Increase In TBARS Levels Research Articles

Glutathione s-transferase as a marker of oxidative stress in human ejaculated spermatozoa from patients with pathospermia

It is believed that the most common causes of male infertility are impairment of spermatogenesis and sperm functions. Glutathione S-transferases (EC 2.5.1.18) play an important role in sperm physiology, specifically in antioxidant protection against oxidative damage. The catalase decomposition of lipid hydro-peroxides forms as a result of oxidative stress. We used a model of superoxide anion-generating system Fe3+/ascorbate or H2O2-induced stress to study the activity of glutathione s transferase in human ejaculated spermatozoa from patients with pathospermia and products of lipid peroxidation (TBARS) as a marker of oxidative stress. In the present study, dose dependent increase in the level of lipid peroxidation was observed for treatment with Fe3+/ascorbate or H2O2. The TBARS level was higher for sperm cells incubated with superoxide anion-generating system Fe3+/ascorbate than for H2O2. GSTs activity increased in spermatozoa treated with increasing concentration of superoxide anion-generating system Fe3+/ascorbate and H2O. We found that both Fe3+/ascorbate and H2O2 displayed similar inhibitory effects on sperm GSTs activity, however H2O2 at low concentrations activated enzyme activity only in normozoospermic samples, which can be explained as a defence response to oxidative stress. The time course of incubation with 100 μM H2O2 showed a sharp decrease in the enzyme activity during the first 5 min of incubation for both normozoospermic and pathozoospermic men. Preincubation of spermatozoa with GSH completely prevented the ROS-induced inhibition on GSTs only in normozoospermic samples. On the other hand, in pathospermic samples protectory effect of GSH was observed only against non-radical (H2O) radical, but not against radical (superoxide anion-generating system Fe3+/ascorbate) species. The results of our study showed higher oxygen-free radical production, evidenced by increased TBARS level in spermatozoa obtained from infertile men than normozoospermic men. The inhibitory effect of the radical (superoxide anion-generating system Fe3+/ascorbate) species on sperm GSTs activity and products of lipid peroxidation in sperm cells of fertile and infertile men were more expressed compared to non-radical (H2O) species. Our results indicate that estimation of sperm GSTs enzyme assays can be used as a bioindicator for impaired male fertility. The obtained results argue for a biological role of sperm GSTs in susceptibility of spermatozoa to oxidative damage and maintaining sperm antioxidant status.

In vivo effects of hemin and nitric oxide donors on parameters of heme metabolism in rat liver and serum

In vivo effects of hemin chloride (15 mg/kg body weight) and donors of nitrogen monoxide (NO) – sodium nitroprusside (SNP, 1 mg/kg) and substrate of NO-synthase L-arginine (L-Arg, 600 mg/kg) on the activity of key enzymes of heme synthesis (5-aminolevulinate synthase, ALAS) and heme degradation (heme oxygenase, HO), on the free heme level in liver and on the content of heme in blood serum of rats were studied. NO donors were administered alone or 30 min before hemin chloride injection. The level of free heme in liver was estimated by the ratio of holoenzyme and total tryptophan 2,3-dioxygenase (TDO) activities. Two hours after hemin chloride administration a significant increase in the level of heme-containing products and lipid peroxidation products (TBARS) was found in blood serum. These changes were accompanied by decrease in ALAS activity and by increase in holoenzyme activity and heme saturation of TDO, which was the result of free heme accumulation in liver. 24 hrs after administration of hemin chloride the content of heme in serum returned to normal level, while level of TBARS remained elevated. 24 hrs after hemin action a significant increase in the activities of HO and ALAS was observed in liver, while the degree of TDO heme saturation decreased, indicating the prevalence of heme degradation over its synthesis. Both NO donors did not affect the accumulation of heme in serum and liver first hours after hemin action. However, the specific features of SNP and L-Arg effects on the key enzyme of heme synthesis in liver and the TBARS level in serum were revealed. L-Arg, unlike SNP, prevented the accumulation of TBARS in serum, but did not prevent a decrease in ALAS activity 2 hrs after hemin chloride injection. The treatment by SNP itself caused an increase in TBARS level in serum, an increase in TDO activity and a decrease in ALAS activity in liver 2 hrs after action. Heme content in serum positively correlated with holoenzyme activity and heme saturation of TDO in liver. The pretreatment with NO donors did not affect the increase in HO activity, however, it blocked the induction of ALAS, a decrease in holoenzyme activity and heme saturation of TDO 24 hrs after the administration of hemin chloride. Thus, both SNP and Arg prevented a decrease in free heme level in liver, which might be due to heme nitrosylation in the presence of NO donors and, as a result, its slower degradation in the heme oxygenase reaction.

Effect of Poly-Unsaturated Fatty Acids Fortification on Growth Performance, Survival, Fatty Acid Composition and Antioxidant Balance of Meagre, Argyrosomus regius Larvae

A total of 120 meagre, Argyrosomus regius, larvae (0.37 ± 0.02 g) were assigned to four treatments (three replicates each) to determine the optimum dietary level of PUFAs, at which there will be the best growth performance, feed utilization, fatty acids composition and antioxidant status. The treatments were a control group (fed a basal diet 3% PUFAs of total fatty acids) and another three groups fed PUFAs supplemented diets at levels 4.55, 6% and 7% for 21 days. The results indicated that increasing dietary PUFAs levels up to 4.5% significantly improved growth and survival compared to the control group. Feed intake, feed conversion ratio and protein utilization were significantly increased with 4.5% PUFAs followed by the control group. The results revealed significant differences in PUFAs among treatments and the best value was reported for the 4.5% PUFAs supplemented diet followed by the control. There is a significant increase in TBARs levels with increasing dietary PUFAs concentration. Meanwhile, the SOD and CAT activities decreased significantly with increasing PUFAs levels. However, TAS decreased significantly with higher PUFAS level (6%) only compared to other treatments. Therefore, the dietary requirements of A. regius larvae is 4.5% PUFAs of total fatty acids.

Ascorbate Attenuates Oxidative Stress and Increased Blood Pressure Induced by 2-(4-Hydroxyphenyl) Amino-1,4-naphthoquinone in Rats.

Quinone derivatives like 2-(4-hydroxyphenyl) amino-1,4-naphthoquinone (Q7) are used as antitumor agents usually associated with adverse effects on the cardiovascular system. The objective of this study was to evaluate the cardioprotective effect of ascorbate on Q7-induced cardiovascular response in Wistar rats. In this study, blood pressure, vascular reactivity, and intracellular calcium fluxes were evaluated in cardiomyocytes and the rat aorta. We also measured oxidative stress through lipid peroxidation (TBARS), superoxide dismutase- (SOD-) like activity, and H2O2 generation. Oral treatment of rats with ascorbate (500 mg/kg) for 20 days significantly (p < 0.05) reduced the Q7-induced increase (10 mg/kg) in blood pressure and heart rate. The preincubation with ascorbate (2 mM) significantly (p < 0.05) attenuated the irregular beating of the atrium induced by Q7 (10−5 M). In addition, ascorbate induced endothelial vasodilation in the presence of Q7 in the intact aortic rings of a rat and reduced the cytosolic calcium levels in vascular smooth muscle cells. Ascorbate also reduced the Q7-induced oxidative stress in vivo. Ascorbate also attenuated Q7-induced SOD-like activity and increased TBARS levels. These results suggest a cardioprotective effect in vivo of ascorbate in animals treated orally with a naphthoquinone derivative by a mechanism involving oxidative stress.

Abstract 008: Leptin Treatment Attenuates Vascular Dysfunction and Inflammation in Mouse Model(s) of Acquired Lipodystrophy via Reducing Nox1-derived Ros

Although extremely efficient at suppressing HIV replication, highly active antiretroviral therapy (HAART) induces lipodystrophy, a metabolic disorder characterized by an abnormal adipose tissue distribution, reduced leptin levels and vascular dysfunction. Leptin replacement therapy (LRT) is currently used to improve metabolic function in patients suffering from congenital lipodystrophy. Here, we analyzed whether LRT restores vascular function and inflammation in mice treated with the antiretroviral agent, ritonavir (Rit). Four weeks of Rit reduced body weight [control (C): 28.4±0.5 vs. Rit: 24.4±0.2g*, *P&lt;0.05] and fat mass (C: 10±1 vs. Rit: 6.5±1 %*) confirming that it induces lipodystrophy. Rit impaired aortic endothelial function [Relaxation to acetylcholine: C: 74±4 vs. Rit: 21±15%*), increased ROS producing enzymes (NOX1 and NOXA1), induced vascular inflammation (increased IL-1β, MCP-1, GATA Binding Protein 3 and INF-γ gene expression) and increased TBARS levels. ROS scavenging via tempol or GKT137117, (Nox1/4 inhibitor) pre-incubation blunted endothelial dysfunction. LRT (10μg/day/7 days, osmotic mini-pump), at the end of the 3-week Rit, restored endothelial function, reduced Nox1 and NOXA1 gene expression and vascular inflammation. NOX1 deficiency in Nox1 KO mice protected mice from Rit-induced endothelial dysfunction and vascular inflammation. Increasing endothelial leptin sensitivity via specific deletion of protein tyrosine phosphatase 1B (Ptp1b) in endothelial cells ( Ptp1b-/-EC mice) protected mice from Rit-induced endothelial dysfunction and reduced Nox1 and NOXA1 gene expression, and vascular inflammation. To address the relevance of these observations to other forms of acquired lipodystrophy, experiments were repeated in mice in which lipodystrophy was induced at 8 week of age, by the deletion of Bscl2, a gene involved in adipocyte maturation. Bscl2 deletion reduced fat mass, and induced endothelial dysfunction via ROS-mediated mechanisms. Again, LRT reverted endothelial dysfunction by downregulating Nox1 expression. All together, these data presents leptin as a key regulator of endothelial oxidative stress level and as a potential avenue for the treatment vascular disease.

Occurrence of oxidative stress in dairy cows seropositives for Brucella abortus

Bovine brucellosis is an important zoonotic disease caused by the bacterium Brucella abortus that leads to economic losses due to animal discard and commercial restrictions. Since positive animals for brucellosis are culled, little is known about the pathogenesis of this disease. Therefore, the aims of this study were to evaluate possible changes in the activity of deaminase adenosine (ADA) and the oxidative stress in cows seropositives for brucellosis (Experiment I), and to evaluate the seroprevalence of B. abortus in dairy cows from the Western state of Santa Catarina, Southern Brazil (Experiment II). The Experiment I evaluated 20 pregnant cows: ten seropositives for B. abortus and ten seronegatives that were used as controls. The ADA activity and markers of oxidative stress (TBARS, catalase (CAT) and superoxide dismutase (SOD)) were evaluated in these animals. A reduction in the activity of ADA and catalase enzymes in seropositive animals was observed (p < 0.001). Conversely, there was an increase in TBARS levels and superoxide dismutase activity in cows infected by B. abortus (p < 0.001). The presence of oxidative stress and a reduction of ADA might be related to the modulation of the inflammatory response. The experiment II was performed due to a high number of herds with restrictions imposed by cases of brucellosis in the state of Santa Catarina in the last two years, and thus, the seroprevalence for B. abortus was evaluated in 1242 serum samples of cows of 69 herds. The serodiagnosis was performed using two tests: buffered acidified antigen and 2-mercaptoethanol. However, none of the serum samples were positive for B. abortus. Although we did not find seropositive animals for brucellosis in our study, the disease still requires continued surveillance, due to its economic impact, and to the oxidative stress caused by it, which may have contributed to cases of abortion in three seropositive cows (Experiment I) in the final third of the gestation.

Acute and long-term effects of intracerebroventricular administration of α-ketoisocaproic acid on oxidative stress parameters and cognitive and noncognitive behaviors.

Maple Syrup Urine Disease (MSUD) is biochemically characterized by elevated levels of leucine, isoleucine and valine, as well as their corresponding transaminated branched-chain α-keto acids in tissue and biological fluids. Neurological symptoms and cerebral abnormalities, whose mechanisms are still unknown, are typical of this metabolic disorder. In the present study, we evaluated the early effects (1h after injection) and long-term effects (15days after injection) of a single intracerebroventricular administration of α-ketoisocaproic acid (KIC) on oxidative stress parameters and cognitive and noncognitive behaviors. Our results showed that KIC induced early and long-term effects; we found an increase in TBARS levels, protein carbonyl content and DNA damage in the hippocampus, striatum and cerebral cortex both one hour and 15days after KIC administration. Moreover, SOD activity increased in the hippocampus and striatum one hour after injection, whereas after 15days, SOD activity decreased only in the striatum. On the other hand, KIC significantly decreased CAT activity in the striatum one hour after injection, but 15days after KIC administration, we found a decrease in CAT activity in the hippocampus and striatum. Finally, we showed that long-term cognitive deficits follow the oxidative damage; KIC induced impaired habituation memory and long-term memory impairment. From the biochemical and behavioral findings, it we presume that KIC provokes oxidative damage, and the persistence of brain oxidative stress is associated with long-term memory impairment and prepulse inhibition.

Application of platelet derived growth factor-BB and diabetic wound healing: the relationship with oxidative events

The reasons that cause delay in wound healing in diabetes are a decrease in the level of growth factors secretion, an increase in the destruction of growth factors and in oxidative stress. Platelet derived growth factor (PDGF) is one of the important growth factors that play a role in all phases of wound healing. This study investigates time-dependent effects of topically PDGF-BB administration on oxidative events on the healing of dorsolateral-excisional wounds in diabetic rats. Forty-two female Wistar-albino rats with streptozotocin-induced diabetes were divided into four groups: control group, untreated group, chitosan-treated group, chitosan + PDGF-BB-treated group. Two identical full-thickness excisional skin wounds were made under anaesthesia in all rats except for the control group. In the PDGF-BB-treated and chitosan-treated groups, the wounds were treated topically PDGF-BB (7 ng/mL, single daily dose) and blank chitosan gel (equal amount) after wounding, respectively. After these administrations, on day 3 and day 7 of wound healing, rats were sacrificed. Thiobarbituric acid reactive substances, glutathione, nitric oxide, ascorbic acid levels, and superoxide dismutase activity in wound tissues were spectrophotometrically measured. PDGF-BB administration significantly increased TBARS levels and non-enzymatic antioxidant levels in early phase of diabetic wound healing. PDGF-BB dramatically reduced NOx levels on day 3 and sharply increased NOx levels on day 7 of wound healing. Consequently, PDGF-BB administration can be effective on oxidative balance in the early phase of diabetic wound healing.

Effect of two exercise varieties on fetuin-A plasma level in experimental diabetic nephropathy

Background Diabetes mellitus is an endocrinological and/or metabolic disorder with an increasing global prevalence and incidence. Fetuin-A is a serum protein that represents an important factor in the pathophysiology of the metabolic syndrome, type 2 diabetes, and in patients with chronic kidney disease. Aim The aim of this work was to study the effect of different exercise varieties on fetuin-A (Fet-A) plasma level in experimental diabetic nephropathy. Material and methods Forty male Wistar rats weighing 150–200 g were used. Ten rats were considered as control (group I). Type 2 diabetes was induced in another 30 rats with the use of streptozotocin. The diabetic rats were divided into three groups as follows: group II, sedentary; group III, chronic regular moderate exercise; and group IV, irregular strenuous exercise. Results In group II, diabetes caused a significant increase in fasting glucose, total cholesterol, triglycerides, and creatinine plasma levels and microalbuminuria as compared with group I. In group III, moderate regular exercise produced a significant decrease in the same parameters as compared with group II. However, in group IV there were similar but less significant changes. Moreover, in group II there was a significant elevation in Fet-A, Interleukin-6, tumor necrosis factor-α, and C-reactive protein plasma levels. However, group III showed a significant reduction in these parameters, whereas in group IV there was a nonsignificant decrease as compared with group II. Moreover, diabetes produced a significant increase in TBARS level with a significant reduction in the antioxidant enzyme activities in kidney tissue as compared with group I. In group III, the exercise regimen produced a significant reduction in the same parameters as compared with group II. However, in group IV, there were similar but nonsignificant changes. Conclusion In type 2 diabetes with nephropathy, regular moderate exercise is more valuable program to reduce Fet-A plasma level and to improve associated renal damage compared with irregular strenuous one.

Perinatal complications, lipid peroxidation, and mental health problems in a large community pediatric sample.

Replicated evidence indicates that perinatal complications are associated with increased markers of oxidative stress and with mental health problems in children. However, there are fewer reports on the impact of perinatal complications in later phases of development. We aimed to investigate the estimated effects of perinatal complications on levels of lipid peroxidation and on psychopathology in children and adolescents. The study is part of the High Risk Cohort Study for Psychiatric Disorders; the population was composed by 554 students, 6-14years of age. Serum levels of malondialdehyde, a product of lipid peroxidation, were measured by the TBARS method. A household interview with parents and caregivers was conducted and included inquiries about perinatal history, the Child Behavior Checklist (CBCL), and parent's evaluation, using the Mini International Psychiatric Interview (MINI). We created a cumulative risk index, conceptualized as each individual's cumulative exposure to perinatal complications. Results indicate that perinatal complications were associated with higher levels of TBARS. After adjusting for age, gender, socio-economic status, CBCL total problems score, parental psychopathology, and childhood maltreatment, children exposed to 3 or more perinatal complications had an 26.9% (95% CI 9.9%, 46.6%) increase in TBARS levels, relative to the unexposed group. Exploratory mediation analysis indicated that TBARS levels partially mediated the association between perinatal complications and externalizing problems. In conclusion, an adverse intrauterine and/or early life environment, as proxied by the cumulative exposure to perinatal complications, was independently associated with higher levels of lipid peroxidation in children and adolescents.

Chronic administration of methionine and/or methionine sulfoxide alters oxidative stress parameters and ALA-D activity in liver and kidney of young rats.

High levels of methionine (Met) and methionine sulfoxide (MetO) are found in several genetic abnormalities. Oxidative stress is involved in the pathophysiology of many inborn errors of metabolism. However, little is known about the role of oxidative damage in hepatic and renal changes in hypermethioninemia. We investigated the effect of chronic treatment with Met and/or MetO on oxidative stress parameters in liver and kidney, as lipid peroxidation (TBARS), total sulfhydryl content (SH), reactive oxygen species (ROS) and enzymes activities superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and delta aminolevulinic dehydratase (ALA-D). Serum biochemical parameters were evaluated. Wistar rats were treated daily with two subcutaneous injections of saline (control), Met (0.2-0.4g/kg), MetO (0.05-0.1g/kg) and the association between these (Met plus MetO) from the 6th to the 28thday of life. Our data demonstrated an increase of glucose and urea levels in all experimental groups. Cholesterol (MetO and Met plus MetO) were decreased and triglycerides (MetO) were increased. SOD (MetO and Met plus MetO) and CAT (Met, MetO and Met plus MetO) activities were decreased, while GPx was enhanced by MetO and Met plus MetO treatment in liver. In kidney, we observed a reduction of SH levels, SOD and CAT activities and an increase of TBARS levels in all experimental groups. ROS levels in kidney were increased in MetO and Met plus MetO groups. ALA-D activity was enhanced in liver (MetO and Met plus MetO) and kidney (Met plus MetO). These findings help to understand the pathophysiology of hepatic and renal alterations present in hypermethioninemia.

Evidence of oxidative stress in brain and liver of young rats submitted to experimental galactosemia.

Galactosemia is a disorder of galactose metabolism, leading to the accumulation of this carbohydrate. Galactosemic patients present brain and liver damage. For evaluated oxidative stress, 30-day-old males Wistar rats were divided into two groups: galactose group, that received a single injection of this carbohydrate (5μmol/g), and control group, that received saline 0.9% in the same conditions. One, twelve or twenty-four hours after the administration, animals were euthanized and cerebral cortex, cerebellum, and liver were isolated. After one hour, it was found a significant increase in TBA-RS levels, nitrate and nitrite and protein carbonyl contents in cerebral cortex, as well as protein carbonyl content in the cerebellum and in hepatic level of TBA-RS, and a significant decrease in nitrate and nitrite contents in cerebellum. TBA-RS levels were also found increased in all studied tissues, as well as nitrate and nitrite contents in cerebral cortex and cerebellum, that also present increased protein carbonyl content and impairments in the activity of antioxidant enzymes of rats euthanized at twelve hours. Finally, animals euthanized after twenty-four hours present an increase of TBA-RS levels in studied tissues, as well as the protein carbonyl content in cerebellum and liver. These animals also present an increased nitrate and nitrite content and impairment of antioxidant enzymes activities. Taken together, our data suggest that acute galactose administration impairs redox homeostasis in brain and liver of rats.

Role of Sulphydral Compounds on Antioxidant Defense Mechanism under High Temperature Stress in Wheat

The role of sulphydral compound viz: thiourea (TU) on the activities of antioxidant enzymes along with membrane thermostability parameters and metabolites contents was studied in high temperature (HT) stressed wheat (Triticum aestivum L. cv. PBW 343) seedlings. The seedlings were raised from seeds previously soaked with TU at different concentration (6 mM and 10 mM). TU pre-treatments modulated the response in shoots under HT by increasing antioxidant enzymes activities except superoxide dismutase and catalase, resulting in decreased lipid peroxidation products. In roots, HT upregulated the activities of ascorbate peroxidase and glutathione peroxidase but downregulated the activities of other enzymes resulting in increased TBARS levels. Proline content increased with TU pre-treatment in both shoots and roots under HT stress. Membrane thermostability was also enhanced with TU pre-treatment in both organs. However, free amino acids decreased with TU pre-treatment.

Selective cytoprotective effect of histamine on doxorubicin-induced hepatic and cardiac toxicity in animal models.

The aim of the present work was to evaluate the potential protective effect of histamine on Doxorubicin (Dox)-induced hepatic and cardiac toxicity in different rodent species and in a triple-negative breast tumor-bearing mice model. Male Sprague Dawley rats and Balb/c mice were divided into four groups: control (received saline), histamine (5 mg/kg for rats and 1 mg/kg for mice, daily subcutaneous injection starting 24 h before treatment with Dox), Dox (2 mg/kg, intraperitoneally injected three times a week for 2 weeks) and Dox+histamine (received both treatments). Tissue toxicity was evaluated by histopathological studies and oxidative stress and biochemical parameters. The combined effect of histamine and Dox was also investigated in vitro and in vivo in human MDA-MB-231 triple-negative breast cancer model. Heart and liver of Dox-treated animals displayed severe histological damage, loss of tissue weight, increased TBARS levels and DNA damage along with an augment in serum creatine kinase-myocardial band. Pretreatment with histamine prevented Dox-induced tissue events producing a significant preservation of the integrity of both rat and mouse myocardium and liver, through the reduction of Dox-induced oxidative stress and apoptosis. Histamine treatment preserved anti-tumor activity of Dox, exhibiting differential cytotoxicity and increasing the Dox-induced inhibition of breast tumor growth. Findings provide preclinical evidence indicating that histamine could be a promising candidate as a selective cytoprotective agent for the treatment of Dox-induced cardiac and hepatic toxicity, and encourage the translation to clinical practice.

Can Ozone Alter the Terpenoid Composition and Membrane Integrity of in vitro Melissa officinalis Shoots?

Ozone affects volatile organic compounds that protect plants from biotic and abiotic stress. In vitro Melissa officinalis shoots were exposed to ozone (200 ppb, 3 h) in controlled environmental conditions: leaf pigments, membrane integrity and headspace composition were assayed during fumigation and after the recovery period (3 h from the beginning of the exposure, FBE). At the end of the exposure, no injury was observed in untreated and treated shoots, although an evident increase in lipid peroxidation was reported (+38.5 and +37.2% of TBARS levels in comparison with controls, respectively after 1 and 3 h FBE). The levels of total carotenoids significantly rose as a normal response mechanism to oxidative stress. SPME-GS-MS analysis showed that, as a consequence of the fumigation, the trends in non-terpenoid compounds increased after 1 and 3 h FBE. This suggests that the concentration and the duration of the treatment were enough to cause a breakdown of cells (as evidenced by increased TBARS levels) and involves an association between volatile products of the lipoxygenase pathway (LOX products) and membrane degradation.

Geranium oil ameliorates endothelial dysfunction in high fat high sucrose diet induced metabolic complications in rats

The protective effect of geranium oil (GO) on insulin resistance, dyslipidemia, endothelial dysfunction and associated cardiovascular changes in rats fed with high fat sucrose (HFS) diet was evaluated. HFS diet (20% fat and 30% sucrose) was fed to wistar rats for 12 weeks to induce metabolic complications and treated with different doses of GO (100, 200 and 400 mg/kg p.o.) for the last 6 weeks. Prolonged administration of HFS diet led to metabolic syndrome characterized by significant increase in plasma glucose, insulin, insulin resistance, triacylglycerol (TG), total cholesterol (TC), low density lipoprotein (LDL) along with decreased high density lipoprotein (HDL), serum nitric oxide (NO) levels and impaired glucose tolerance. Furthermore HFS diet resulted in significant increase in mean arterial pressure, electrocardiographic changes and reduced acetylcholine induced endothelial dependent relaxation of rat aorta along with elevated oxidative stress (reduced superoxide dismutase, catalase, glutathione S transferase and increased TBARS level). Treatment with GO positively modulated the altered parameters in dose dependent manner suggesting overall beneficial effects of GO on HFS diet associated detrimental changes.

Effects of oxytetracycline exposure in Oncorhynchus mykiss: oxidative defence system, peroxidative damage and neurotoxicity

Event Abstract Back to Event Effects of oxytetracycline exposure in Oncorhynchus mykiss: oxidative defence system, peroxidative damage and neurotoxicity Sara Rodrigues1*, Sara C. Antunes1, Alberto T. Correia2 and Bruno S. Nunes3 1 FCUP and CIIMAR, Portugal 2 UFP and CIIMAR, Portugal 3 CESAM and DBio, Portugal In recent years, the presence and effects of pharmaceutical drugs in aquatic ecosystems has received increasing attention from the scientific community. The increasing use of pharmaceutical drugs, such as antibiotics, is cause of concern due to their potential biochemical and physiological deleterious effects. Antibiotics are particularly important because they include a variety of substances widely used in medical and veterinary practice, livestock production and aquaculture. These compounds, such as oxytetracycline (OXY), may act not only on cultured organisms, but also in non-target species. OXY is tetracycline, being used worldwide in aquacultures, due to its high efficacy against bacterial diseases (e.g. vibriosis, enteric redmouth, and also furunculosis). The present study aimed to assess the toxic effects of OXY in the freshwater fish Oncorhynchus mykiss. Fish were exposed during 96 h to OXY in concentrations of 0.005, 0.050, 0.500, 5.00 and 50.0 mg/L. In order to evaluate OXY effects in the rainbow trout, biochemical markers were analyzed, include those focused on oxidative stress parameters [catalase (CAT), total glutathione peroxidase (GPx), glutathione reductase (GRed), and glutathione-S-transferases (GSTs) activities); lipid peroxidation levels (TBARS levels), in liver and gills]; and neurotransmission, (acetylcholinesterase AChE, in muscle and eyes). The here-obtained data showed the occurrence of oxidative stress, reflected by an increased activity of GPx, GRed and GSTs (in gills) and increase of TBARS levels in liver. Additionally, it was possible to observe significant alterations in AChE activities, with decreases in the eyes and increases in muscle. Short-term effects of antibiotics were observed indicating that physiological impairment in fish may occur, with the involvement of multiple organs and biochemical pathways. The global significance of the entire set of results is discussed, giving emphasis to the ecological relevance of the responses. Keywords: Oxytetracycline, rainbow trout, Oxidative Stress, Lipid Peroxidation, neurotransmission Conference: XV European Congress of Ichthyology, Porto, Portugal, 7 Sep - 11 Sep, 2015. Presentation Type: Poster Presentation Topic: Physiology, Behavior and Toxicology Citation: Rodrigues S, Antunes SC, Correia AT and Nunes BS (2015). Effects of oxytetracycline exposure in Oncorhynchus mykiss: oxidative defence system, peroxidative damage and neurotoxicity. Front. Mar. Sci. Conference Abstract: XV European Congress of Ichthyology. doi: 10.3389/conf.FMARS.2015.03.00202 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 07 Dec 2015; Published Online: 07 Dec 2015. * Correspondence: Dr. Sara Rodrigues, FCUP and CIIMAR, Porto, Portugal, up201208875@fc.up.pt Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract Supplemental Data The Authors in Frontiers Sara Rodrigues Sara C Antunes Alberto T Correia Bruno S Nunes Google Sara Rodrigues Sara C Antunes Alberto T Correia Bruno S Nunes Google Scholar Sara Rodrigues Sara C Antunes Alberto T Correia Bruno S Nunes PubMed Sara Rodrigues Sara C Antunes Alberto T Correia Bruno S Nunes Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Berberine Reduces Neurotoxicity Related to Nonalcoholic Steatohepatitis in Rats.

Berberine is a plant alkaloid that has several pharmacological effects such as antioxidant, antilipidemic, and anti-inflammatory effects. Nonalcoholic steatohepatitis (NASH) triggers different aspects of disorders such as impaired endogenous lipid metabolism, hypercholesterolemia, oxidative stress, and neurotoxicity. In this study, we examined the mechanism by which NASH induces neurotoxicity and the protective effect of berberine against both NASH and its associated neurotoxicity. NASH induced rats showed significant impairments in lipid metabolism with increased serum triglycerides, cholesterol, and low-density lipoprotein (LDL). The NASH induced group also demonstrated a significant oxidative stress which is characterized by increased TBARs level and decreased antioxidant capacity such as GSH and SOD levels. Moreover, the NASH induction was associated with inflammation which was demonstrated by increased TNFα and nitric oxide levels. Hyperglycemia and hyperinsulinemia were observed in the NASH induced group. Also, our results showed a significant increase in the expression of the acetylcholine esterase (AChE) and amyloid beta precursor protein (AβPP). These changes were significantly correlated with decreased insulin degrading enzyme (IDE) and beta-amyloid40 (Aβ 40) and increased beta-amyloid42 (Aβ 42) in the hippocampal region. Daily administration of berberine (50 mg/kg) for three weeks ameliorated oxidative stress, inflammation, hyperlipidemia, hyperglycemia, hyperinsulinemia, and the observed neurotoxicity.

Aldehydes participation in oxidative stress in rat thymocytes in vitro.

A variety of lipid radicals are formed under oxidative stress development. The further oxidation of these radicals leads to formation of numerous aldehydes. They can form postsynthetic modifications in proteins and nucleic acids that disrupt their functions. In the present study aldehydes role in the formation of oxidative stress parameters in rat thymocytes was investigated. Two models were used: iron-stimulated oxidative stress and exogenous aldehydes exposure to thymocytes. For oxidative stress induction, thymocytes (2 x 10(6) cells/ml HBSS, pH 7.2) were exposed to different concentrations of FeSO4 (20, 30, 40 microM) and ascorbic acid (100 microM) for 6 h. It resulted in increase of levels of aldehydes 29 times (90 +/- 6 nmol/10(7) cells), these changes led to increase of TBARS levels 4.4 times; the levels of protein CO groups 10 times, cell mitochondrial activity and low-molecular weight SH groups were decreased 1.5 and 2.3 times, respectively. Treatment with aldehydes acceptor dimedone (200 microM) significantly decreased the levels of aldehydes 3.7 times, TBARS 1.6 times and protein CO groups 5 times. It was shown that the levels of cell mitochondrial activity increase 1.4 times and the levels of SH groups 1.8 times. To compare the effects of aldehydes in induction of oxidative stress, thymocytes (2 x 10(6) cells/ml HBSS, pH 7.2) were exposed to 50-600 microM formaldehyde (FA), 50-600 microM glyoxal (GL), 50-600 microM methylglyoxal (MGL), 1-15 microM acrolein (ACR) for 6 h. TBARS levels were increased for FA 1.3 times and for other aldehydes about 5-7 times. The levels of protein CO groups were increase for FA 3.7 times, for MGL 7 times, for GL 13 times, for ACR 22 times. Levels of SH groups were decreased for FA 1.5 times, for MGL 2.6 times, for GL 3 times, for ACR 9 times. A decrease of cell mitochondrial activity 1.5 times observe for all aldehydes. Obtained results prove the aldehydes participation in the formation of oxidative stress parameters and their capability to oxidative stress induction in the rat thymocytes.

Effects of quercetin on oxidative stress biomarkers in methimazole - induced hypothyroid rats.

The objective of the present study was to evaluate the effect of quercetin on oxidative stress biomarkers in methimazole (MMI) - induced hypothyroidism male rats. Hypothyroidism was induced by administering MMI at 20 mg/100 ml in the drinking water, for 1 month. After achieved hypothyroidism, rats received orally 10 or 25 mg/kg of quercetin (QT) for 8 weeks. 60 male wistar rats were randomly divided into 6 groups (group I, control; group II, QT10; group III, QT25; group IV, hypothyroid; group V, hypothyroid+QT10; group VI, hypothyroid+QT25). Liver, kidney and serum TBARS levels significantly increased in hypothyroid rats when compared to controls, along with increased protein carbonyl (PCO) in liver and increased ROS levels in liver and kidney tissues. QT10 and QT25 were effective in decreasing TBARS levels in serum and kidney, PCO levels in liver and ROS generation in liver and kidney. MMI - induced hypothyroidism also increased TBARS levels in cerebral cortex and hippocampus that in turn were decreased in rats treated with QT25. Moreover, the administration of QT25 to hypothyroid rats resulted in decreased SOD activities in liver and whole blood and increased liver CAT activity. Liver and kidney ascorbic acid levels were restored with quercetin supplementation at both concentrations. QT10 and QT25 also significantly increased total oxidative scavenging capacity in liver and kidney tissues from hypothyroid rats. These findings suggest that MMI - induced hypothyroidism increases oxidative stress parameters and quercetin administration could exert beneficial effects against redox imbalance in hypothyroid status.