ErbB4 signals Neuregulin1-stimulated cell proliferation and c-fos gene expression through phosphorylation of serum response factor by mitogen-activated protein kinase cascade

The temporal relationship of hepatic steatosis and changes in liver oxidative stress and fatty acid (FA) composition to the development of non-alcoholic steatohepatitis (NASH) remain to be clearly defined. Recently, we developed an experimental model of hepatic steatosis and NASH, the transgenic spontaneously hypertensive rat (SHR) that overexpresses a dominant positive form of the human SREBP-1a isoform in the liver. These rats are genetically predisposed to hepatic steatosis at a young age that ultimately progresses to NASH in older animals. Young transgenic SHR versus SHR controls exhibited simple hepatic steatosis which was associated with significantly increased hepatic levels of oxidative stress markers, conjugated dienes, and TBARS, with decreased levels of antioxidative enzymes and glutathione and lower concentrations of plasma α- and γ-tocopherol. Transgenic rats exhibited increased plasma levels of saturated FA, decreased levels of n?3 and n?6 polyunsaturated FA (PUFA), and increased n?6/n?3 PUFA ratios. These results are consistent with the hypothesis that excess fat accumulation in the liver in association with increased oxidative stress and disturbances in the metabolism of saturated and unsaturated fatty acids may precede and contribute to the primary pathogenesis of NASH.     

Lack of correlation between TBARS production and PUFA degradation during incubation of membrane erythrocytes in an OH⋅ (Fe2+/H2O2) generator system

We investigated the effects of an OH^⋅ (Fe²⁺/H₂O₂) generator system of erythrocyte membrane, particularly the time-course of lipid peroxidation as estimated by measurement of conjugated dienes, thiobarbituric reactive substances (TBARS), lipofuscin-like pigments, and α-tocopherol. Polyunsaturated fatty acids (PUFAs), especially arachidonic acid (20∶4 ω 6) and docosahexenoic acid (22∶6 ω 3), were also measured. Erythrocyte membranes were suspended in phosphate buffer containing Fe²⁺ (200 μM) and H₂O₂ (1.42 mM), and incubated in a shaking water bath at 37°C. Initially, there was an increase in TBARS and lipofuscin-like pigments, two well-known end products of PUFA oxidative degradation, whereas PUFAs remained unchanged (incubation time: 1 h). After two or more hours of incubation, marked lipid peroxidation was noted, with the appearance of conjugated dienes and a decrease of PUFAs, indicating that lipid peroxidation had occurred after a lag phase during which TBARS were not produced from PUFAs. This suggests that another OH^⋅ target was involved.     

Detection of retinal lipid hydroperoxides in experimental uveitis.

In our on-going studies of experimental uveitis, we previously obtained a preliminary indication of phagocyte-mediated retinal lipid peroxidation by measuring conjugated dienes (CD), thiobarbituric acid reactive substances (TBARS) and fluorescent chromolipids. Using gas chromatography/mass spectrometry (GC/MS), the current study detected hydroperoxide-derived 10-, 11-, 13-, 14-, and 17-hydroxydocosahexaenoic acid (HDHE) in retinal membranes. Docosahexaenoic acid (22:6) is the major polyunsaturated fatty acid (PUFA) in photoreceptor membranes. Hydroperoxides from other retinal PUFA were found also. Arachidonic acid (20:4) yielded 8-, 9-, 11-, 12-hydroxyeicosatetraenoic acid (HETE) as major products. Since 12-HETE could also arise from lipoxygenase catalyzed oxygenation of free 20:4, the source of 12-HETE could be both peroxidative and lipoxygenase pathways. Concomitantly, peroxidative loss of 22:6 and accumulation of 20:4 were also noted. At the peak of inflammation, loss of 22:6 was close to 50% of the original amount in the control retinas. In the same time period, 20:4 increased more than two-fold. The present data suggest that the oxygen radicals derived from phagocytes initiate the retinal lipid peroxidation, and the resultant formation of hydroperoxides, oxidative loss of 22:6 and accumulation of 20:4 appear to serve as amplification factors in subsequent biochemical events, such as chemotaxis of PMNs and activation of cyclooxygenase.     

Dietary Enrichment with Medium Chain Triglycerides (AC-1203) Elevates Polyunsaturated Fatty Acids in the Parietal Cortex of Aged Dogs: Implications for Treating Age-Related Cognitive Decline

Dogs demonstrate an age-related cognitive decline, which may be related to a decrease in the concentration of omega-3 polyunsaturated fatty acids (n-3 PUFA) in the brain. Medium chain triglycerides (MCT) increase fatty acid oxidation, and it has been suggested that this may raise brain n-3 PUFA levels by increasing mobilization of n-3 PUFA from adipose tissue to the brain. The goal of the present study was to determine whether dietary MCT would raise n-3 PUFA concentrations in the brains of aged dogs. Eight Beagle dogs were randomized to a control diet (n = 4) or an MCT (AC-1203) enriched diet (n = 4) for 2 months. The animals were then euthanized and the parietal cortex was removed for phospholipid, cholesterol and fatty acid determinations by gas-chromatography. Dietary enrichment with MCT (AC-1203) resulted in a significant increase in brain phospholipid and total lipid concentrations (P < 0.05). In particular, n-3 PUFA within the phospholipid, unesterified fatty acid, and total lipid fractions were elevated in AC-1203 treated subjects as compared to controls (P < 0.05). Brain cholesterol concentrations did not differ significantly between the groups (P > 0.05). These results indicate that dietary enrichment with MCT, raises n-3 PUFA concentrations in the parietal cortex of aged dogs.     

Associations of maternal prenatal dietary intake of n-3 and n-6 fatty acids with maternal and umbilical cord blood levels

Maternal n-3 and n-6 polyunsaturated fatty acid (PUFA) status may influence birth outcomes and child health. We assessed second trimester maternal diet with food frequency questionnaires (FFQs) (n=1666), mid-pregnancy maternal erythrocyte PUFA concentrations (n=1550), and umbilical cord plasma PUFA concentrations (n=449). Mean (SD) maternal intake of total n-3 PUFA was 1.17 g/d (0.43), docosahexaenoic and eicosapentaenoic acids (DHA+EPA) 0.16 g/d (0.17), and total n-6 PUFA 12.25 g/d (3.25). Mean maternal erythrocyte and cord plasma PUFA concentrations were 7.0% and 5.2% (total n-3), 5.0% and 4.6% (DHA+EPA), and 27.9% and 31.4% (total n-6). Mid-pregnancy diet–blood and blood–blood correlations were strongest for DHA+EPA (r=0.38 for diet with maternal blood, r=0.34 for diet with cord blood, r=0.36 for maternal blood with cord blood), and less strong for n-6 PUFA. The FFQ is a reliable measure of elongated PUFA intake, although inter-individual variation is present     

Protective role of intraperitoneally administered vitamin E and selenium on the antioxidative defense mechanisms in rats with diabetes induced by streptozotocin

The aim of this work was to determine the protective effects of intraperitoneally administered vitamin E and selenium (as Na₂SeO₃, Se) on the lipid peroxidation as thiobarbituric acid reactive substances (TBARS) and vitamin E levels, glutathione peroxidase (GSH-Px), reduced glutathione (GSH) activities in the plasma, red blood cell (RBC), liver, and muscle of rats with streptozotocin-induced diabetes. Fifty adult male Wistar rats were used and all rats were randomly divided into five groups. The first group was used as a control and the second group as a diabetic control. A placebo was given to first and second groups by injection. The third group was intraperitoneally administered with vitamin E (20 mg over 24 h), the fourth group with Se (0.3 mg over 24 h), and the fifth group with vitamin E and Se combination (COM) (20 mg vitamin E + 0.3 mg Se over 24 h). This administration was done for 25 days and the TBARS, vitamin E, GSH-Px, GSH levels in the plasma, RBC, liver, and muscle samples were determined. The vitamin E level in the plasma and liver was significantly (p < 0.05) higher in the control than in the diabetic control group. Also, the TBARS levels in the RBC, liver, and muscle were significantly (p < 0.05) lower in the control than in the diabetic control group. However, GSH-Px and GSH activities in RBC, liver, and muscle were not statistically different between the control and the diabetic control groups. The vitamin E levels in plasma and liver (p < 0.01 and p < 0.001) and GSH-Px activities (p < 0.01, p < 0.001) in RBC were significantly higher in vitamin E, Se, and COM groups than in both control and diabetic control groups. However, the TBARS levels of RBC, muscle, and liver in vitamin E and Se administered groups were significantly (p < 0.05-p < 0.001, respectively) decreased. These results indicate that intraperitoneally administered vitamin E and Se have significant protective effects on the blood, liver, and muscle against oxidative damage of diabetes. The abstract of this study was presented in Physiological Research 48(Suppl. 1), S99 (1999).     

Day-night variations in pro-oxidant reactions of hypothalamic,hepatic and pancreatic tissue in mice with spontaneous obesity (Neotomodon alstoni)

Objectives: The present work compares the pro-oxidant properties in hypothalamic, hepatic, and pancreatic tissue of spontaneously obese and lean Neotomodon alstoni during day and night. Methods: Lipid peroxidation from hypothalamus, liver, and pancreas from lean and obese mice were quantified by the two-thiobarbituric acid method. Lipid peroxidation in vivo was also determined by means of detection of conjugated dienes in lipid extracts. Results: Hypothalamic tissue from obese Neotomodon showed a notorious increase (nearly 700%) in the production of thiobarbituric acid-reactive substances (TBARS) at day, either in basal as well as in an assay supplemented with Fe²⁺; the presence of conjugated dienes was also notably greater (76%) at day. Hypothalamus of lean mice presented an increase (170%) in assay supplemented with Fe²⁺. Hepatic tissue in obese mice showed diurnal increasing in TBARS + Fe²⁺ (34%) and in conjugated dienes (38%), while lean mice showed only a diurnal increase (45%) in TBARS + Fe²⁺. Pancreatic tissue from obese mice presented a diurnal increasing in basal TBARS (130%) but a decrease (72%) in TBARS + Fe²⁺. Presence of conjugated dienes was also decreased during the day in lean (60%) and in obese (40%) mice. Conclusions: In the obese Neotomodon, there is a larger day–night change in pro-oxidant status in the hypothalamus and in pancreas than the one observed in the liver, suggesting a differential equilibrium between oxidative reactions and antioxidant defenses in the different tissues during the day–night cycle.     

Dietary Omega-3 Polyunsaturated Fatty Acids Alter the Fatty Acid Composition of Hepatic and Plasma Bioactive Lipids in C57BL/6 Mice: A Lipidomic Approach

Background

Omega (n)-3 polyunsaturated fatty acids (PUFA) are converted to bioactive lipid components that are important mediators in metabolic and physiological pathways; however, which bioactive compounds are metabolically active, and their mechanisms of action are still not clear. We investigated using lipidomic techniques, the effects of diets high in n-3 PUFA on the fatty acid composition of various bioactive lipids in plasma and liver.

Methodology and Principal Findings

Female C57BL/6 mice were fed semi-purified diets (20% w/w fat) containing varying amounts of n-3 PUFA before mating, during gestation and lactation, and until weaning. Male offspring were continued on their mothers’ diets for 16 weeks. Hepatic and plasma lipids were extracted in the presence of non-naturally occurring internal standards, and tandem electrospray ionization mass spectrometry methods were used to measure the fatty acyl compositions. There was no significant difference in total concentrations of phospholipids in both groups. However, there was a significantly higher concentration of eicosapentaenoic acid containing phosphatidylcholine (PC), lysophosphatidylcholine (LPC), and cholesteryl esters (CE) (p < 0.01) in the high n-3 PUFA group compared to the low n-3 PUFA group in both liver and plasma. Plasma and liver from the high n-3 PUFA group also had a higher concentration of free n-3 PUFA (p < 0.05). There were no significant differences in plasma concentrations of different fatty acyl species of phosphatidylethanolamine, triglycerides, sphingomyelin and ceramides.

Conclusions/Significance

Our findings reveal for the first time that a diet high in n-3 PUFA caused enrichment of n-3 PUFA in PC, LPC, CE and free fatty acids in the plasma and liver of C57BL/6 mice. PC, LPC, and unesterified free n-3 PUFA are important bioactive lipids, thus altering their fatty acyl composition will have important metabolic and physiological roles.     

Monounsaturated diet lowers LDL oxidisability in type IIb and type IV dyslipidemia without affecting coenzyme Q10 and vitamin E contents.

The purpose of the present study was to evaluate the effects of MUFA vs PUFA enriched diets on the plasma and LDL lipid profile and antioxidant contents in mild hypercholesterolemic and triglyceridemic subjects. The study was divided in two consecutive diet periods. Two groups of 11 dyslipidemic patients each (type IIb and type IV) were recruited and during the first period (lasting four weeks) received a linoleic rich diet while during the following four weeks took an oleate rich diet. Both groups showed no significant changes in cholesterol and TG concentration either in plasma or in LDL. Coenzyme Q10 and vitamin E were also unaffected by the dietary treatments. LDL proneness to be oxidatively modified increased after dietary PUFA administration and markedly decreased following the virgin olive oil enriched diet. In fact, LDL from hypertrigliceridemic subjects on a oleate-enriched diet displayed a 26% (p < 0.05) longer lag-phase in conjugated dienes generation than during linoleate-enriched diet and at recruitment. In hypercholesterolemic subjects similar results were obtained: the lag-phase was 28% longer after MUFA diet that after PUFA diet. No differences were found in the maximum propagation rate and maximum concentration of conjugated dienes among dietary periods and at recruitment. Since we found that the vit. E and CoQ10 levels in plasma and in LDL particles remained unchanged during the course of the study, we may conclude that LDL proneness to undergo oxidative modifications is mainly the result of compositional change due to the enrichment from the different diets of the relative fats.     

Fatty Acid Composition and the Oxidation of Low-Density Lipoproteins

The effect of the fatty acid composition of low-density lipoprotein (LDL) on copper-ion-catalyzed oxidation of isolated LDL was examined in 18 normolipidemic men. The decrease in LDL linoleic acid concentration (ΔL) during oxidation was found to be strongly correlated with initial LDL linoleic acid concentration (r = 0.976, n = 18, P < 0.001), whereas the production of thiobarbituric acid reacting substances (TBARS) was not. The concentration of oleic acid in LDL was then increased significantly (mean increase 20%, P < 0.05) in 8 male volunteers by a daily dietary supplement of rapeseed oil/muesli for 4 weeks. The mean delay before copper-ion-catalyzed production of conjugated dienes (the lag phase) was significantly (P < 0.001) greater in LDL isolated after the study period (67 min) than that of before the study period (40 mm). The rate of formation of conjugated dienes, ΔL and TBARS production during oxidation of LDL was not significantly altered by the rapeseed oil/muesli supplement. These results suggest that the linoleic acid content of LDL is a determinant of individual variability in LDL oxidation, and that a rapeseed oil/muesli dietary supplement reduces the susceptibility of LDL to oxidation.     

Comparison between in vitro lipid peroxidation in fresh sheep platelets and peroxidative processes during sheep platelet ageing under storage at 4 degrees C.

Incubation of sheep platelet crude membranes with xanthine oxidase (XO)/hypoxanthine/Fe(2+)-ADP revealed: (i) a fast peroxidative response - with a maximal linear rate of 14 nmol malondialdehyde (MDA) equivalents/mg protein, as evidenced by the thiobarbituric acid test - and a decrease in the polyunsaturated fatty acid (PUFA) content of the platelet crude membranes; (ii) a decrease in the lipid fluidity in the deep lipid core of the membranes but not at the membrane surface; (iii) a dramatic inhibitory effect on glucose 6-phosphatase (Glc-6-Pase) but not on acetylcholinesterase activity. Platelets were also aged by storage at 4 degrees C in their own plasma or in Seto additive solution. In these media, platelet aggregates were visible and the effects on platelet phospholipids, PUFA, lipid extract fluorescence, crude membrane fluidity and membrane-bound enzyme activities were assessed for comparison with those observed in in vitro lipid peroxidation. The sensitivity of membranes from stored platelets to lipid peroxidation was also assessed. Storage of platelets in plasma for 5 days was associated with different changes in their crude membranes such as decreases in arachidonic acid contents, the decrease not being avoided by the presence of phospholipase A(2) inhibitors, increases in MDA equivalents, conjugated dienes and lipid extract fluorescence, decreases in the amounts of MDA equivalents formed by platelet crude membranes treated with the oxidizing agents, changes in membrane fluidity and inhibition of Glc-6-Pase. All these alterations were less pronounced or even abolished after platelet storage in Seto. These findings suggest that platelet lipid peroxidation due to XO/hypoxanthine/Fe(2+)-ADP and platelet membrane alterations observed after platelet ageing under storage at 4 degrees C share common features. Also, as regards the prevention of peroxidative processes, Seto solution permits better storage of sheep platelets than plasma.     

Different bioavailability in humans of wheat and fish selenium as measured by blood platelet response to increased dietary Se

The bioavailabilities of selenium (Se) from Se-rich fish species and Se-rich wheat were compared in a study involving 32 healthy volunteers. Initial serum Se values were 109±16 μg/L (mean±SD). For 6 wk, one group (n=11) included Se-rich bread in their diet, bringing daily average intake of Se up to 135±25 μg/d. Another group (n=11) consumed Se-rich fish daily (average Se intake: 115±31 μg/d), whereas the control group (n=10) ate their normal diet, providing 77±25 μg Se/d. Serum Se increased by 17% (P<0.01), and platelet Se increased by 30% (P<0.01) in the wheat group. Although platelet Se decreased by 11% in the fish group, no changes in serum and platelet Se in the fish or control group reached statistical significance. Glutathione peroxidase (EC 1.11.1.9; GSH-Px) activity in serum and platelets did not change during the study, nor did platelet mercury (Hg) content. Since the dietary intake of Hg, arsenium (As), and fatty acids could not satisfactorily explain the lack of response in the fish group, the results are indicative of low bioavailability of fish Se in humans. At present, wheat Se seems to be the most important factor contributing to the body stores of Se in this study population. Dr. Norheim died on January 9, 1991.     

Local and systemic oxidant/antioxidant status before and during lung cancer radiotherapy

To examine local and systemic oxidative status of lung cancer (LC) and oxidant effects of radiotherapy (RT), this study evaluated antioxidants and markers of oxidative and nitrosative stress in bronchoalveolar lavage (BAL) fluid and in the blood of 36 LC patients and 36 non-cancer controls at baseline and during and after RT for LC. LC patients had higher baseline serum urate, plasma nitrite and lower serum oxidized proteins than controls (p=0.016, p<0.001 and p=0.027, respectively), but BAL fluid oxidative stress markers were similar. RT tended to raise some antioxidants, however, significant increases were seen in serum urate, conjugated dienes and TBARS (p=0.044, p=0.034 and p=0.004, respectively) 3 months after RT. High urate at baseline may compensate against the oxidative stress caused by LC. RT shifts the oxidant/antioxidant balance towards lipid peroxidation, although the antioxidant defense mechanisms of the body appear to counteract the increased oxidative stress rather effectively.     

Concurrent measurement of (Na+,K+)-ATPase activity and lipid peroxides in rat brain following reversible global ischemia

Lipid peroxides, quantitated as lipid conjugated dienes, and (Na⁺,K⁺)-ATPase activity were assayed concurrently in brains of control rats and in three groups subjected to 30 min of reversible forebrain ischemia followed by 0, 1, and 4 hr of recirculation. Multiple small samples were taken from lateral, dorsolateral and medial cortex, hippocampus, thalamus and striatum following in situ freezing. (Na⁺,K⁺)-ATPase activity was elevated in hippocampus, dorsolateral and lateral cortex (P<0.10) and in thalamus (P<0.05) following 30 min ischemia. ATPase activity in medial cortex continued to increase during the first 1 hr of recirculation (P<0.10). Following 4 hr of recirculation, decreased enzyme activities were observed in all of these regions (lateral cortex and hippocampus,P<0.10). No changes in ATPase activity were observed in samples from striatum. Of the regional samples assayed for lipid peroxide content, the incidence of conjugated dienes as a function of recirculation time was 6% (0 hr), 23% (1 hr), and 17% (4 hr). For these samples, plots of normalized ATPase activity vs. tissue conjugated diene concentration revealed that normalized ATPase activity varied with recirculation time, but was independent of the magnitude of the lipid peroxidative process (expressed in terms of tissue conjugated diene concentration). These results suggest that disturbances in membrane structure and function presumed to arise from lipid peroxidation are not responsible for the behavior of the ATPase under the current in vivo conditions.     

N-3 fatty acid supplementation decreases plasma homocysteine in diabetic dyslipidemia treated with statin-fibrate combination

The aim of this study was to study the effect of adding polyunsaturated fatty acid (PUFA) n-3 or placebo (containing oleic acid) to a combined statin-fibrate treatment on plasma lipoproteins, lipoperoxidation, glucose homeostasis, total homocysteine (tHcy) and microalbuminuria (MA) in patients with diabetic dyslipidemia (DDL). Twenty-four patients, who did not fulfill the recommended target lipid values with combined hypolipidemic therapy (pravastatin 20 mg+micronized fenofibrate 200 mg daily), were supplemented with 3.6 g PUFA n-3 daily for 3 months or placebo (olive oil) for the next 3 months. The concentrations of plasma lipids, fatty acid (FA) profiles of phosphatidylcholine (PC), cholesteryl esters (CE) and triglycerides (TG), tHcy levels, concentrations of conjugated dienes (CD) in low-density lipoprotein (LDL), and MA were determined in baseline state, after the PUFA n-3 and placebo treatment period. Supplementation with PUFA n-3 led to a significant decrease in plasma tHcy (-29%, P < .01) and TG (-28%, P < .05) levels, as well as to a significant decrease in MA (-24%, P < .05). The decrease in MA correlated significantly with the increase in total PUFA n-3 (r = -.509, P < or = .05) and docosahexaenoic acid (r = -.52, P < .01) in TG. The concentrations of CD in LDL increased significantly (+15%, P < .05). The supplementation with PUFA n-3 to the combined statin-fibrate treatment in patients with DDL decreased the TG and tHcy levels as well as MA. It could lead to decreased risk of atherothrombosis and delay of diabetic nephropathy onset and progression.     

Tea catechins inhibit cholesterol oxidation accompanying oxidation of low density lipoprotein in vitro

Endogenous oxidized cholesterols are potent atherogenic agents. Therefore, the antioxidative effects of green tea catechins (GTC) against cholesterol oxidation were examined in an in vitro lipoprotein oxidation system. The antioxidative potency of GTC against copper catalyzed LDL oxidation was in the decreasing order (-)-epigalocatechin gallate (EGCG)=(-)-epicatechin gallate (ECG)>(-)-epicatechin (EC)=(+)-catechin (C)>(-)-epigallocatechin (EGC). Reflecting these activities, both EGCG (74%) and ECG (70%) inhibited the formation of oxidized cholesterol, as well as the decrease of linoleic and arachidonic acids, in copper catalyzed LDL oxidation. The formation of oxidized cholesterol in 2,2'-azobis(2-amidinopropane) hydrochloride (AAPH)-mediated oxidation of rat plasma was also inhibited when the rats were given diets containing 0.5% ECG or EGCG. In addition, EGCG and ECG highly inhibited oxygen consumption and formation of conjugated dienes in AAPH-mediated linoleic acid peroxidative reaction. These two species of catechin also markedly lowered the generation of hydroxyl radical and superoxide anion. Thus, GTC, especially ECG and EGCG, seem to inhibit cholesterol oxidation in LDL by combination of interference with PUFA oxidation, the reduction and scavenging of copper ion, hydroxyl radical generated from peroxidation of PUFA and superoxide anion.     

Role of the Lower and Upper Intestine in the Production and Absorption of Gut Microbiota-Derived PUFA Metabolites

In vitro studies have suggested that isolated gut bacteria are able to metabolize PUFA into CLA (conjugated linoleic acids) and CLnA (conjugated linolenic acids). However, the bioavailability of fatty acid metabolites produced in vivo by the gut microbes remains to be studied. Therefore, we measured intestinal concentration and plasma accumulation of bacterial metabolites produced from dietary PUFA in mice, first injected with a lipoprotein lipase inhibitor, then force-fed with either sunflower oil (200 µl) rich in n-6 PUFA or linseed oil (200 µl) rich in n-3 PUFA. The greatest production of bacterial metabolites was observed in the caecum and colon, and at a much lesser extent in the jejunum and ileum. In the caecal content, CLA proportions were higher in sunflower oil force-fed mice whereas CLnA proportions were higher in linseed oil force-fed mice. The accumulation of the main metabolites (CLA cis-9,trans-11-18:2 and CLnA cis-9,trans-11,cis-15-18:3) in the caecal tissue was not associated with their increase in the plasma, therefore suggesting that, if endogenously produced CLA and CLnA have any biological role in host metabolism regulation, their effect would be confined at the intestinal level, where the microbiota is abundant.     

Effect of nutrition on fatty acid profiles of riverine, lacustrine, and aquaculture-raised salmonids of pre-alpine habitats

We examined trophic positions and fatty acid concentrations of riverine, lacustrine, and aquaculture diet and fish in Austrian pre-alpine aquatic ecosystems. It was hypothesized that dietary fatty acid (FA) profiles largely influence the FA composition of the salmonids Salvelinus alpinus, Salmo trutta, and Oncorhynchus mykiss. We analyzed trophic positions using stable isotopes (δ¹⁵N) and tested for correlations with polyunsaturated fatty acid (PUFA) concentrations. Gut content analysis revealed benthos (rivers), pellets (aquaculture), and zooplankton (lakes) as the predominant diet source. Results of dorsal muscle tissues analysis showed that the omega-3 PUFA, docosahexaenoic acid (DHA; 22:6n − 3), was the mostly retained PUFA in all fish of all ecosystems, yet with the highest concentrations in S. alpinus from aquaculture (mean: 20 mg DHA/g dry weight). Moreover, we found that eicosapentaenoic acid (EPA; 20:5n − 3) in fish of natural habitats (rivers, lakes) was the second most abundant PUFA (3–5 mg/g DW), whereas aquaculture-raised fish had higher concentrations of the omega-6 linoleic acid (18:2n – 6; 9–11 mg/g DW) than EPA. In addition, PUFA patterns showed that higher omega-3/-6 ratios in aquacultures than in both riverine and lacustrine fish. Data of this pilot field study suggest that salmonids did not seem to directly adjust their PUFA to dietary PUFA profiles in either natural habitats or aquaculture and that some alterations of PUFA are plausible. Finally, we suggest that trophic positions of these freshwater salmonids do not predict PUFA concentrations in their dorsal muscle tissues.     

Rutin improves the antioxidant status in streptozotocin-induced diabetic rat tissues

Rutin, a polyphenolic flavonoid, was investigated for its antioxidant potential in streptozotocin (STZ)-induced diabetic rats. Rats were rendered diabetic by a single intraperitoneal injection of streptozotocin (50 mg/kg). The levels of fasting plasma glucose and insulin were estimated. Lipid peroxidative products and antioxidants were estimated in liver, kidney and brain. Histopathological studies were carried out in these tissues. A significant (p < 0.05) increase in the levels of fasting plasma glucose, lipid peroxidative products (thiobarbituric acid reactive substances [TBARS] and lipid hydroperoxides [HP]) and a significant (p < 0.05) decrease in plasma insulin, enzymic antioxidants (superoxide dismutase [SOD], catalase, glutathione peroxidase [GPx] and glutathione reductase [GRx]) and nonenzymic antioxidants (reduced glutathione [GSH], vitamin C and E) in diabetic liver, kidney and brain were observed. Oral administration of rutin (100 mg/kg) for a period of 45 days significantly (p < 0.05) decreased fasting plasma glucose, increased insulin levels and improved the antioxidant status of diabetic rats by decreasing lipid peroxidative products and increasing enzymic and nonenzymic antioxidants. Normal rats treated with rutin (100 mg/kg) showed no significant (p < 0.05) effect on any of the parameters studied. Histopathological studies of the liver, kidney and brain showed the protective role of rutin. Thus, our study clearly shows that rutin has antioxidant effect in STZ-induced experimental diabetes.