Oxidative stress induced by corticosterone administration in broiler chickens (Gallus gallus domesticus) 2. Short-term effect

Two trials were conducted to evaluate the effects of short-term administration of corticosterone (CORT) on the induction of oxidative injury in broiler chickens (Gallus gallus domesticus). Twelve broiler chickens of 30 and of 40 days of age were respectively employed in Trial 1 and 2. Half of the chickens were administered subcutaneously with CORT (4 mg/kg body weight [BW] in corn oil), while another half served as controls (corn oil) in each trail. In Trial 1, a blood sample was obtained from each chicken immediately before administration and at 1 and 3 h after injection. In Trial 2, the liver and heart were obtained after 3 h of CORT exposure. Short-term administration of CORT resulted in enhanced proteolysis and gluconeogenesis. There were no obvious changes in lipid peroxidation status of the heart and liver, whereas a decrease in lipid peroxidation in the plasma was observed after acute CORT exposure. The significantly increased plasma nonenzymatic antioxidants (uric acid [UA] and total antioxidant capacity) in concert with the enhanced enzymatic antioxidant activity (SOD in heart) during short-term CORT administration indicate preventive changes to counteract the oxidative injury, and these may be tissue specific.     

Acute heat stress induces oxidative stress in broiler chickens

The stress responses and possible oxidative damage in plasma, liver and heart were investigated in broiler chickens acutely exposed to high temperature. Eighty 5-week old broiler chickens were exposed to 32 degrees C for 6h. The extent of lipid peroxidation, activities of superoxide dismutase and total antioxidant power in plasma, liver and heart tissues were investigated. Meanwhile, the blood metabolites such as glucose, urate, triiodothyronine, thyroxine, corticosterone, ceruloplasmin and creatine kinase were measured before and after 3 and 6h of heat exposure. The results showed that oxidative stress could be induced in 5-week old broiler chickens by acute heat exposure (32 degrees C, 6h). The results suggest that the elevated body temperature can induce the metabolic changes that are involved in the induction of oxidative stress. The liver is more susceptible to oxidative stress than heart during acute heat exposure in broiler chickens. The oxidative stress should be considered as part of the stress response of broiler chickens to heat exposure.     

Impaired development of broiler chickens by stress mimicked by corticosterone exposure

The effects of corticosterone (CORT) administration on the development of muscular tissues of broiler chickens (Gallus gallus domesticus) fed with diets differing in lipid content were investigated. The experimental chickens were given one of two experimental diets: high lipid diet (9.9% crude fat) or control diet, from 21 d of age. At 28 d of age, half of the chickens in each dietary treatment were exposed to CORT treatment, supplemented with 30 mg CORT/kg diet for 12 days, while the other half continued to consume the former diet. The zootechnical parameters were recorded at 21, 28, 35 and 39 d, and a blood sample was obtained from 8 birds of each group, respectively. The growth performance of broiler chickens was significantly depressed by CORT administration, but not by dietary treatment. Corticosterone treatment resulted in enhanced energy expenditure. The results indicate that the development of breast muscle was more susceptible to stress mimicked by CORT administration. The results suggest that corticosterone administration enhanced hepatic fatty acid synthesis and resulted in the redistribution of energy to abdominal store from peripheral tissues. Diet rich in lipid content was favorable to the central fat deposit in stressed broiler chickens.     

Altered development and protein metabolism in skeletal muscles of broiler chickens (Gallus gallus domesticus) by corticosterone

Two trials were conducted to investigate the effect of corticosterone (CORT) on protein metabolism and the amino acid composition in muscle tissues of broiler chickens (Gallus gallus domesticus). In Trial 1, two groups of 30 broiler chickens were subjected to control or CORT treatment (30 mg/kg diet) from 28 to 39 days of age. In Trial 2, three groups of chickens of 28 days of age were randomly subjected to one of the following treatments for 7 days: CORT (30 mg/kg diet), pair-fed (maintaining the same feed intake as CORT treatment) and control treatments. The body mass gain and feed efficiency was significantly decreased by CORT treatment, while the food intake was decreased. The breast and thigh masses (% body mass) were significantly suppressed by CORT treatment, while the abdominal fat and liver masses (%) were obviously increased. The plasma levels of glucose, urate and total amino acid were significantly elevated by CORT treatment. The capacity for protein synthesis, estimated by RNA:protein ratio, were significantly suppressed by CORT in M. pectoralis major and M. biceps femoris. The 3-methylhistidine concentrations were significantly increased in both M. pectoralis major and M. biceps femoris of CORT chickens, compared to control but not the pair-fed chickens. The amino acid composition of M. pectoralis major and M. biceps femoris was not significantly affected by CORT treatment. In conclusion, the arrested growth in skeletal muscles induced by CORT administration has tissue specificity. The CORT treatment retards the growth of skeletal muscle by suppressed protein synthesis and augmented protein catabolism.     

Effect of splenosid on lipid peroxidation process and glutathione antioxidant system in rats exposed to fractionated radiation

The dynamics of lipid peroxidation, antioxidant glutathione system condition in blood and viscerals (brain, heart, liver, spleen) of rats which were fractionally irradiated (10 fractions) in the total dose 1.0 Gy and oxidative homeostasis increase of primary and secondary lipid peroxidation products and glutathione system disturbances were established in the irradiated rats. The administration of splenosid diminished the disturbances of oxidative homeostasis but does not completely normalize the latter. The administration of splenosid during the irradiation course and after its finishing is more effective than only during the irradiation course.     

Effects of Corticosterone and Dietary Energy on Immune Function of Broiler Chickens

An experiment was conducted to investigate the effects of dietary energy level on the performance and immune function of stressed broiler chickens (Gallus gallus domesticus). A total of 96 three-day-old male broiler chickens (Ross × Ross) were divided into two groups. One group received a high energy (HE) diet and the other group received a low energy (LE) diet for 7 days. At 5 days of age, the chickens from each group were further divided into two sub-groups and received one of the following two treatments for 3 days: (1) subcutaneous injection of corticosterone, twice per day (CORT group; 2 mg of CORT/kg BW in corn oil) and (2) subcutaneous injection of corn oil, twice per day (Control/Sham treatment group). At 10 days of age, samples of blood, duodenum, jejunum, and ileum were obtained. Compared with the other three groups, the LE group treated with CORT had the lowest average daily gain (ADG) and the poorest feed conversion ratio (FCR, P < 0.05). Furthermore, CORT treatment decreased the relative weight (RW) of the bursa independent of the dietary energy level, but it decreased the RW of the thymus only in the chickens fed the LE diet. By contrast, CORT administration decreased the RW of the spleen only in the chickens fed the HE diet (P < 0.05). The plasma total protein, albumin, tumor necrosis factor alpha, interleukin 2 and immunoglobulin G (IgG) levels were affected by the CORT treatment (P < 0.05); however, these factors were not significantly affected by the dietary energy level. Toll-like receptor-5 mRNA level was down-regulated by CORT injection in the duodenum and ileum (P < 0.05) and showed a trend of down-regulation in the jejunum (P=0.0846). The present study showed that CORT treatment induced immunosuppressive effects on the innate immune system of broiler chickens, which were ameliorated by consumption of higher dietary energy.     

Effects of acute heat stress and subsequent stress removal on function of hepatic mitochondrial respiration,ROS production and lipid peroxidation in broiler chickens

In order to investigate the effects of acute heat stress and subsequent stress removal on function of hepatic mitochondrial respiration, production of reactive oxygen species (ROS) and lipid peroxidation in broiler chickens, 128 six-week-old broiler chickens were kept in a controlled-environment chamber. The broiler chickens were initially kept at 25 °C (relative humidity, RH, 70 ± 5%) for 6 d and subsequently exposed to 35 °C (RH, 70 ± 5%) for 3 h, then the heat stress was removed and the temperature returned to 25 °C (RH, 70 ± 5%). Blood and liver samples were obtained before heat exposure and at 0 (at the end of the three-hour heating episode, this group is also abbreviated as the HT group), 1, 2, 4, 8, 12 h after the stress was removed. The results showed that acute heat stress induced a significant production of ROS, function of the mitochondrial respiratory chain, antioxidative enzymes [superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)] activity, and formation of malondialdehybe (MDA). Within the first 12 h after removal of the heat stress, the acute modification of the above parameters induced by heat stress gradually approached to pre-heat levels. The results of the present study suggest that acute exposure to high temperatures may depress the activity of the mitochondrial respiratory chain. This leads to over-production of ROS, which ultimately results in lipid peroxidation and oxidative stress. When the high temperature was removed, the production of ROS, mitochondrial respiratory function and oxidative injury that were induced by acute heat exposure gradually approached the levels observed before heating, in a time-dependent manner.     

Suppression of oxidative stress in aging NZB/NZW mice: effect of fish oil feeding on hepatic antioxidant status and guanidino compounds

Oxidative stress caused by excessive reactive species (RS) and lipid peroxidation is known to be casually linked to age-related inflammation. To test the hypothesis that fish oil (FO) intake has a beneficial effect on nephritis due to its suppressive action of oxidative stress and the enhancement of antioxidant defenses, we examined the effect of dietary FO on various oxidative stress-related parameters and guanidino compound (GC) levels using (NZB × NZW) F₁ (B/W) mice. These mice were fed diets supplemented with either 5% corn oil (control) or 5% FO. At 4 and 9 months of age, the hepatic oxidative status was estimated by assessing RS generation produced from xanthine oxidase, the prostaglandin pathway and lipid peroxidation. To evaluate the effect of FO on redox status, including antioxidant defenses, GSH and GSSG levels and antioxidant enzyme activities were measured. To correlate the extent of oxidative status with the nephritic condition, creatinine, guanidino acetic acid and arginine levels were measured. Results indicated that increased levels of lipid peroxidation, RS generation and xanthine oxidase activity with age were all significantly suppressed by FO feeding. Furthermore, reduced GSH levels, GSH/GSSG ratio and antioxidant enzyme activities in the FO-fed mice were effectively enhanced compared to the corn oil-fed mice. Among several GCs, the age-related increase of creatinine level was blunted by FO. Based on these results, we propose that dietary FO exerts beneficial effects in aged, nephritic mice by suppressing RS, superoxide and lipid peroxidation, and by maintaining a higher GSH/GSSG ratio and antioxidant enzyme activities.     

Effect of dietary lipid and vitamin E on mitochondrial lipid peroxidation and hepatic injury in the bile duct-ligated rat.

To assess whether lipid peroxidation of hepatic mitochondria is associated with cholestatic hepatic injury we examined the effect of bile duct ligation (BDL) versus sham surgery on mitochondrial lipids of rats maintained on one of seven diets. Diets included vitamin E-deficient (E-) and vitamin E-sufficient (E+) combined with normal lipid (11.9% calories as stripped corn oil), high lipid (35% calories as stripped corn oil), or n-3 fatty acid (fish oil) supplementation. Rats were killed 17 days after surgery, mitochondria were isolated by differential centrifugation, and lipid-conjugated dienes and thiobarbituric acid-reacting substances (TBARS) were measured in mitochondrial lipids as indices of lipid peroxidation. BDL resulted in significant increases in lipid peroxidation in all dietary groups. The E- high lipid diets (with either corn oil or fish oil) were associated with higher lipid peroxide and serum bilirubin values in BDL rats compared to the normal lipid diets. Fish oil supplementation did not ameliorate cholestatic or oxidative injury. Serum alanine aminotransferase, bilirubin, alkaline phosphatase, and cholylglycine levels correlated significantly with levels of mitochondrial conjugated dienes and TBARS. These data suggest that free radical stress occurs during BDL in the rat and may result in mitochondrial lipid peroxidation, and that diets high in lipid may increase free radical damage to hepatic mitochondria. The role of free radicals in cholestatic hepatic injury requires further investigation.     

Lipid peroxidation and glutathione system in hyperlipemic rabbits: influence of olive oil administration

We studied the effect of supplementation (10% w/w) of a hyperlipemic diet (1% cholesterol) with olive oil (OLIV) for 6 weeks in four groups of 10 rabbits each. At the end of this period, we determined lipid peroxidation, glutathione content, and glutathione peroxidase, reductase and transferase activities in liver, brain, heart, aorta and platelets. The atherogenic diet increased tissue lipid peroxidation and decreased the protective antioxidant effect of glutathione. Dietary supplementation with olive oil reduced tissue lipid peroxidation by 71.6% in liver, 20.3% in brain, 84.5% in heart, 63.6% in aorta, 72% in platelets. The ratios total/oxidized glutathione were increased in all tissues (49% in liver, 48% in brain, 45% in heart, 83% in aorta, 70% in platelets). Olive oil increased glutathione peroxidase and transferase activities in all tissues. We conclude that in rabbits made hyperlipemic with a diet rich in saturated fatty acids, olive oil decreased tissue oxidative stress.     

Circaannual changes in antioxidants and oxidative stress in the heart and liver in rats

Reactive oxygen species are formed in physiological and pathological conditions in mammalian tissues. Because of their high reactivity, they may interact with biomolecules, inducing oxidative injury. Increases in lipid peroxidation can result in oxidative damage to cellular membranes. Protection against oxidative damage is provided by enzymatic and non-enzymatic antioxidant defenses. Antioxidant enzyme activities and lipid peroxidation, as an index of oxidative stress injury, were evaluated in different seasons over one year in the heart and liver of rats, maintained on a 12 h light and dark cycle. Glutathione peroxidase and catalase activities, in both tissues, were maximal in the summer season. Lipid peroxidation in the heart was maximal in the spring as compared to the other seasons and it did not vary in the liver during the year. These findings suggest that any study of antioxidants or oxidative stress must take into account such seasonal variations for a more precise analysis of changes due to any pathological condition.     

Oral exposure to Microcystis increases activity-augmented antioxidant enzymes in the liver of loach (Misgurnus mizolepis) and has no effect on lipid peroxidation

Recently, eutrophication has induced severe cyanobacterial blooms in the Naktong River, the second largest river of Korea. In the present study, lipid peroxidation and the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, were evaluated in the liver of loach (Misgurnus mizolepis) that were orally exposed to a low dose of Microcystis through dietary supplementation with bloom scum. Loach received 75 mg of dry cells/kg body weight mass (equal to 10 microg microcystin-RR/kg body mass), for 28 days under controlled conditions. Antioxidant enzymatic activity and lipid peroxidation were measured after termination of exposure. The activities of antioxidant enzyme were significantly increased in the livers of toxin-exposed loach after 28 days of exposure, as compared to control fish. However, lipid peroxidation remained stable in both groups. These results suggest that antioxidant enzymes were able to eliminate oxidative stress induced by low concentrations of microcystins and to prevent increased lipid peroxidation in the liver of loach.     

Preconditioning with physiological levels of ethanol protect kidney against ischemia/reperfusion injury by modulating oxidative stress

Background

Oxidative stress due to excessive production of reactive oxygen species (ROS) and subsequent lipid peroxidation plays a critical role in renal ischemia/reperfusion (IR) injury. The purpose of current study is to demonstrate the effect of antecedent ethanol exposure on IR-induced renal injury by modulation of oxidative stress.

Materials and Methods

Bilateral renal warm IR was induced in male C57BL/6 mice after ethanol or saline administration. Blood ethanol concentration, kidney function, histological damage, inflammatory infiltration, cytokine production, oxidative stress, antioxidant capacity and Aldehyde dehydrogenase (ALDH) enzymatic activity were assessed to evaluate the impact of antecedent ethanol exposure on IR-induced renal injury.

Results

After bilateral kidney ischemia, mice preconditioned with physiological levels of ethanol displayed significantly preserved renal function along with less histological tubular damage as manifested by the reduced inflammatory infiltration and cytokine production. Mechanistic studies revealed that precondition of mice with physiological levels of ethanol 3 h before IR induction enhanced antioxidant capacity characterized by significantly higher superoxidase dismutase (SOD) activities. Our studies further demonstrated that ethanol pretreatment specifically increased ALDH2 activity, which then suppressed lipid peroxidation by promoting the detoxification of Malondialdehyde (MDA) and 4-hydroxynonenal (HNE).

Conclusions

Our results provide first line of evidence indicating that antecedent ethanol exposure can provide protection for kidneys against IR-induced injury by enhancing antioxidant capacity and preventing lipid peroxidation. Therefore, ethanol precondition and ectopic ALDH2 activation could be potential therapeutic approaches to prevent renal IR injury relevant to various clinical conditions.     

Enhanced heme oxygenase activity increases the antioxidant defense capacity of guinea pig liver upon acute cobalt chloride loading: comparison with rat liver

Changes in the activity of so-called oxidative stress defensive enzymes, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and heme oxygenase, as well as changes in lipid peroxidation and reduced glutathione levels, were measured in guinea pig and rat liver after acute cobalt loading. Cobalt chloride administration produced a much higher degree of lipid peroxidation in guinea pig than in rat liver compared with the control animals. The intrahepatic reduced glutathione content in control guinea pig was higher than that in rat, but was equally decreased in both species after cobalt administration. The enzymatic scavengers of free radicals, superoxide dismutase, catalase and glutathione peroxidase, were significantly decreased in rat liver after acute cobalt loading, and as a compensatory reaction, the heme oxygenase activity was increased (seven-fold). In guinea pig liver, only superoxide dismutase activity was depleted in response to cobalt-induced oxidative stress, while catalase and glutathione peroxidase were highly activated and the heme oxygenase activity was dramatically increased (13-fold). It is assumed that enhanced heme oxygenase activity may have important antioxidant significance by increasing the liver oxidative-stress defense capacity.     

Melatonin exerts a more potent effect than S-adenosyl-l-methionine against iron metabolism disturbances, oxidative stress and tissue injury induced by obstructive jaundice in rats

Melatonin and S-adenosyl-l-methionine (SAMe) prevent oxidative stress and tissue dysfunction in obstructive jaundice (OJ). Lipid peroxidation is exacerbated in the presence of trace amounts of iron (Fe). The study investigated the regulation by melatonin and SAMe the induction of oxidative stress, iron metabolism disturbances and tissue injury in an experimental model of OJ. Different parameters of lipid peroxidation, antioxidant status, tissue injury and Fe metabolism were determined in liver and blood. OJ induced Fe accumulation in liver, and increased transferrin (Tf) saturation and loosely bound Fe content in blood. Melatonin, and SAMe at lesser extent, enhanced protein Tf content in liver and blood, that reduced loosely bound Fe content in blood. Melatonin and SAMe did not affect ferritin (FT) and Tf mRNA expression, but reduced Tf receptor (TfR) mRNA expression in liver. In conclusion, the effect of melatonin and SAMe on Fe metabolism may be included in the beneficial properties of these agents on lipid peroxidation and tissue injury induced by OJ.     

Protective effects of an extract of young radish (Raphanus sativus L) cultivated with sulfur (sulfur-radish extract) and of sulforaphane on carbon tetrachloride-induced hepatotoxicity

The protective effects of an extract of young radish (Raphanus sativus L) cultivated with sulfur (sulfur-radish extract) and of sulforaphane, an isothiocyanate, on carbon tetrachloride (CCl(4))-induced liver injury were observed in mice. CCl(4) produced a marked increase in the serum level of alanine aminotransferase (ALT), primed lipid peroxidation, and resulted in intense necrosis due to oxidative stress. Oral administration of the sulfur-radish extract and of sulforaphane after CCl(4)-induced liver injury both decreased the serum level of ALT, reduced the necrotic zones, inhibited lipid peroxidation, and induced phase 2 enzymes without affecting cytochrome P450-2E1 (CYP2E1). These results suggest that the administration of the sulfur-radish extract and of sulforaphane may partially prevent CCl(4)-induced hepatotoxicity, possibly by indirectly acting as an antioxidant by improving the detoxification system.     

Attenuation of TCDD-induced oxidative stress by 670 nm photobiomodulation in developmental chicken kidney

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a potent developmental teratogen inducing oxidative stress and sublethal changes in multiple organs, provokes developmental renal injuries. In this study, we investigated TCDD-induced biochemical changes and the therapeutic efficacy of photobiomodulation (670 nm; 4 J/cm(2)) on oxidative stress in chicken kidneys during development. Eggs were injected once prior to incubation with TCDD (2 pg/g or 200 pg/g) or sunflower oil vehicle control. Half of the eggs in each dose group were then treated with red light once per day through embryonic day 20 (E20). Upon hatching at E21, the kidneys were collected and assayed for glutathione peroxidase, glutathione reductase, catalase, superoxide dimutase, and glutathione-S-transferase activities, as well as reduced glutathione and ATP levels, and lipid peroxidation. TCDD exposure alone suppressed the activity of the antioxidant enzymes, increased lipid peroxidation, and depleted available ATP. The biochemical indicators of oxidative and energy stress in the kidney were reversed by daily phototherapy, restoring ATP and glutathione contents and increasing antioxidant enzyme activities to control levels. Photobiomodulation also normalized the level of lipid peroxidation increased by TCDD exposure. The results of this study suggest that 670 nm photobiomodulation may be useful as a noninvasive treatment for renal injury resulting from chemically induced cellular oxidative and energy stress.     

Further prove on oxidative stress in alloxan diabetic rat tissues

After intravenous administration of alloxan monohydrate (AL) diabetes developed in rats. Forty-eight hours after the injection the animals were sacrificed, their blood was collected in heparin containing tubes and the tissues were dissected and frozen (-70 degrees C) until their homogenization for pro- and antioxidant testing. Our results can be summarised as follows: (i) In the blood hemolysate the lipid peroxidation slightly elevated and the activity of antioxidant enzymes and reduced glutathione decreased. (ii) Similar phenomena could be observed in the different examined organ homogenates. The organs tested for pro- and antioxidant system were as follows: the liver, heart, skeletal muscle, kidney and pancreas. In our present work we attempt to confirm the data in support of the oxidative predominance over antioxidants in oxidative stress of AL diabetic rats.     

Effect of Bilirubin on Lipid Peroxidation, Sphingomyelinase Activity, and Apoptosis Induced by Sphingosine and UV Irradiation

The effect of bilirubin (BR) on sphingomyelin cycle activity, lipid peroxidation (LPO), and apoptosis induced by sphingosine and UV irradiation has been studied in vivo. Neutral Mg²⁺-dependent sphingomyelinase (SMase) activity and LPO level were monitored in heart, kidney, and liver of mice after administration of BR. BR inhibited both LPO and SMase activities in heart and kidney. BR induced a mild increase in LPO level and moderate increase in lipid contents in liver, consistent with the functional role of liver in both BR and lipid metabolism. BR injected to mice causes simultaneous and unidirectional alterations in both LPO level and SMase activity with a significant (p < 0.05) positive linear correlation between these two parameters. Sphingosine administration results in increased lipid peroxidation in murine liver. Data on DNA fragmentation indicate that exogenous BR may effectively protect thymus cells against sphingosine- and UV-mediated apoptosis. These results have revealed a biochemical association between oxidative stress and BR on one hand and the sphingomyelin cycle and apoptotic cell death on the other hand. Our data show that BR as an antioxidant, due to its effect on the sphingomyelin cycle, can protect membrane lipids against peroxidation and cells against apoptosis induced by various factors.     

Alpha-lipoic acid supplementation: tissue glutathione homeostasis at rest and after exercise.

Antioxidant nutrients have demonstrated potential in protecting against exercise-induced oxidative stress. alpha-Lipoic acid (LA) is a proglutathione dietary supplement that is known to strengthen the antioxidant network. We studied the effect of intragastric LA supplementation (150 mg/kg, 8 wk) on tissue LA levels, glutathione metabolism, and lipid peroxidation in rats at rest and after exhaustive treadmill exercise. LA supplementation increased the level of free LA in the red gastrocnemius muscle and increased total glutathione levels in the liver and blood. The exercise-induced decrease in heart glutathione S-transferase activity was prevented by LA supplementation. Exhaustive exercise significantly increased thiobarbituric acid-reactive substance levels in the liver and red gastrocnemius muscle. LA supplementation protected against oxidative lipid damage in the heart, liver, and red gastrocnemius muscle. This study reports that orally supplemented LA is able to favorably influence tissue antioxidant defenses and counteract lipid peroxidation at rest and in response to exercise.