scholarly journals Phytic Acid Inhibits Lipid PeroxidationIn Vitro

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Alicja Zajdel ◽  
Adam Wilczok ◽  
Ludmiła Węglarz ◽  
Zofia Dzierżewicz
Keyword(s):  
Lipid Peroxidation ◽  
Linoleic Acid ◽  
Phytic Acid ◽  
Inhibitory Effect ◽  
Acid Oxidation ◽  
Colonic Epithelial Cells ◽  
Linoleic Acid Oxidation ◽  
Small Intestinal

Phytic acid (PA) has been recognized as a potent antioxidant and inhibitor of iron-catalyzed hydroxyl radical formation underin vitroandin vivoconditions. Therefore, the aim of the present study was to investigate, with the use of HPLC/MS/MS, whether PA is capable of inhibiting linoleic acid autoxidation and Fe(II)/ascorbate-induced peroxidation, as well as Fe(II)/ascorbate-induced lipid peroxidation in human colonic epithelial cells. PA at 100 μM and 500 μM effectively inhibited the decay of linoleic acid, both in the absence and presence of Fe(II)/ascorbate. The observed inhibitory effect of PA on Fe(II)/ascorbate-induced lipid peroxidation was lower (10–20%) compared to that of autoxidation. PA did not change linoleic acid hydroperoxides concentration levels after 24 hours of Fe(II)/ascorbate-induced peroxidation. In the absence of Fe(II)/ascorbate, PA at 100 μM and 500 μM significantly suppressed decomposition of linoleic acid hydroperoxides. Moreover, PA at the tested nontoxic concentrations (100 μM and 500 μM) significantly decreased 4-hydroxyalkenal levels in Caco-2 cells which structurally and functionally resemble the small intestinal epithelium. It is concluded that PA inhibits linoleic acid oxidation and reduces the formation of 4-hydroxyalkenals. Acting as an antioxidant it may help to prevent intestinal diseases induced by oxygen radicals and lipid peroxidation products.

Oxidation of alpha 1-protease inhibitor: role of lipid peroxidation products

1989 ◽  
Vol 66 (5) ◽  
pp. 2211-2215 ◽  
Author(s):  
V. Mohsenin ◽  
J. L. Gee
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Stearic Acid ◽  
Protease Inhibitor ◽  
Alpha Tocopherol ◽  
Inhibitory Capacity ◽  
Buffer Control

Previously we demonstrated that in vivo exposure of humans to NO2 resulted in significant inactivation of alpha 1-protease inhibitor (alpha 1-PI) in the bronchoalveolar lavage fluid. However, alpha 1-PI retains its elastase inhibitory activity in vitro when exposed to 10 times the concentration of NO2 used in vivo. We suggested exogenous oxidants such as O2 and NO2 exert their effect in vivo in part through lipid peroxidation. We investigated the mechanism of inactivation of alpha 1-PI in the presence or absence of lipids under oxidant atmosphere. alpha 1-PI in solutions containing phosphate buffer (control), 0.1 mM stearic acid (saturated fatty acid, 18:0), or 0.1 mM linoleic acid (polyunsaturated fatty acid, 18:2) was exposed to either N2 or NO2 (50 ppm for 4 h). Elastase inhibitory capacity of alpha 1-PI was significantly diminished in the presence of 0.1 mM linoleic acid and under NO2 atmosphere (75 +/- 8% of control, P less than 0.01), whereas there was no change in elastase inhibitory capacity of alpha 1-PI in the presence or absence (buffer only) of 0.1 mM stearic acid under a similar condition (109 +/- 11 and 94 +/- 6%, respectively). The inactivated alpha 1-PI as the result of peroxidized lipid could be reactivated by dithiothreitol and methionine sulfoxide peptide reductase, suggesting oxidation of methionine residue at the elastase inhibitory site. Furthermore the inhibitory effect of peroxidized lipid on alpha 1-PI could be prevented by glutathione and glutathione peroxidase and to some extent by alpha-tocopherol.

scholarly journals A Synthetic Peptide Corresponding to the Extracellular Loop 2 Region of Claudin-4 Protects against Clostridium perfringens EnterotoxinIn VitroandIn Vivo

2014 ◽  
Vol 82 (11) ◽  
pp. 4778-4788 ◽  
Author(s):  
Archana Shrestha ◽  
Susan L. Robertson ◽  
Jorge Garcia ◽  
Juliann Beingasser ◽  
Bruce A. McClane ◽  
...  
Keyword(s):  
Clostridium Perfringens ◽  
Synthetic Peptide ◽  
Inhibitory Effect ◽  
Intestinal Loop ◽  
Extracellular Loop ◽  
Content Type ◽  
Potential Therapeutic Application ◽  
Small Intestinal

ABSTRACTClostridium perfringensenterotoxin (CPE) action starts when the toxin binds to claudin receptors. Claudins contain two extracellular loop domains, with the second loop (ECL-2) being slightly smaller than the first. CPE has been shown to bind to ECL-2 in receptor claudins. We recently demonstrated that Caco-2 cells (a naturally CPE-sensitive enterocyte-like cell line) can be protected from CPE-induced cytotoxicity by preincubating the enterotoxin with soluble full-length recombinant claudin-4 (rclaudin-4), which is a CPE receptor, but not with recombinant nonreceptor claudins, such asrclaudin-1. The current study evaluated whether a synthetic peptide corresponding to the claudin-4 ECL-2 sequence can similarly inhibit CPE actionin vitroandin vivo. Significant protection of Caco-2 cells was also observed using eitherrclaudin-4 or the claudin-4 ECL-2 peptide in both a preincubation assay and a coincubation assay. This inhibitory effect was specific, sincerclaudin-1 and a synthetic peptide based on the claudin-1 ECL-2 offered no protection to Caco-2 cells. However, the claudin-4 ECL-2 peptide was unable to neutralize cytotoxicity if CPE had already bound to Caco-2 cells. When the study was repeatedin vivousing a rabbit small intestinal loop assay, preincubation or coincubation of CPE with the claudin-4 ECL-2 peptide significantly and specifically inhibited the development of CPE-induced luminal fluid accumulation and histologic lesions in rabbit small intestinal loops. No similarin vivoprotection from CPE was afforded by the claudin-1 ECL-2 peptide. These results suggest that claudin-4 ECL-2 peptides should be further investigated for their potential therapeutic application against CPE-associated disease.

scholarly journals circRNA_0046367 Prevents Hepatoxicity of Lipid Peroxidation: An Inhibitory Role against Hepatic Steatosis

2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Xing-Ya Guo ◽  
Jian-Neng Chen ◽  
Fang Sun ◽  
Yu-Qin Wang ◽  
Qin Pan ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Hepatic Steatosis ◽  
Transcriptional Activation ◽  
Regulatory System ◽  
Inhibitory Effect ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Triglyceride Accumulation

Hepatic steatosis reflects the miRNA-related pathological disorder with triglyceride accumulation and lipid peroxidation, which leads to nonalcoholic steatohepatitis, liver fibrosis/cirrhosis, and even hepatocellular carcinoma. Circular RNA (circRNA)/miRNA interaction reveals a novel layer of epigenetic regulation, yet the miRNA-targeting circRNA remains uncertain in hepatic steatosis. Here, we uncover circRNA_0046367 to be endogenous modulator of miR-34a that underlies hepatic steatosis. In contrast to its expression loss during the hepatocellular steatosis in vivo and in vitro, circRNA_0046367 normalization abolished miR-34a’s inhibitory effect on peroxisome proliferator-activated receptorα(PPARα) via blocking the miRNA/mRNA interaction with miRNA response elements (MREs). PPARαrestoration led to the transcriptional activation of genes associated with lipid metabolism, including carnitine palmitoyltransferase 2 (CPT2) and acyl-CoA binding domain containing 3 (ACBD3), and then resulted in the steatosis resolution. Hepatotoxicity of steatosis-related lipid peroxidation, being characterized by mitochondrial dysfunction, growth arrest, and apoptosis, is resultantly prevented after the circRNA_0046367 administration. These findings indicate a circRNA_0046367/miR-34a/PPARαregulatory system underlying hepatic steatosis. Normalized expression of circRNA_0046367 may ameliorate the lipoxidative stress on the basis of steatosis attenuation. circRNA_0046367, therefore, is suggested to be potential approach to the therapy of lipid peroxidative damage.

scholarly journals Peroxynitrite mediated linoleic acid oxidation and tyrosine nitration in the presence of synthetic neuromelanins.

2000 ◽  
Vol 47 (4) ◽  
pp. 931-940 ◽  
Author(s):  
K Stepień ◽  
A Wilczok ◽  
A Zajdel ◽  
A Dzierzega-Lecznar ◽  
T Wilczok
Keyword(s):  
Linoleic Acid ◽  
Protective Effect ◽  
Inhibitory Effect ◽  
Oxidation Products ◽  
Acid Oxidation ◽  
Tyrosine Nitration ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Linoleic Acid Oxidation ◽  
Synthetic Model

Peroxynitrite-mediated linoleic acid oxidation and tyrosine nitration were analysed in the presence of synthetic model neuromelanins: dopamine (DA) -melanin, cysteinyldopamine (CysDA) -melanin and various DA/CysDA copolymers. The presence of melanin significantly decreased the amount of 3-nitrotyrosine formed. This inhibitory effect depended on the type and concentration of melanin polymer. It was found that incorporation of CysDA-derived units into melanin attenuated its protective effect on tyrosine nitration induced by peroxynitrite. In the presence of bicarbonate, the melanins also inhibited 3-nitrotyrosine formation in a concentration dependent manner, although the extent of inhibition was lower than in the absence of bicarbonate. The tested melanins inhibited peroxynitrite-induced formation of linoleic acid hydroperoxides, both in the absence and in the presence of bicarbonate. In the presence of bicarbonate, among the oxidation products appeared 4-hydroxynonenal (HNE). CysDA-melanin inhibited the formation of HNE, while DA-melanin did not affect the aldehyde level. The results of the presented study suggest that neuromelanin can act as a natural scavenger of peroxynitrite.

scholarly journals AKTIVITAS ANTIOKSIDAN EKSTRAK BIJI DUWET (Syzygium cumini Linn.) PADA PEROKSIDASI LIPIDA SECARA IN VITRO

2016 ◽  
Vol 36 (01) ◽  
pp. 30 ◽  
Author(s):  
Rohadi Rohadi ◽  
Sri Rahadjo ◽  
Lip Izul Falah ◽  
Umar Santoso
Keyword(s):  
Antioxidant Activity ◽  
Linoleic Acid ◽  
Reducing Power ◽  
Seed Extract ◽  
Total Phenolic ◽  
Acid Oxidation ◽  
Syzygium Cumini ◽  
Antioxidant Power ◽  
Linoleic Acid Oxidation

All parts of Syzygium cumini Linn. (duwet) were widely used for medicinal plant in the treatment of various deseases.The seed extract was used to lower blood glucose. Cumini's seed had higher phenolic fractions than others. It were prepared by extracted of duwet seed "Genthong" varieties, using various extractants such as 85% ethyl acetate, 50% methanol and 50% ethanol. Duwet seed extract collected then was determined of phenolics compound and antioxidant activity assayed by measuring 2,2-diphenyl-1-picrylhydrazylradical (DPPH) scavenging activity, reducing Ferric ion (Fe3+) power and inhibition of linoleic acid oxidation. The objective was to select one of the extractant which gave highest yield and polyphenolic content and its stronger antioxidant activity. Extractant 50% methanol gave highest the extract yields was 16.29 % (db.) and phenolics compounds of extract was composed: total phenolic 45.99±0.25 g-GAE/100 g-extract; total flavonoid 2.28±0.07 g-QE/100 g-extract and total tannin 26.9±0.07 g-TAE/100 g-extract. All of extract exhibited strong on behalf of RSA-DPPH assay 87-95% (100  g-mL-l) and reducing power, nevertheless in inhibition of linoleic acid oxidation was moderate 49-55% (400  g-mL-l).Keywords: Syzygium cumini Linn, seed, antioxidant, extraction ABSTRAKTanaman duwet (Syzygium cumini Linn.) pada semua kompartemennya dimanfaatkan masyarakat untuk pengobatansuatu penyakit. Ekstrak bijinya dimanfaatkan untuk penurun gula darah. Bijinya merupakan bagian tanaman yang kaya senyawa polifenol. Fraksi kaya senyawa fenolik dipreparasi dengan mengekstraksi biji duwet varietas "Genthong", dengan tiga jenis ekstraktan; etil acetat 85%, metanol 50% dan etanol 50%. Ekstrak biji duwet (EBD) yang diperoleh dianalisis kelompok senyawa fenolik dan aktivitas antioksidan menggunakan metode uji penangkapan radikal DPPH (2,2-diphenil 1-picrylhydrazyl), uji reduksi ion Feri (ferric reduction antioxidant power-FRAP) dan uji penghambatan peroksidasi asam lemak linoleat. Tujuan penelitian adalah memilih satu dari tiga ekstraktan yang menghasilkaan ekstrak, dengan yield dan kadar senyawa polifenolik terbesar serta sifat antioksidatif terkuat. Yield dengan ekstraktan Met-OH-50%, sebesar 16,29% (db), senyawa fenoliknya sebesar 45,99 ±0,25 g-GAE/100 g-EBD; 2,28±0,07 g-QE/100 g-EBD dan 26,9±0,07 g-TAE/100 g-EBD. Ketiga ekstrak kuat dalam uji penangkapan radikal DPPH antara 87-95 % (100 g-mL-l) dan uji reduksi ion Feri (Fe3+), moderat pada uji penghambatan peroksidasi lipid, 49-52 % pada 400  g- mL-l.Kata kunci: Biji duwet (Syzygium cumini Linn.), antioksidan, ekstraksi

scholarly journals Antioxidant and Hepatoprotective Effects of Polyphenols in Leaves of Artemisia Princeps Pamp

2007 ◽  
Vol 2 (11) ◽  
pp. 1934578X0700201
Author(s):  
Shizuo Toda
Keyword(s):  
Lipid Peroxidation ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Glutamic Oxaloacetic Transaminase ◽  
Serum Glutamic Oxaloacetic Transaminase ◽  
Artemisia Princeps ◽  
Hepatoprotective Effects ◽  
Protein Fragmentation

The leaves of Artemisia princeps Pamp have been used for tea and food in Japan. The polyphenols of the leaves have inhibitory effects against lipid peroxidation and protein fragmentation by free radicals in vitro and an inhibitory effect on galactosamine -lipopolysaccharide induced hepatotoxicity in vivo. The levels of serum glutamic oxaloacetic transaminase and glutamic pyruvic transaminase, lipid peroxidation in serum and liver by hepatotoxity were depressed by polyphenols in A. princeps Pamp. The depression of gluthathione and superoxide dismutase in plasma and liver by hepatotoxity were elevated by polyphenols in A. princeps Pamp. These results demonstrated that polyphenols in A. princeps Pamp have antioxidant and hepatoprotective effects.

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