gut. We therefore tested to what extent these antioxidants can sustain the viability of F. prausnitzii at ambient air. The present results show that cysteine can facilitate the survival of F. prausnitzii upon exposure to air, and that this effect is significantly enhanced the by addition of riboflavin and the cryoprotectant inulin. The highly oxygen-sensitive gut bacterium F. prausnitzii can be kept alive at ambient air for 24 h when formulated with the antioxidants cysteine and riboflavin plus the cryoprotectant inulin. Improved formulations were obtained by addition of the bulking agents corn starch and wheat bran. Our present findings pave the way towards the biomedical exploitation of F. prausnitzii in redox-based therapeutics for treatment of dysbiosis-related inflammatory disorders of the human gut.
Particulate matter air pollution causes oxidant-mediated increase in gut permeability in mice
Ece A Mutlu, Phillip A Engen, Saul Soberanes, Daniela Urich, Christopher B Forsyth, Recep Nigdelioglu, Sergio E Chiarella, Kathryn A Radigan, Angel Gonzalez, Shriram Jakate, Ali Keshavarzian, GR Budinger, G?khan M Mutlu
Particle and Fibre Toxicology , 2011, DOI: 10.1186/1743-8977-8-19
Abstract: We measured PM-induced cell death and mitochondrial ROS generation in Caco-2 cells stably expressing oxidant sensitive GFP localized to mitochondria in the absence or presence of an antioxidant. C57BL/6 mice were exposed to a very high dose of urban PM from Washington, DC (200 μg/mouse) or saline via gastric gavage and small bowel and colonic tissue were harvested for histologic evaluation, and RNA isolation up to 48 hours. Permeability to 4kD dextran was measured at 48 hours.PM induced mitochondrial ROS generation and cell death in Caco-2 cells. PM also caused oxidant-dependent NF-κB activation, disruption of tight junctions and increased permeability of Caco-2 monolayers. Mice exposed to PM had increased intestinal permeability compared with PBS treated mice. In the small bowel, colocalization of the tight junction protein, ZO-1 was lower in the PM treated animals. In the small bowel and colon, PM exposed mice had higher levels of IL-6 mRNA and reduced levels of ZO-1 mRNA. Increased apoptosis was observed in the colon of PM exposed mice.Exposure to high doses of urban PM causes oxidant dependent GI epithelial cell death, disruption of tight junction proteins, inflammation and increased permeability in the gut in vitro and in vivo. These PM-induced changes may contribute to exacerbations of inflammatory disorders of the gut.In human populations, investigators have associated PM exposure with an increasing number of adverse health outcomes including all-cause mortality, cardiovascular mortality, accelerated atherosclerosis in postmenopausal women, loss of lung function in healthy adults, impaired lung development in children, exacerbations of obstructive lung disease, pneumonia and increased risk of venous thromboembolism [1-11]. Recently, Kaplan et al reported that individuals younger than 23 years were more likely to be diagnosed with Crohn's disease if they lived in regions with higher NO2 concentrations [12], a marker of traffic related pollution that correlates
Influence of Various Antioxidants on the Characteristics of Plain Yogurt  [PDF]
Blake Brignac, Kayanush J. Aryana
Food and Nutrition Sciences (FNS) , 2012, DOI: 10.4236/fns.2012.39168
Abstract: Free radical damage has been implicated in ageing and in certain degenerative conditions such as Alzheimer’s disease and other forms of dementia. Ageing is also associated with a progressive decline in the function of the immune system and an increased susceptibility to infection. Antioxidants protect the body from free radical damage. Vitamin E is the major antioxidant vitamin in body tissues and is considered the first line of defense against cell membrane damage. Other antioxidant defenses that protect the body from free radical damage include vitamin C and beta carotene. Yogurt is considered a healthy food product and its sales have been steadily increasing over the past 5 years. The objective was to study the influence of various antioxidants on the quality characteristics of yogurt. The antioxidants Vitamin C, vitamin E and beta carotene individually and in combination were incorporated at 100% of their respective recommended dietary allowance of 60 mg, 12 mg and 3 mg in 240 mL of yogurt. Yogurt manufacture and all experiments were conducted in triplicate. Use of antioxidants in yogurt manufacture significantly influenced yogurt viscosity, flavor, appearance, body texture but did not influence syneresis, lactic acid bacterial counts and pH.Depending upon the application antioxidants can be recommended in yogurt manufacture.
Structural, Chemical and Biological Aspects of Antioxidants for Strategies Against Metal and Metalloid Exposure  [PDF]
Swaran J. S. Flora
Oxidative Medicine and Cellular Longevity , 2009, DOI: 10.4161/oxim.2.4.9112
Abstract: Oxidative stress contributes to the pathophysiology of exposure to heavy metals/metalloid. Beneficial renal effects of some medications, such as chelation therapy depend at least partially on the ability to alleviate oxidative stress. The administration of various natural or synthetic antioxidants has been shown to be of benefit in the prevention and attenuation of metal induced biochemical alterations. These include vitamins, N-acetylcysteine, α-lipoic acid, melatonin, dietary flavonoids and many others. Human studies are limited in this regard. Under certain conditions, surprisingly, the antioxidant supplements may exhibit pro-oxidant properties and even worsen metal induced toxic damage. To date, the evidence is insufficient to recommend antioxidant supplements in subject with exposure to metals. Prospective, controlled clinical trials on safety and effectiveness of different therapeutic antioxidant strategies either individually or in combination with chelating agent are indispensable. The present review focuses on structural, chemical and biological aspects of antioxidants particularly related to their chelating properties.
The Evolution of Mutualism in Gut Microbiota Via Host Epithelial Selection  [PDF]
Jonas Schluter,Kevin R. Foster
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1001424
Abstract: The human gut harbours a large and genetically diverse population of symbiotic microbes that both feed and protect the host. Evolutionary theory, however, predicts that such genetic diversity can destabilise mutualistic partnerships. How then can the mutualism of the human microbiota be explained? Here we develop an individual-based model of host-associated microbial communities. We first demonstrate the fundamental problem faced by a host: The presence of a genetically diverse microbiota leads to the dominance of the fastest growing microbes instead of the microbes that are most beneficial to the host. We next investigate the potential for host secretions to influence the microbiota. This reveals that the epithelium–microbiota interface acts as a selectivity amplifier: Modest amounts of moderately selective epithelial secretions cause a complete shift in the strains growing at the epithelial surface. This occurs because of the physical structure of the epithelium–microbiota interface: Epithelial secretions have effects that permeate upwards through the whole microbial community, while lumen compounds preferentially affect cells that are soon to slough off. Finally, our model predicts that while antimicrobial secretion can promote host epithelial selection, epithelial nutrient secretion will often be key to host selection. Our findings are consistent with a growing number of empirical papers that indicate an influence of host factors upon microbiota, including growth-promoting glycoconjugates. We argue that host selection is likely to be a key mechanism in the stabilisation of the mutualism between a host and its microbiota.
The Evolution of Mutualism in Gut Microbiota Via Host Epithelial Selection  [PDF]
Jonas Schluter ,Kevin R. Foster
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1001424
Abstract: The human gut harbours a large and genetically diverse population of symbiotic microbes that both feed and protect the host. Evolutionary theory, however, predicts that such genetic diversity can destabilise mutualistic partnerships. How then can the mutualism of the human microbiota be explained? Here we develop an individual-based model of host-associated microbial communities. We first demonstrate the fundamental problem faced by a host: The presence of a genetically diverse microbiota leads to the dominance of the fastest growing microbes instead of the microbes that are most beneficial to the host. We next investigate the potential for host secretions to influence the microbiota. This reveals that the epithelium–microbiota interface acts as a selectivity amplifier: Modest amounts of moderately selective epithelial secretions cause a complete shift in the strains growing at the epithelial surface. This occurs because of the physical structure of the epithelium–microbiota interface: Epithelial secretions have effects that permeate upwards through the whole microbial community, while lumen compounds preferentially affect cells that are soon to slough off. Finally, our model predicts that while antimicrobial secretion can promote host epithelial selection, epithelial nutrient secretion will often be key to host selection. Our findings are consistent with a growing number of empirical papers that indicate an influence of host factors upon microbiota, including growth-promoting glycoconjugates. We argue that host selection is likely to be a key mechanism in the stabilisation of the mutualism between a host and its microbiota.
The Oxidant-Scavenging Abilities in the Oral Cavity May Be Regulated by a Collaboration among Antioxidants in Saliva, Microorganisms, Blood Cells and Polyphenols: A Chemiluminescence-Based Study  [PDF]
Isaac Ginsburg, Ron Kohen, Miri Shalish, David Varon, Ella Shai, Erez Koren
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0063062
Abstract: Saliva has become a central research issue in oral physiology and pathology. Over the evolution, the oral cavity has evolved the antioxidants uric acid, ascorbate reduced glutathione, plasma-derived albumin and antioxidants polyphenols from nutrients that are delivered to the oral cavity. However, blood cells extravasated from injured capillaries in gingival pathologies, or following tooth brushing and use of tooth picks, may attenuate the toxic activities of H2O2 generated by oral streptococci and by oxidants generated by activated phagocytes. Employing a highly sensitive luminol-dependent chemiluminescence, the DPPH radical and XTT assays to quantify oxidant-scavenging abilities (OSA), we show that saliva can strongly decompose both oxygen and nitrogen species. However, lipophilic antioxidant polyphenols in plants, which are poorly soluble in water and therefore not fully available as effective antioxidants, can nevertheless be solubilized either by small amounts of ethanol, whole saliva or also by salivary albumin and mucin. Plant-derived polyphenols can also act in collaboration with whole saliva, human red blood cells, platelets, and also with catalase-positive microorganisms to decompose reactive oxygen species (ROS). Furthermore, polyphenols from nutrient can avidly adhere to mucosal surfaces, are retained there for long periods and may function as a “slow- release devises” capable of affecting the redox status in the oral cavity. The OSA of saliva is due to the sum result of low molecular weight antioxidants, albumin, polyphenols from nutrients, blood elements and microbial antioxidants. Taken together, saliva and its antioxidants are considered regulators of the redox status in the oral cavity under physiological and pathological conditions.
Depletion of Murine Intestinal Microbiota: Effects on Gut Mucosa and Epithelial Gene Expression  [PDF]
Dag Henrik Reikvam,Alexander Erofeev,Anders Sandvik,Vedrana Grcic,Frode Lars Jahnsen,Peter Gaustad,Kathy D. McCoy,Andrew J. Macpherson,Leonardo A. Meza-Zepeda,Finn-Eirik Johansen
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0017996
Abstract: Inappropriate cross talk between mammals and their gut microbiota may trigger intestinal inflammation and drive extra-intestinal immune-mediated diseases. Epithelial cells constitute the interface between gut microbiota and host tissue, and may regulate host responses to commensal enteric bacteria. Gnotobiotic animals represent a powerful approach to study bacterial-host interaction but are not readily accessible to the wide scientific community. We aimed at refining a protocol that in a robust manner would deplete the cultivable intestinal microbiota of conventionally raised mice and that would prove to have significant biologic validity.
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