共查询到20条相似文献,搜索用时 93 毫秒
1.
Medeiros MC Mello A Gemelli T Teixeira C de Almeida M de Andrade RB Wannmacher CM Guerra RB Gomez R Funchal C 《Neurochemical research》2012,37(5):928-934
Selenium (Se) is an essential mineral for mammals. It is a nutrient related to the complex metabolic and enzymatic functions.
Although Se has important physiological functions in the cells, organic compounds of Se can be extremely toxic, and may affect
the central nervous system. This study aims to investigate the effect of the chronic treatment with the vinyl chalcogenide
3-methyl-1-phenyl-2-(phenylseleno)oct-2-en-1-one on some parameters of oxidative stress in the brain of rats. Animals received
the vinyl chalcogenide (125, 250 or 500 μg/kg body weight) intraperitoneally once a day during 30 days. The cerebral cortex,
the hippocampus, and the cerebellum were dissected and homogenized in KCl. Afterward, thiobarbituric acid reactive substances
(TBARS), carbonyl, sulfhydryl, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were
measured in the brain. Results showed that the organoselenium enhanced TBARS in the cerebral cortex of rats but the compound
was not able to change carbonyl levels. Furthermore, the organoselenium reduced thiol groups measured by the sulfhydryl assay
in all tissues studied. The activity of the antioxidant enzyme CAT was increased by the organochalcogen in the cerebral cortex
and in the cerebellum, and the activity of SOD was increased in the hippocampus. On the other hand, the activity of the antioxidant
enzyme GPx was reduced in all brain structures. Our findings indicate that this organoselenium compound induces oxidative
stress in different brain regions of rats, corroborating to the fact that this tissue is a potential target for organochalcogen
action. 相似文献
2.
Cláudia Funchal Carlos Augusto Souza Carvalho Tanise Gemelli Andressa S. Centeno Robson Brum Guerra Mirian Salvador Caroline Dani Adriana Coitinho Rosane Gomez 《Cellular and molecular neurobiology》2010,30(7):1135-1142
Organotellurium compounds have been synthesized since 1840, but pharmacological and toxicological studies about them are still
incipient. Therefore, the objective of this study was to verify the effect of acute administration of the organochalcogen
3-butyl-1-phenyl-2-(phenyltelluro)oct-en-1-one on some parameters of oxidative stress in the brain of 30-day-old rats. Animals
were treated intraperitoneally with a single dose of the organotellurium (125, 250, or 500 μg/kg body weight) and sacrificed
60 min after the injection. The cerebral cortex, the hippocampus, and the cerebellum were dissected and homogenized in KCl.
Afterward, thiobarbituric acid reactive substances (TBARS), carbonyl, sulfhydryl, catalase (CAT), superoxide dismutase (SOD),
nitric oxide (NO) formation, and hydroxyl radical production were measured in the brain. The organotellurium enhanced TBARS
in the cerebral cortex and the hippocampus, and increased protein damage (carbonyl) in the cerebral cortex and the cerebellum.
In contrast, the compound provoked a reduced loss of thiol groups measured by the sulfhydryl assay in all the tissues studied.
Furthermore, the activity of the antioxidant enzyme CAT was reduced by the organochalcogen in the cerebral cortex and the
cerebellum, and the activity of SOD was inhibited in all the brain tissues. Moreover, NO production was increased in the cerebral
cortex and the cerebellum by this organochalcogen, and hydroxyl radical formation was also enhanced in the cerebral cortex.
Our findings indicate that this organotellurium compound induces oxidative stress in the brain of rats, corroborating that
this tissue is a potential target for organochalcogen action. 相似文献
3.
Harish G Venkateshappa C Mahadevan A Pruthi N Srinivas Bharath MM Shankar SK 《Neurochemistry international》2011,59(7):1029-1042
The equilibrium between antioxidant function and oxidative stress is implicated in brain pathology. However, human studies on oxidant and antioxidant markers rely on postmortem tissue that might be affected by pre and postmortem factors. To evaluate the effect of these variables, we tested whether antioxidant enzymes [superoxide dismutase (SOD), catalase] glutathione (GSH) and related enzymes [gamma glutamylcysteine ligase (GCL), GSH peroxidase (GPx), GSH reductase (GR), GSH-S-transferase (GST)] and malondialdehyde (MDA, marker of lipid peroxidation) are affected in postmortem human brains (n = 50) by increase in postmortem interval (2.5–26 h), gender difference and agonal state [based on Glasgow coma scale (GCS): range: 3–15] in different anatomical regions-frontal cortex (FC), cerebellum (CB) medulla oblongata (MO), substantia nigra (SN) and hippocampus (HC). While SOD and catalase activities were relatively unaltered, GR and GPx activities were affected by agonal state (GR in CB, p < 0.05; GPx in MO, p < 0.05) indicating altered GSH dynamics during the secondary events following neuronal injury. MO, SN and HC displayed low GSH compared to FC and CB. Total GSH level was decreased with PMI (MO, p = 0.02) which could be partly attributed to increase in MDA levels with increasing PMI in MO (p < 0.05). Total GSH level was higher in CB (p < 0.017) and MO (p < 0.04) in female brains compared to males. Interestingly, HC and SN regions showed significant stability in most of the markers tested. We suggest that while SOD and catalase were relatively unaffected by the pre and postmortem factors, GSH and its metabolic enzymes were significantly altered and this was more pronounced in MO of postmortem human brains. These data highlight the influence of pre and postmortem factors on GSH dynamics and the inherent differences in brain regions, with implications for studies on brain pathophysiology employing human samples. 相似文献
4.
The age-related changes in the activities of antioxidant enzymes of mitochondrial and cytosolic fractions were measured in different regions of the central nervous system (CNS) in 10 and 32 months old guinea pigs. In old animals, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were reduced (p < 0.05) in all the regions of CNS studied but catalase (CAT) declined significantly only in the cerebral cortex, hypothalamus and cerebellum. Glutathione reductase (GRd) activity declined in cerebral cortex and hypothalamus in the cytosolic fractions and only in cerebellum in the mitochondrial fraction. It is concluded that age-related decline in the activities of antioxidant enzymes is both region and enzyme specific. The endogenous lipid peroxide was found to be significantly higher (p < 0.05) in the 32 month old animals whereas, lipid peroxidation after incubating the tissue homogenate in air was found to be lower (p < 0.05). The in vitro mitochondrial lipid peroxidation decreased with age. The results indicate that accumulation of lipid peroxides takes place with ageing but the susceptibility of lipid peroxidation decreases in the older animals. 相似文献
5.
Sathyasaikumar KV Swapna I Reddy PV Murthy ChR Dutta Gupta A Senthilkumaran B Reddanna P 《Neurochemical research》2007,32(3):517-524
Hepatic Encephalopathy (HE) is one of the most common complications of acute liver diseases and is known to have profound
influence on the brain. Most of the studies, available from the literature are pertaining to whole brain homogenates or mitochondria.
Since brain is highly heterogeneous with functions localized in specific areas, the present study was aimed to assess the
oxidative stress in different regions of brain-cerebral cortex, cerebellum and pons medulla during acute HE. Acute liver failure
was induced in 3-month old adult male Wistar rats by intraperitoneal injection of thioacetamide (300 mg/kg body weight for
two days), a well known hepatotoxin. Oxidative stress conditions were assessed by free radical production, lipid peroxidation,
nitric oxide levels, GSH/GSSG ratio and antioxidant enzyme machinery in three distinct structures of rat brain-cerebral cortex,
cerebellum and pons medulla. Results of the present study indicate a significant increase in malondialdehyde (MDA) levels,
reactive oxygen species (ROS), total nitric oxide levels [(NO) estimated by measuring (nitrites + nitrates)] and a decrease
in GSH/GSSG ratio in all the regions of brain. There was also a marked decrease in the activity of the antioxidant enzymes-glutathione
peroxidase, glutathione reductase and catalase while the super oxide dismutase activity (SOD) increased. However, the present
study also revealed that pons medulla and cerebral cortex were more susceptible to oxidative stress than cerebellum. The increased
vulnerability to oxidative stress in pons medulla could be due to the increased NO levels and increased activity of SOD and
decreased glutathione peroxidase and glutathione reductase activities. In summary, the present study revealed that oxidative
stress prevails in different cerebral regions analyzed during thioacetamide-induced acute liver failure with more pronounced
effects on pons medulla and cerebral cortex.
Murthy Ch.R.K—Deceased while in service. 相似文献
6.
7.
Juliano M. Vieira Fabiano B. Carvalho Jessié M. Gutierres Mayara S. P. Soares Pathise S. Oliveira Maribel A. Rubin 《Redox report : communications in free radical research》2017,22(6):493-500
Objective: Here we investigated the impact of chronic high-intensity interval training (HIIT) and caffeine consumption on the activities of Na+-K+-ATPase and enzymes of the antioxidant system, as well as anxiolytic-like behaviour in the rat brain.Methods: Animals were divided into groups: control, caffeine (4?mg/kg), caffeine (8?mg/kg), HIIT, HIIT plus caffeine (4?mg/kg) and HIIT plus caffeine (8?mg/kg). Rats were trained three times per week for 6 weeks, and caffeine was administered 30 minutes before training. We assessed the anxiolytic-like behaviour, Na+-K+-ATPase, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, levels of reduced glutathione (GSH) and thiobarbituric acid reactive substances (TBARS) in the brain.Results and discussion: HIIT-induced anxiolytic-like behaviour increased Na+-K+-ATPase and GPx activities and TBARS levels, altered the activities of SOD and CAT in different brain regions, and decreased GSH levels. Caffeine, however, elicited anxiogenic-like behaviour and blocked HIIT effects. The combination of caffeine and HIIT prevented the increase in SOD activity in the cerebral cortex and GPx activity in three brain regions. Our results show that caffeine promoted anxiogenic behaviour and prevented HIIT-induced changes in the antioxidant system and Na+-K+-ATPase activities. 相似文献
8.
Latini A Ferreira GC Scussiato K Schuck PF Solano AF Dutra-Filho CS Vargas CR Wajner M 《Cellular and molecular neurobiology》2007,27(4):423-438
1. Glutaric acidemia type I (GA I) is a neurometabolic disorder caused by deficiency of glutaryl-CoA dehydrogenase, which
leads to tissue accumulation of predominantly glutaric acid (GA) and also 3-hydroxyglutaric acid to a lesser amount. Affected
patients usually present progressive cortical atrophy and acute striatal degeneration attributed to the toxic accumulating
metabolites.
2. In the present study, we determined a number of oxidative stress parameters, namely chemiluminescence, thiobarbituric acid-reactive
substances (TBA-RS), total antioxidant reactivity (TAR), glutathione (GSH) levels, and the activities of catalase and glutathione
peroxidase (GPx), in various tissues from rats chronically exposed to GA or to saline (controls). High GA concentrations,
similar to those found in glutaric aciduria type I, were induced in the brain by three daily subcutaneous injections of saline-buffered
GA (5 μmol/g body weight) to Wistar rats of 5–22 days of life. The parameters were assessed 12 h after the last GA administration
in different brain structures, skeletal muscle, heart, liver, erythrocytes, and plasma. The lipid peroxidation parameters
chemiluminescence and/or TBA-RS measurements were found significantly increased in midbrain, liver, and erythrocytes of GA-injected
rats. The activity of GPx was significantly reduced in midbrain and markedly increased in liver. TAR measurement was significantly
reduced in midbrain and liver. Furthermore, GSH levels were reduced in liver and heart.
We also investigated the acute in vivo effect of GA administration on the same oxidative stress parameters in cerebral structures and erythrocytes from 22-day-old
rats. We found that TBA-RS values were significantly increased in erythrocytes, TAR levels were markedly decreased in midbrain
and cerebellum, and GPx activity mildly reduced in the midbrain.
3. These data showing an imbalance between antioxidant defences and oxidative damage, particularly in midbrain, liver, and
erythrocytes from GA-injected rats, indicate that oxidative stress might be involved in GA toxicity and that the midbrain,
where the striatum is located, is the brain structure more susceptible to GA chronic and acute exposition. 相似文献
9.
Essential elements, mainly selenium and zinc, were involved in protection against oxidative stress in cells. Oxidation could
lead to the formation of free radicals that have been implicated in the pathogenesis of many diseases, including leukemia.
Leukemia is a neoplastic disease that is susceptible to antioxidant enzyme and essential elements alterations. This study
was undertaken to examine the levels of essential elements, antioxidant enzymes activities, and their relationships with different
types of leukemia. Serum selenium, zinc, and copper concentrations, red blood cell glutathione peroxidase (GPx) activities,
plasma Cu−Zn superoxide dismutase (Cu−Zn SOD) activities and lipid peroxidation (LPO) levels were determined in 49 patients
with different types of leukemia before initial treatment. Serum selenium and zinc concentrations were lower in leukemia patients
than those of controls (p<0.01). Serum copper concentration was higher in leukemia patients than that of controls (p<0.01). The activities GPx and Cu−Zn SOD were significantly increased in leukemia patients, especially with acute leukemia
(AL), acute lymphoid leukemia (ALL), and acute nonlymphoid leukemia (ANLL) (p<0.05), whereas no difference was found between those of chronic myelogeneous leukemia and the controls. The levels of LPO
were normal as controls. Serum selenium concentration was not correlated with GPx, and serum levels of zinc and copper were
not related to Cu−Zn SOD. Serum zinc levels had a negative correlation with the absolute peripheral blast cells, whereas serum
copper had a positive correlation with the absolute peripheral blast cells. Increased GPx and Cu−Zn SOD activities and normal
levels of LPO, which were a protective responses, were an indicator of mild oxidative stress; it mights indicate that the
essentials elements alterations in leukemia patients were mostly dependent on tumor activity. Changes of their levels demonstrated
that there are low selenium, zinc, and high copper status in leukemia patients. The decrease of plasma zinc and increase of
the Cu/Zn ratio could be the index that showed an unfavorable prognosis of acute leukemia. 相似文献
10.
In the present investigation, we studied the possible potentiating effect of salicylic acid (SA) under Cd toxicity in Oryza sativa L. leaves. Cd treatments for 24 h reduced the shoot length, dry biomass and total chlorophyll content followed by high Cd
accumulation in shoots. About 16 h presoaking with SA resulted in partial protection against Cd, as observed by minor changes
in length, biomass and total chlorophyll. SA priming resulted in low Cd accumulation. Enhanced thiobarbituric acid reactive
substances (TBARS), hydrogen peroxide (H2O2) and superoxide anion (O2
−) content were seen when Cd was applied alone, while under SA priming the extent of TBARS, H2O2 and O2
− were significantly low, suggesting SA-regulated protection against oxidative stress. The antioxidant enzymes like Catalase
(CAT), guaiacol peroxidase (GPx), glutathione reductase (GR) and superoxide dismutase (SOD) showed varied activities under
Cd alone. CAT activity increased after Cd treatment, followed by a decline in GPX and GR activity. SOD also declined at the
highest concentrations with an initial increase. Under SA-priming conditions, the efficiency of the antioxidant enzymes was
significantly elevated. GPx and SOD activity showed significant increase in activity. The ascorbate activity increased after
Cd treatment, followed by a decline in glutathione under SA-free condition. SA priming showed gradual increase in these non-enzymic
antioxidants. Our results indicate that Cd-induced oxidative stress can be regulated by SA. 相似文献
11.
Anthocyanins (ANT) are polyphenolic flavonoids with antioxidant and neuroprotective properties. This study evaluated the effect of ANT treatment on cognitive performance and neurochemical parameters in an experimental model of sporadic dementia of Alzheimer's type (SDAT). Adult male rats were divided into four groups: control (1 ml/kg saline, once daily, by gavage), ANT (200 mg/kg, once daily, by gavage), streptozotocin (STZ, 3 mg/kg) and STZ plus ANT. STZ was administered via bilateral intracerebroventricular (ICV) injection (5 μl). ANT were administered after ICV injection for 25 days. Cognitive deficits (short-term memory and spatial memory), oxidative stress parameters, and acetylcholinesterase (AChE) and Na+-K+-ATPase activity in the cerebral cortex and hippocampus were evaluated. ANT treatment protected against the worsening of memory in STZ-induced SDAT. STZ promoted an increase in AChE and Na+-K+-ATPase total and isoform activity in both structures; ANT restored this change. STZ administration induced an increase in lipid peroxidation and decrease in the level of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), in the cerebral cortex; ANT significantly attenuated these effects. In the hippocampus, an increase in reactive oxygen species (ROS), nitrite and lipid peroxidation levels, and SOD activity and a decrease in CAT and GPx activity were seen after STZ injection. ANT protected against the changes in ROS and antioxidant enzyme levels. In conclusion, the present study showed that treatment with ANT attenuated memory deficits, protected against oxidative damage in the brain, and restored AChE and ion pump activity in an STZ-induced SDAT in rats. 相似文献
12.
Acute hyperammonemia (HA) induced oxidative stress in the brain is considered to play critical roles in the neuropathology
of end stage hepatic encephalopathy (HE). Moderate grade HA led minimal/moderate type HE is more common in the patients with
chronic liver failure. However, implication of oxygen free radical (
\textO 2 - {\text{O}}_{ 2}^{ - } ) based oxidative mechanisms remain to be defined during moderate grade HA. This article describes profiles of all the antioxidant
enzymes Vis a Vis status of oxidative stress/damage in the brain slices exposed to 0.1–1 mM ammonia, reported to exist in
the brain of animals with chronic liver failure and in liver cirrhotic patients. Superoxide dismutase catalyzes the first
step of antioxidant mechanism and, with concerted activity of catalase, neutralizes
\textO 2 - {\text{O}}_{ 2}^{ - } produced in the cells. Both these enzymes remained unchanged up to 0.2–0.3 mM ammonia, however, with significant increments
(P < 0.01–0.001) in the brain slices exposed to 0.5–1 mM ammonia. This was consistent with the similar pattern of production
of reactive oxygen species in the brain slices. However, level of lipid peroxidation remained unchanged throughout the ammonia
treatment. Synchronized activities of glutathione peroxidase and glutathione reductase regulate the level of glutathione to
maintain reducing equivalents in the cells. The activities of both these enzymes also increased significantly in the brain
slices exposed to 0.5–1 mM ammonia with concomitant increments in GSH/GSSG ratio and in the levels of total and protein bound
thiol. The findings suggest resistance of brain cells from ammonia induced oxidative damage during moderate grade HA due to
concordant activations of antioxidant enzymes. 相似文献
13.
《Redox report : communications in free radical research》2013,18(2-3):75-80
AbstractProtective effects of NOS inhibitors and free radical scavengers in cerebral ischemia are well documented. The present study was undertaken to determine the possible effects of NOS inhibition on brain antioxidants. Levels of both enzymatic [glutathione peroxidase (GPx), catalase and superoxide dismutase (SOD)] and non-enzymatic [reduced glutathione (GSH)] antioxidants following nitric oxide synthase (NOS) inhibition by NG-nitro-L-arginine methyl ester (L-NAME), D-NAME or 7-nitro-indazole (7-NI) have been investigated. NOS activity and antioxidant levels in the rat cerebellum and medulla were estimated 1 h after treatment with L-NAME (10, 30 and 100 mg/kg, i.p.), D-NAME (100 mg/kg, i.p.) or 7-NI (25 mg/kg, i.p.). L-NAME and 7-NI inhibited NOS activity in a dose-dependent manner. D-NAME also exhibited significant NOS inhibition. The activity of SOD and the GSH level remained unaltered following NOS inhibition. However, L-NAME and D-NAME at 100 mg/kg attenuated GPx activity in the cerebellum, though 7-NI had no effect. L-NAME inhibited catalase activity in medulla only at 30 mg/kg, but had no effect in cerebellum. However, 7-NI (25 mg/kg), D-NAME and L-NAME at 100 mg/kg did not affect catalase activity in the rat brain. Thus, NOS inhibition by the three agents did not have major effects on brain antioxidant levels. 相似文献
14.
Background
Higher aluminum (Al) content in infant formula and its effects on neonatal brain development are a cause for concern. This study aimed to evaluate the distribution and concentration of Al in neonatal rat brain following Al treatment, and oxidative stress in brain tissues induced by Al overload.Methods
Postnatal day 3 (PND 3) rat pups (n =46) received intraperitoneal injection of aluminum chloride (AlCl3), at dosages of 0, 7, and 35 mg/kg body wt (control, low Al (LA), and high Al (HA), respectively), over 14 d.Results
Aluminum concentrations were significantly higher in the hippocampus (751.0 ± 225.8 ng/g v.s. 294.9 ± 180.8 ng/g; p < 0.05), diencephalon (79.6 ± 20.7 ng/g v.s. 20.4 ± 9.6 ng/g; p < 0.05), and cerebellum (144.8 ± 36.2 ng/g v.s. 83.1 ± 15.2 ng/g; p < 0.05) in the HA group compared to the control. The hippocampus, diencephalon, cerebellum, and brain stem of HA animals displayed significantly higher levels of lipid peroxidative products (TBARS) than the same regions in the controls. However, the average superoxide dismutase (SOD) activities in the cerebral cortex, hippocampus, cerebellum, and brain stem were lower in the HA group compared to the control. The HA animals demonstrated increased catalase activity in the diencephalon, and increased glutathione peroxidase (GPx) activity in the cerebral cortex, hippocampus, cerebellum, and brain stem, compared to controls.Conclusion
Aluminum overload increases oxidative stress (H2O2) in the hippocampus, diencephalon, cerebellum, and brain stem in neonatal rats. 相似文献15.
Lead-induced increase in antioxidant enzymes and lipid peroxidation products in developing rat brain 总被引:6,自引:0,他引:6
Kiran Kumar Bokara Erika Brown Rashidi McCormick Prabhakara Rao Yallapragada Sharada Rajanna Rajanna Bettaiya 《Biometals》2008,21(1):9-16
Pregnant rats were treated with 0.4% lead acetate through drinking water from 6th day of gestation and this treatment was
continued till 21 post natal days (PND). Four regions of the brain namely hippocampus, cerebellum, frontal cortex and brain
stem were dissected at 10, 20, 30 and 40 PND for estimation of lipid peroxidation products (LPP), catalase (CAT) and superoxide
dismutase (SOD). The results indicate that there was a significant (P < 0.05) increase of LPP in exposed rats than their corresponding control at 10, 20 and 30 PND both in hippocampus and cerebellum.
At PND 40, the LPP of control and exposed were found to be almost same in both the tissues indicating recovery from lead toxicity.
CAT activity was significantly (P < 0.05) high in hippocampus of exposed rats up to PND 30 but up to PND 20 in cerebellum and frontal cortex. However, in brain
stem, a significant (P < 0.05) increase in CAT activity was observed only at PND 10. A significant (P < 0.05) increase in SOD activity was observed up to PND 30 both in hippocampus and cerebellum on lead exposure. Frontal cortex
exhibited a similar significant (P < 0.05) increase of SOD activity up to PND 20 and for brain stem up to PND 10. There was no significant change in the activity
of antioxidant enzymes (CAT and SOD) and LPP in all the four brain tissues of control and exposed rats at PND 40 indicating
recovery from lead-induced oxidative stress.
This research work was presented as a poster in Annual Biomedical Research Conference for Minority Students (ABRCMS) at Dallas,
Texas, USA, during November 10–13, 2004 and the abstract was printed on page 231 of the Conference Proceedings 相似文献
16.
Rodrigo Binkowski de Andrade Tanise Gemelli Robson B. Guerra Caroline Dani Clovis Milton Duval Wannmacher Rosane Gomez Cláudia Funchal 《Cell biochemistry and function》2014,32(5):438-444
The mechanisms that lead to the onset of organoselenium intoxication are still poorly understood. Therefore, in the present study, we investigated the effect of acute administration of 3‐methyl‐1‐phenyl‐2‐(phenylseleno)oct‐2‐en‐1‐one on some parameters of oxidative stress and on the activity of creatine kinase (CK) in different brain areas and on the behaviour in the open field test of 90‐day‐old male rats. Animals (n = 10/group) were treated intraperitoneally with a single dose of the organoselenium (125, 250 or 500 µg kg?1), and after 1 h of the drug administration, they were exposed to the open field test, and behaviour parameters were recorded. Immediately after they were euthanized, cerebral cortex, hippocampus and cerebellum were dissected for measurement of thiobarbituric acid reactive substances (TBARS), carbonyl, sulfhydryl, catalase (CAT), superoxide dismutase (SOD) and CK activity. Our results showed that the dose of 500 µg kg?1 of the organoselenium increased the locomotion and rearing behaviours in the open field test. Moreover, the organochalcogen enhanced TBARS in the cerebral cortex and cerebellum and increased the oxidation of proteins (carbonyl) only in the cerebral cortex. Sulfhydryl content was reduced in all brain areas, CAT activity enhanced in the hippocampus and reduced in the cerebellum and SOD activity increased in all brain structures. The organoselenium also inhibited CK activity in the cerebral cortex. Therefore, changes in motor behaviour, redox state and energy homeostasis in rats treated acutely with organoselenium support the hypotheses that the brain is a potential target for the organochalcogen action. Copyright © 2014 John Wiley & Sons, Ltd. 相似文献
17.
Pedro Tauler Antoni Aguiló Nuria Cases Antoni Sureda Fernando Gimenez Gerardo Villa 《Free radical research》2013,47(10):1101-1107
Long-duration or damaging exercise initiates reactions that resemble the acute phase response to infection and induces neutrophil priming for oxidative activity. Our objective was to establish the status of the antioxidant defences and of the oxidative equilibrium in the neutrophils of sportsmen prior to and after intense physical exercise. Nine voluntary male professional cyclists participated in this study. The exercise was a cycling mountain stage (171 km) and the cyclists took a mean - SEM of 270 - 12 min to complete it. We determined the activities of catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), the levels and activity of superoxide dismutase (SOD), the concentrations of ascorbate, glutathione and glutathione disulphide (GSSG) and DNA levels in neutrophils. The cycling stage decreased enzyme activities expressed per DNA units: CAT (33%), SOD (38%), GPx (65%); increased ascorbate concentration in neutrophils and decreased the GSH/GSSG ratio and the enzyme activities expressed per DNA units. Neutrophils could contribute to plasma antioxidant defences against oxidative stress induced by exercise because they probably provide antioxidant enzymes and ascorbate. 相似文献
18.
Background and Purpose
Liver dysfunction led hyperammonemia (HA) causes a nervous system disorder; hepatic encephalopathy (HE). In the brain, ammonia induced glutamate-excitotoxicity and oxidative stress are considered to play important roles in the pathogenesis of HE. The brain ammonia metabolism and antioxidant enzymes constitute the main components of this mechanism; however, need to be defined in a suitable animal model. This study was aimed to examine this aspect in the rats with acute liver failure (ALF).Methods
ALF in the rats was induced by intraperitoneal administration of 300 mg thioacetamide/Kg. b.w up to 2 days. Glutamine synthetase (GS) and glutaminase (GA), the two brain ammonia metabolizing enzymes vis a vis ammonia and glutamate levels and profiles of all the antioxidant enzymes vis a vis oxidative stress markers were measured in the cerebral cortex and cerebellum of the control and the ALF rats.Results
The ALF rats showed significantly increased levels of ammonia in the blood (HA) but little changes in the cortex and cerebellum. This was consistent with the activation of the GS-GA cycle and static levels of glutamate in these brain regions. However, significantly increased levels of lipid peroxidation and protein carbonyl contents were consistent with the reduced levels of all the antioxidant enzymes in both the brain regions of these ALF rats.Conclusion
ALF activates the GS-GA cycle to metabolize excess ammonia and thereby, maintains static levels of ammonia and glutamate in the cerebral cortex and cerebellum. Moreover, ALF induces oxidative stress by reducing the levels of all the antioxidant enzymes which is likely to play important role, independent of glutamate levels, in the pathogenesis of acute HE. 相似文献19.
Biswaranjan Paital G.B.N. Chainy 《Comparative biochemistry and physiology. Toxicology & pharmacology : CBP》2010,151(1):142-151
The effects of salinity (10, 17 and 35 ppt) on O2 consumption, CO2 release and NH3 excretion by crabs and oxidative stress parameters and antioxidant defenses of its tissues were reported. An increase in salinity caused a decrease in O2 consumption and CO2 release and an increase in ammonia excretion by crabs. Lipid peroxidation, protein carbonyl, H2O2 levels and total antioxidant capacity of the tissues elevated significantly at 35 ppt salinity except in abdominal muscle where H2O2 content was low. Ascorbic acid content of tissues was higher at 17 ppt salinity than at 10 and 35 ppt salinities. With increasing salinity, a gradual decrease in SOD, an increase in catalase, no change in GPx and a decrease followed by an increase in GR activities were recorded for abdominal muscle. While for hepatopancreas, an increase followed by a decrease in SOD and catalase, decrease in GPx and GR activities were noticed with increasing salinity. In the case of gills, a decrease followed by an increase in SOD, a decrease in catalase and GPx and an increase in GR activities were noted when the salinity increased from 10 ppt to 35 ppt. These results suggest that salinity modulation of oxidative stress and antioxidant defenses in Scylla serrata is tissue specific. 相似文献
20.
Casado A Encarnación López-Fernández M Concepción Casado M de La Torre R 《Neurochemical research》2008,33(3):450-458
It has been reported that oxidative stress may play a role in the pathogenesis of dementia of the Alzheimer type (AD) and
the cerebral ischemia which causes vascular dementia (VD). We measured malondialdehyde (MDA) levels and superoxide dismutase
(SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) activities in blood samples from patients
with AD and VD and in healthy non-demented controls (CTR) which similar ages to the patients, in order to evaluate the degree
of oxidative stress in patients with AD and VD. A sample of 150 subjects consisting of 50 patients with AD; 50 patients with
VD and 50 CTR, aged from 65 to 85 years on, was analyzed. Most of the changes observed were in SOD activity and MDA levels. Catalase activity were least affected. Significant differences were observed in SOD and GR activity between males and females in CRT and in patients with AD, but
not in VD. We have found a decrease in antioxidant enzymes activities (SOD, CAT, GPx and GR) in patients with AD and VD and
significant differences were observed between CRT and AD patients for ages from 65 to 74, 75 to 84 and from 85 years to 94 years
in SOD activity and MDA levels (P < 0.001). MDA levels increase with age in VD, AD and CTR. No significant variation with respect to sex were detected, but
significant variations in MDA levels were detected between CRT and patients with VD and AD (P < 0.001). We conclude that oxidative stress plays an important role in the brain damage for both AD and VD, being observed
higher levels of oxidative stress for AD that for VD. 相似文献