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Oxidative Products (oxidative + products)
Selected AbstractsEvaluation of Lipid Oxidation and Oxidative Products as Affected by Pork Meat Cut, Packaging Method, and Storage Time during Frozen Storage (,10 °C)JOURNAL OF FOOD SCIENCE, Issue 2 2007S.Y. Park ABSTRACT:, Lipid oxidation and oxidative volatiles as affected by pork meat cut and packaging method during frozen storage at ,10 °C were evaluated. Pork belly cut had higher thiobarbituric acid reactive substance (TBARS) and pH values than did the loin, whereas the loin had higher free fatty acid (FFA) values than that of the belly cut. Peroxide values increased with increased storage time, but were not affected by pork meat cut and packaging method. Volatiles with carbon numbers less than 10 in the belly cut were higher than those in the loin cut, whereas those with carbon numbers greater than 10 in the loin cut were higher than those in belly cut. Most volatiles were decreased with increased storage time, except for propane. Both 4-pentenal and 4-methyl-2-hexanone in the belly cut showed a positive correlation with FFA, whereas 2,4-dimethyl-1-heptene and 9-octadecenal in the loin cut were positively correlated with TBARS and FFA, respectively, even though the values were not high enough to predict the degree of lipid oxidation. [source] Evaluation of the radioprotective effect of Liv 52 in miceENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 7 2006Ganesh C. Jagetia Abstract Liv 52 is a mixture of botanicals that is used clinically to treat various hepatic disorders. In this study, the radioprotective activity of Liv 52 was evaluated in mice given whole-body exposure to different doses of ,-radiation. In addition, a series of studies was conducted to explore the mechanism of radioprotection. Radioprotection was evaluated by the ability of Liv 52 to reduce both the frequency of bone marrow micronucleated erythrocytes and the lethality produced by 60Co ,-radiation. Mice were treated by oral gavage once daily for seven consecutive days with 500 mg/kg body weight Liv 52 or carboxymethylcellulose vehicle prior to radiation. Micronucleated polychromatic erythrocytes (MPCEs), micronucleated normochromatic erythrocytes (MNCEs), and the PCE/NCE ratio were measured at 0.25,14 days after exposure to whole-body radiation doses of 0, 0.5, 1.5, 3.0, or 4.5 Gy; animal survival was monitored after doses of 7, 8, 9, 10, 11, or 12 Gy. Pretreatment of mice with Liv 52 significantly reduced the frequency of radiation-induced MPCEs and MNCEs. Irradiation reduced the PCE/NCE ratio in a dose-related manner for up to 7 days following irradiation; Liv 52 pretreatment significantly mitigated against these reductions. Liv 52 treatment also reduced the symptoms of radiation sickness and increased mouse survival 10 and 30 days after irradiation. Liv 52 pretreatment elevated the levels of reduced glutathione (GSH), increased the activities of glutathione transferase, GSH peroxidase, GSH reductase, superoxide dismutase, and catalase, and lowered lipid peroxidation (LPx) and the activities of alanine amino transferase and aspartate aminotransferase 30 min after exposure to 7 Gy of ,-radiation. Liv 52 pretreatment also reduced radiation-induced LPx and increased GSH concentration 31 days following the exposure. The results of this study indicate that pretreatment with Liv 52 reduces the genotoxic and lethal effects of ,-irradiation in mice and suggest that this radioprotection may be afforded by reducing the toxic effects of the oxidative products of irradiation. Environ Mol. Mutagen., 2006. © 2006 Wiley-Liss, Inc. [source] Homocysteine-induced decrease in endothelin-1 production is initiated at the extracellular level and involves oxidative productsFEBS JOURNAL, Issue 20 2001Séverine Drunat The increased cardiovascular risk associated with hyperhomocysteinemia has been partly related to homocysteine (Hcy)-induced endothelial cell dysfunction. However, the intra or extracellular starting point of the interaction between Hcy and endothelial cells, leading to cellular dysfunction, has not yet been identified. We investigated the effects of both intracellular and extracellular Hcy accumulation on endothelin-1 (ET-1) synthesis by cultured human endothelial cells. Incubation of cultures with methionine (1.0 mmol·L,1) for 2 h induced a slight increase in cellular Hcy content but no change in ET-1 production. Incubation of cells with Hcy (0.2 mmol·L,1) led to a significant fall in ET-1 generation, accompanied by a significant increase in cellular Hcy content. Addition of the amino-acid transport system L substrate 2-amino-2-norbornane carboxylic acid had no effect on the Hcy-induced decrease in ET-1 production but significantly inhibited the Hcy-induced increase in the cellular Hcy content. Incubation of cells with a lower Hcy concentration (0.05 mmol·L,1) also reduced ET-1 production without increasing the cellular Hcy content. Co-incubation with extracellular free-radical inhibitors (superoxide dismutase, catalase and mannitol) markedly reduced the effect of Hcy on ET-1 production. Thus, it is extracellular Hcy accumulation that triggers the decrease in ET-1 production by endothelial cells through oxidative products. [source] Oxidative metabolism by Thalassiosira weissflogii (Bacillariophyceae) of a diol-ester of okadaic acid, the diarrhetic shellfish poisoningJOURNAL OF PHYCOLOGY, Issue 2 2000Anthony J. Windust Previous investigations into the comparative toxicity of the diarrhetic shellfish poisoning (DSP) toxins to Thalassiosira weissflogii (Grun.) Fryxell et Hasle found that this diatom oxidatively metabolized okadaic acid diol-ester (OA diol-ester) to a more water-soluble product. This oxidative transformation of OA diol-ester by the diatom is significant for two reasons. First, it is known that dinophysistoxin-4 (DTX-4), the primary DSP toxin produced by the dinoflagellate Exuviaella lima (Ehr.) Butschli, will be hydrolyzed to the diol-ester following cell rupture (e.g. ingestion by a predator). Second, it implies that the ester, an uncharged, lipophilic intermediate, can easily enter cells and therefore may play an important role in the uptake and transfer of DSP toxins through the food web. It has been suggested that the water soluble DTX-4 may also be the form in which DSP toxins are excreted from the producing cell. Therefore, the stability of DTX-4 was examined when incubated either in fresh seawater medium into which washed cells of E. lima were introduced or in seawater medium conditioned by E. lima cells. Rapid hydrolysis of DTX-4 to the diol-ester took place in both cases. Thus, regardless of the route by which DTX-4 is liberated from the cell, either by cell disruption or excretion, the diol-ester will be the dominant form of the toxin to challenge associated organisms. To examine the metabolism of OA diol-ester by T. weissflogii in more detail, serial cultures of the diatom were challenged with OA diol-ester at a concentration of 2.0 ,g·mL,1. The metabolism and fate of the diol-ester in both cellular and medium fractions were monitored over 3 days using liquid chromatography with either ultraviolet (LC-UV) or mass spectrometric (LC-MS) detection. During the course of the experiment, all of the diol-ester was metabolized. LC-MS analysis revealed the presence of multiple oxidative products of OA diol-ester in the medium fraction, including a carboxylic acid derivative. The major metabolites were isolated in sufficient quantity to permit structural elucidation by NMR and MS. All the metabolites identified resulted from oxidation of the diol-ester side chain with the primary sites of attack at the terminal, subterminal, and unsaturated carbons. OA was found in both cellular and medium fractions, and its production was directly correlated with the metabolism of the diol-ester. The relative partitioning of both OA diol-ester and its oxidation products between cells and medium supports the contention that OA diol-ester can readily enter cells, be metabolized, and then excreted in more water-soluble forms. [source] Oxidative stress in developmental brain disordersNEUROPATHOLOGY, Issue 1 2009Masaharu Hayashi Oxidative stress is one of the predisposing factors in adult neurological disorders. We have examined the involvement of oxidative stress in child-onset neurodegenerative disorders, and here we review the findings from our analysis. In cases of Cockayne syndrome, the oxidative products of lipids and proteins were increased in the globus pallidus; however, oxidative nucleotide damage that coincided with reduced copper/zinc superoxide dismutase (Cu/ZnSOD) expression was observed in cases of xeroderma pigmentosum, and these patients also presented increased oxidative stress markers in urine samples. In spinal muscular atrophy, lipid peroxidation in conjunction with oxidative DNA damage was observed in motor neurons. Cases of subacute sclerosing panencephalitis presented oxidative nucleoside damage in cerebral cortical neurons at early disease stages, which were subsequently replaced by lipid peroxidation in glial cells of cerebral white matter. In relation to progressive myoclonic epilepsy, oxidative damage to DNA, proteins, and lipids appeared to coincide with cerebral and cerebellar cortical lesions of neuronal ceroid-lipofuscinosis. Patients with Lafora disease also presented an increase in oxidative stress markers for DNA and/or lipids in the brain and urine. These findings imply involvement of oxidative stress in developmental brain disorders; antioxidant agents could prove to be useful for treating patients with those disorders. [source] Neurofibrillary tangles and deposition of oxidative products in the brain in cases of myotonic dystrophyNEUROPATHOLOGY, Issue 2 2006Reiko Oyamada Myotonic dystrophy (MyD) is a neuromuscular degenerative disorder that is neuropathologically characterized by minor changes, such as the presence of neurofibrillary tangles (NFT), thalamic inclusions and functional brainstem lesions. In the current study, we conducted an immunohistochemical analysis to examine the distribution of NFT and formation of oxidative products in the brain specimens of 12 patients with MyD. Neurofibrillary tangles were found in the limbic system and/or the brainstem of all the cases examined but there were no senile plaques. The density of distribution of the NFT was not significantly correlated with clinicopathological findings, although cases with fewer NFT in the brain frequently showed sleep disturbances and lack of spontaneity. Nuclear and cytoplasmic immunoreactivities for 8-hydroxy-2,-deoxyguanosine and advanced glycation end products were observed in the glial cells and/or neurons in the brainstem, but not in the cerebral cortex. On the other hand, 10 out of the 12 cases showed cytoplasmic immunoreactivity for 4-hydroxy-2-nonenal-modified protein (4-HNE) in neurons of the temporal cortex and raphe nucleus. Deposition of 4-HNE was also recognized in the hippocampus and mesencephalic central gray matter, but not in the subiculum. The distribution pattern of the immunoreactivity for 4-HNE showed no clear correlation with either the psychological disturbances or the distribution of the NFT. Altered expression of monoaminergic neurons in the brainstem of MyD patients has already been reported, and it is worth noting that most of our cases showed NFT in the brainstem. The selective deposition of 4-HNE in the limbic system and brainstem suggests that lipid peroxidation may be involved in the neurodegenerative process in MyD. Using immunohistochemical analysis to determine the distribution of neurotransmitters in the mesencephalic central gray matter and/or pontine raphe nucleus may help elucidate the relationship between the clinical abnormalities, distribuion of NFT, and 4-HNE deposition in the brain in patients with MyD. [source] Identification of 1-palmitoyl-2-linoleoyl-phosphatidylethanolamine modifications under oxidative stress conditions by LC-MS/MSBIOMEDICAL CHROMATOGRAPHY, Issue 6 2009M. Rosário M. Domingues Abstract Phosphatidylethanolamines are a major class of phospholipids found in cellular membranes. Identification of the alterations in these phospholipids, induced by free radicals, could provide new tools for in vivo diagnosis of oxidative stress. In this study, 1-palmitoyl-2-linoleoyl-phosphatidylethanolamine oxidation products, induced by the hydroxyl radical, were studied using LC-MS and LC-MS/MS. Data obtained allowed the identification and separation of isomeric oxidative products with modifications in the sn -2 acyl chain, attributed to long- and short-chain products. Among long-chain products keto, keto-hydroxy, hydroxy, poly-hydroxy, peroxy and hydroxy,peroxy derivatives were identified. Product ions formed by loss of two H2O molecules vs loss of HOOH, allowed the identification of, respectively, di- (or poli-) hydroxy vs peroxy derivatives. Location of functional groups was determined by the product ions formed by cleavage of C,C bonds, in the vicinity of the oxidation positions, allowing the identification of C9, C12 and C13 as the predominant substituted positions. Short-chain products identified comprised aldehydes, hydroxy-aldehydes and carboxylic derivatives, with modified sn -2 acyl lengths of C7,C9 and C11, C12. Among the short-chain products identified, C9 products showed higher relative abundance. Copyright © 2009 John Wiley & Sons, Ltd. [source] A New Amphiphilic Derivative, N -{[4-(Lactobionamido)methyl]benzylidene}- 1,1-dimethyl-2-(octylsulfanyl)ethylamine N -Oxide, Has a Protective Effect Against Copper-Induced Fulminant Hepatitis in Long,Evans Cinnamon Rats at an Extremely Low Concentration Compared with Its Original Form , -Phenyl- N -(tert -butyl) NitroneCHEMISTRY & BIODIVERSITY, Issue 9 2007Taketoshi Asanuma Abstract An amphiphilic , -phenyl- N- (tert -butyl) nitrone (PBN) derivative, N -{[4-(lactobionamido)methyl]benzylidene}-1,1-dimethyl-2-(octylsulfanyl)ethylamine N -oxide (LPBNSH), newly synthesized from its original form PBN in hopes of clinical use, was intraperitoneally administered to Long,Evans Cinnamon (LEC) rats every 2 days at the concentrations of 0.1, 0.5, 1.0, and 2.0,mg/kg. We found that LPBNSH protected against copper-induced hepatitis with jaundice in LEC rats at concentrations of 0.1 and 0.5,mg/kg, which were extremely low compared with that of PBN. It also effectively prevented the loss of body weight, reduced the death rate, and suppressed the increase in serum aspartate aminotransferase and alanine aminotransferase values arising from fulminant hepatitis with jaundice at the same concentrations. Similar results were observed when PBN was administered at the concentration of 150,mg/kg. Immunohistochemical analysis of 8-hydroxy-2,-deoxyguanosine and measurement of thiobarbituric acid-reactive substances in the liver showed that LPBNSH largely suppressed the formation of these oxidative products at same concentrations. No difference in the abnormal accumulation of copper in the liver between the LPBNSH administered and control groups was observed. From these results, it was concluded that LPBNSH exhibited liver-protective effects against fulminant hepatitis with jaundice at ca. 1/1000, 500 the molar concentration of PBN and, therefore, was clinically promising. [source] | |||||||||||||