Lipid peroxidation as one mode of action in ochratoxin A toxicity in rats and chicks

1997 ◽  
Vol 77 (2) ◽  
pp. 287-292 ◽  
Author(s):  
Dirk Hoehler ◽  
Ronald R. Marquardt ◽  
Andrew A.F. Rohlich
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Ochratoxin A ◽  
Sunflower Oil ◽  
Mode Of Action ◽  
Unsaturated Fatty Acids ◽  
Corn Oil ◽  
Iron Catalyst ◽  
Different Tissues

The objective of this study was to determine whether lipid peroxidation is one mode of action in ochratoxin A (OA) toxicity in vivo. Lipid peroxidation was monitored by analyzing malondialdehyde (MDA) in different tissues by HPLC. A refinement study on the MDA assay was carried out, which showed the importance of the addition of an iron catalyst for the decomposition of hydroperoxides to yield a maximum amount of MDA from a given sample. The rat experiment was designed in a 2 × 2 factorial arrangement using 4 × 6 animals. The four different diets were fed for 21 d and contained either 1% corn oil and 9% tallow (Diets I and III) or 10% corn oil (Diets II and IV); in groups III and IV, 5 mg OA were added per kilogram of diet. For the chick experiment 4 × 8 Leghorn cockerels received diets for 14 d with no added sunflower oil (Diets I and III), whereas the diets of groups II and IV were supplemented with 2.5% sunflower oil. In groups III and IV, 2.5 mg OA were added per kilogram of diet. In both experiments OA decreased the performance of the animals significantly. In the rat experiment an increased lipid peroxidation due to a higher dietary level of unsaturated fatty acids could be obtained, when muscle samples were oxidatively stressed with Fe3+ and ascorbic acid. In the chick experiment there were very clear effects of the dietary treatment on the MDA concentrations of different tissues, as both a higher supply with unsaturated fatty acids and OA increased most of the MDA values significantly. These data suggest that lipid peroxides are formed in vivo by OA, but the effects may vary considerably from species to species, and may also be influenced by other factors. Key words: Ochratoxin A, lipid peroxidation, malondialdehyde, rat, chick

Glucose-stimulated acrolein production from unsaturated fatty acids

2004 ◽  
Vol 23 (2) ◽  
pp. 101-105 ◽  
Author(s):  
R Medina-Navarro ◽  
G Duran-Reyes ◽  
M Diaz-Flores ◽  
J J Hicks ◽  
J Kumate R
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Unsaturated Fatty Acids ◽  
Tissue Injury ◽  
Acid Product ◽  
Hydroperoxide Formation ◽  
Fatty Acid Product ◽  
Arachidonic Acids

Glucose auto-oxidation may be a significant source of reactive oxygen species (ROS), and also be important in the lipid peroxidation process, accompanied by the release of toxic reactive products. We wanted to demonstrate that acrolein can be formed directly and actively from free fatty acids in a hyperglycemic environment. A suspension of linoleic and arachidonic acids (2.5 mM) was exposed to different glucose concentrations (5, 10 and 15 mmol/L) in vitro. The samples were extracted with organic solvents, partitioned, followed at 255 / 267 nm, and analysed using capillary electrophoresis and mass spectroscopy. The total release of aldehydes significantly (P ≤ 0.01) increased from 1.0 to 5.1, 8.3 and 13.1 μmol/L after 6 hours of incubation, proportional to glucose concentrations. It was possible to verify a correlate hydroperoxide formation as well. Among the lipid peroxidation products, acrolein (5% of total) and its condensing product, 4-hydroxy-hexenal, were identified. From the results presented here, it was possible to demonstrate the production of acrolein, probably as a fatty acid product, due to free radicals generated from the glucose auto-oxidation process. The results led us to propose that acrolein, which is one of the most toxic aldehydes, is produced during hyperglycemic states, and may lead to tissue injury, as one of the initial problems to be linked to high levels of glucose in vivo.

scholarly journals Pengimbuhan Minyak Jagung Terproteksi dengan Berbagai Level Protein Ransum Sapi Friesian Holstein Meningkatkan Kadar Asam Lemak Tidak Jenuh Susu

2018 ◽  
Vol 19 (1) ◽  
pp. 100
Author(s):  
Danes Suhendra ◽  
Sudjatmogo Sudjatmogo ◽  
Widiyanto Widiyanto
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Protein Level ◽  
Crude Protein ◽  
Unsaturated Fatty Acids ◽  
Corn Oil ◽  
Monounsaturated Fatty Acids ◽  
Milk Fatty Acids ◽  
Iodin Number

This study was aimed to examine level supplemenation of corn oil (CO) as a source of protected poly unsaturated fatty acids (PUFA) and various crude protein (CP) levels in diets to ruminal iodin number and milk fatty acids of Friesian Holstein. The research done through two stages, using in vivo method and in vivo method. The corn oil protection is performed by saponification using KOH and then tranformed using CaCl2 to calcium salt. Research use two treatment factors with three replications, the first factor was supplementation of PUFA (L) with details L0 (Without protection), L1 (supplementation 75% Protected CO), and L2 (Supplementation 80% Protected CO) and the second factor is the P1 crude protein level (CP 12%) and P2 (CP 16%). The results showed that there was no interaction effect between the supplementation of protected CO with protein level to the ruminal iodin number, saturated fatty acid (SFA), unsaturated fatty acid (UFA), linoleic acid (LA), monounsaturated fatty acids (MUFA) and polyunsaturated fatty acid (PUFA) milk. The parameters are iodin number and milk fatty acids. Result of this research show that supplementation of protected CO increased the ruminal iodin number (P<0.01), UFA (P=), LA (P=) and milk PUFA (P=). Supplementation protected CO decrease milk SFA (P=). It can be concluded that supplementation of protected CO increases milk UFA of FH.

scholarly journals Studies of the long-term regulation of hepatic pyruvate dehydrogenase kinase

1998 ◽  
Vol 329 (1) ◽  
pp. 89-94 ◽  
Author(s):  
C. Mary SUGDEN ◽  
G. D. Lee FRYER ◽  
A. Karen ORFALI ◽  
A. David PRIESTMAN ◽  
Elaine DONALD ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Pyruvate Dehydrogenase ◽  
Unsaturated Fatty Acids ◽  
Fold Increase ◽  
Membrane Lipid ◽  
Dietary Lipid ◽  
Pyruvate Dehydrogenase Kinase ◽  
Plasma Insulin Concentration

The administration of a low-carbohydrate/high-saturated-fat (LC/HF) diet for 28 days or starvation for 48 h both increased pyruvate dehydrogenase kinase (PDHK) activity in extracts of rat hepatic mitochondria, by approx. 2.1-fold and 3.5-fold respectively. ELISAs of extracts of hepatic mitochondria, conducted over a range of pyruvate dehydrogenase (PDH) activities, revealed that mitochondrial immunoreactive PDHKII (the major PDHK isoform in rat liver) was significantly increased by approx. 1.4-fold after 28 days of LC/HF feeding and by approx. 2-fold after 48 h of starvation. The effect of LC/HF feeding to increase hepatic PDHK activity was retained through hepatocyte preparation, but was decreased on 21 h culture with insulin (100μ-i.u./ml). A sustained (24 h) 2-4-fold elevation in plasma insulin concentration in vivo (achieved by insulin infusion via an osmotic pump) suppressed the effect of LC/HF feeding so that hepatic PDHK activities did not differ significantly from those of (insulin-infused) control rats. The increase in hepatic PDHK activity evoked by 28 days of LC/HF feeding was prevented and reversed (within 24 h) by the replacement of 7% of the dietary lipid with long-chain ω-3 fatty acids. Analysis of hepatic membrane lipid revealed a 1.9-fold increase in the ratio of total polyunsaturated ω-3 fatty acids to total mono-unsaturated fatty acids. The results indicate that the increased hepatic PDHK activities observed in livers of LC/HF-fed or 48 h-starved rats are associated with long-term actions to increase hepatic PDHKII concentrations. The long-term regulation of hepatic PDHK by LC/HF feeding might be achieved through an impaired action of insulin to suppress PDHK activity. In addition, the fatty acid composition of the diet, rather than the fat content, is a key influence.

scholarly journals Analysis of the Carry-Over of Ochratoxin A from Feed to Milk, Blood, Urine, and Different Tissues of Dairy Cows Based on the Establishment of a Reliable LC-MS/MS Method

Molecules ◽  
2019 ◽  
Vol 24 (15) ◽  
pp. 2823 ◽  
Author(s):  
Zhiqi Zhang ◽  
Zhichen Fan ◽  
Dongxia Nie ◽  
Zhihui Zhao ◽  
Zheng Han
Keyword(s):  
Dairy Cows ◽  
Ochratoxin A ◽  
Limit Of Quantification ◽  
Fresh Milk ◽  
Liquid Chromatography Tandem Mass ◽  
Ochratoxin Α ◽  
Carry Over ◽  
First Time ◽  
Different Tissues

A rapid and reliable liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was developed for simultaneous determination of ochratoxin A (OTA) and its metabolite ochratoxin α (OTα), for the first time, in dairy cow plasma, milk, urine, heart, liver, spleen, lung, and kidney. The established method was extensively validated by determining the linearity (R2 ≥ 0.990), sensitivity (lower limit of quantification, 0.1–0.2 ng mL−1), recovery (75.3–114.1%), precision (RSD ≤ 13.6%), and stability (≥83.0%). Based on the methodological advances, the carry-over of OTA was subsequently studied after oral administration of 30 μg/kg body weight OTA to dairy cows. As revealed, OTA and OTα were detected in urine, with maximal concentrations of 1.8 ng mL−1 and 324.6 ng mL−1, respectively, but not in milk, plasma, or different tissues, verifying the protection effects of rumen flora against OTA exposure for dairy cows. Moreover, 100 fresh milk samples randomly collected from different supermarkets in Shanghai were also analyzed, and no positive samples were found, further proving the correctness of the in vivo biotransformation results. Thus, from the currently available data, regarding OTA contamination issues on dairy cows, no significant health risks were related to OTA exposure due to the consumption of these products.

scholarly journals The Involvement of Energy Metabolism and Lipid Peroxidation in Lignin Accumulation of Postharvest Pumelos

Membranes ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 269
Author(s):  
Huiling Yan ◽  
Junjia Chen ◽  
Juan Liu
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Energy Metabolism ◽  
Unsaturated Fatty Acids ◽  
Saturated Fatty Acids ◽  
Energy Charge ◽  
Succinic Dehydrogenase ◽  
Membrane Integrity ◽  
Lignin Accumulation ◽  
Juice Sacs

Lignification is especially prominent in postharvest pumelo fruit, which greatly impairs their attractiveness and commercial value. This study investigated the energy metabolism and lipid peroxidation and their relationship with accumulated lignin content in juice sacs of “Hongroumiyou” (HR) during 90 d of storage at 25 °C. The results indicated that, the alterations of energy metabolism in juice of sacs of postharvest pumelos was featured by a continuous decline in energy charge and ATP/ADP; an increase in succinic dehydrogenase (SDH) activity before 30 d and increases in activities of cytochrome c oxidase (CCO) and F0F1-ATPase before 60 d; but declines in activities of Ca2+-ATPase and H+-ATPase. Additionally, enhanced contents of H2O2, O2−, and –OH scavenging rate; increased malondialdehyde (MDA) content; and transformation of unsaturated fatty acids (USFA) to saturated fatty acids (USFA) and reduced USFA/SFA (U/S) could result in lipid peroxidation and membrane integrity loss. Moreover, correlation analysis showed that lignin accumulation was in close relation to energy metabolism and lipid peroxidation in juice sacs of postharvest pumelos. These results gave evident credence for the involvement of energy metabolism and lipid peroxidation in the lignin accumulation of HR pumelo fruit during postharvest storage.

scholarly journals The role of lipid components of the diet in the regulation of the fatty acid composition of the rat liver endoplasmic reticulum and lipid peroxidation

1978 ◽  
Vol 174 (2) ◽  
pp. 585-593 ◽  
Author(s):  
Catherine T. Hammer ◽  
Eric D. Wills
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Endoplasmic Reticulum ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acids ◽  
Acid Composition ◽  
Corn Oil ◽  
Lipid Peroxide

The fatty acid compositions of the lipids and the lipid peroxide concentrations and rates of lipid peroxidation were determined in suspensions of liver endoplasmic reticulum isolated from rats fed on synthetic diets in which the fatty acid composition had been varied but the remaining constituents (protein, carbohydrate, vitamins and minerals) kept constant. Stock diet and synthetic diets containing no fat, 10% corn oil, herring oil, coconut oil or lard were used. The fatty acid composition of the liver endoplasmic reticulum lipid was markedly dependent on the fatty acid composition of the dietary lipid. Feeding a herring-oil diet caused incorporation of 8.7% eicosapentaenoic acid (C20:5) and 17% docosahexaenoic acid (C22:6), but only 5.1% linoleic acid (C18:2) and 6.4% arachidonic acid (C20:4), feeding a corn-oil diet caused incorporation of 25.1% C18:2, 17.8% C20:4 and 2.5% C22:6 fatty acids, and feeding a lard diet caused incorporation of 10.3% C18:2, 13.5% C20:4 and 4.3% C22:6 fatty acids into the liver endoplasmic-reticulum lipids. Phenobarbitone injection (100mg/kg) decreased the incorporation of C20:4 and C22:6 fatty acids into the liver endoplasmic reticulum of rats fed on a lard, corn-oil or herring-oil diet. Microsomal lipid peroxide concentrations and rates of peroxidation in the presence of ascorbate depended on the nature and quantity of the polyunsaturated fatty acids in the diet. The lipid peroxide content was 1.82±0.30nmol of malonaldehyde/mg of protein and the rate of peroxidation was 0.60±0.08nmol of malonaldehyde/min per mg of protein after feeding a fat-free diet, and the values were increased to 20.80nmol of malonaldehyde/mg of protein and 3.73nmol of malonaldehyde/min per mg of protein after feeding a 10% herring-oil diet in which polyunsaturated fatty acids formed 24% of the total fatty acids. Addition of α-tocopherol to the diets (120mg/kg of diet) caused a very large decrease in the lipid peroxide concentration and rate of lipid peroxidation in the endoplasmic reticulum, but addition of the synthetic anti-oxidant 2,6-di-t-butyl-4-methylphenol to the diet (100mg/kg of diet) was ineffective. Treatment of the animals with phenobarbitone (1mg/ml of drinking water) caused a sharp fall in the rate of lipid peroxidation. It is concluded that the polyunsaturated fatty acid composition of the diet regulates the fatty acid composition of the liver endoplasmic reticulum, and this in turn is an important factor controlling the rate and extent of lipid peroxidation in vitro and possibly in vivo.

scholarly journals Overlapping Repressor Binding Sites Result in Additive Regulation of Escherichia coli FadH by FadR and ArcA

2010 ◽  
Vol 192 (17) ◽  
pp. 4289-4299 ◽  
Author(s):  
Youjun Feng ◽  
John E. Cronan
Keyword(s):  
Escherichia Coli ◽  
Fatty Acids ◽  
Cyclic Amp ◽  
Unsaturated Fatty Acids ◽  
Genetic Regulation ◽  
Receptor Protein ◽  
Anaerobic Conditions ◽  
Mobility Shift ◽  
Long Chain

ABSTRACT Escherichia coli fadH encodes a 2,4-dienoyl reductase that plays an auxiliary role in β-oxidation of certain unsaturated fatty acids. In the 2 decades since its discovery, FadH biochemistry has been studied extensively. However, the genetic regulation of FadH has been explored only partially. Here we report mapping of the fadH promoter and document its complex regulation by three independent regulators, the fatty acid degradation FadR repressor, the oxygen-responsive ArcA-ArcB two-component system, and the cyclic AMP receptor protein-cyclic AMP (CRP-cAMP) complex. Electrophoretic mobility shift assays demonstrated that FadR binds to the fadH promoter region and that this binding can be specifically reversed by long-chain acyl-coenzyme A (CoA) thioesters. In vivo data combining transcriptional lacZ fusion and real-time quantitative PCR (qPCR) analyses indicated that fadH is strongly repressed by FadR, in agreement with induction of fadH by long-chain fatty acids. Inactivation of arcA increased fadH transcription by >3-fold under anaerobic conditions. Moreover, fadH expression was increased 8- to 10-fold under anaerobic conditions upon deletion of both the fadR and the arcA gene, indicating that anaerobic expression is additively repressed by FadR and ArcA-ArcB. Unlike fadM, a newly reported member of the E. coli fad regulon that encodes another auxiliary β-oxidation enzyme, fadH was activated by the CRP-cAMP complex in a manner similar to those of the prototypical fad genes. In the absence of the CRP-cAMP complex, repression of fadH expression by both FadR and ArcA-ArcB was very weak, suggesting a possible interplay with other DNA binding proteins.

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