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1.
To investigate the influence of selenium on body weights and the immune organ indexes in ducklings administrated with aflatoxin
B1 (AFB1), 90 7-day-old ducklings were randomly divided into three groups (groups I–III). Group I was used as a blank control. Group
II was administered with AFB1 (0.1 mg/kg body weight). Group III was administered with AFB1 (0.1 mg/kg body weight) plus sodium selenite (1 mg/kg body weight). All treatments were given once daily for 21 days. It
showed that the ducklings’ bursa of fabricius, thymus indexes, and body weights in group II significantly decreased when compared
with group I (P < 0.01). Furthermore, the spleen indexes significantly decreased (P < 0.01). However, the ducklings’ bursa of fabricius and thymus indexes, body weights in group III ducklings significantly
increased when compared with group II (P < 0.01). In addition, the spleen indexes significantly decreased (P < 0.01). These results revealed that AFB1 significantly affect ducklings’ growth and immune organs development. However, selenium significantly ameliorated the negative
effects induced by AFB1. 相似文献
2.
Shi D Guo S Liao S Su R Guo M Liu N Li P Tang Z 《Biological trace element research》2012,145(3):312-317
To investigate the protection of selenium on hepatic mitochondrial functions, 90 7-day-old ducklings were randomly divided
into three groups (groups I–III). Group I was used as a blank control. Group II was administered with aflatoxin B1 (0.1 mg/kg body weight). Group III was administered with aflatoxin B1 (0.1 mg/kg body weight) plus selenium (sodium selenite, 1 mg/kg body weight). All treatments were given once daily for 21 days.
The results showed that the activities of hepatic mitochondrial complexes I–IV in group II ducklings significantly decreased
when compared with group I (P < 0.01). Furthermore, the activities of hepatic mitochondrial complexes I–IV in group III significantly increased when compared
with group II (P < 0.05). The hepatic mitochondrial respiratory control ratio (RCR) in group II ducklings significantly decreased when compared
with group I (P < 0.01). In addition, the hepatic mitochondrial RCR in group III significantly increased when compared with group II (P < 0.05). These results revealed that the aflatoxin B1 significantly induced hepatic mitochondrial dysfunction in the activities of hepatic mitochondrial respiratory chain complexes
I–IV and the RCR in ducklings. However, sodium selenite could significantly ameliorate the negative effect induced by aflatoxin
B1. 相似文献
3.
The aim of the study was to investigate the effect of selenium on hepatic mitochondrial antioxidant capacity in ducklings
administrated with aflatoxin B1 (AFB1). Ninety 7-day-old ducklings were randomly divided into three groups (groups I–III). Group I was used as a blank control.
Group II was administered with AFB1 (0.1 mg/kg body weight). Group III was administered with AFB1 (0.1 mg/kg body weight) plus selenium (sodium selenite, 1 mg/kg body weight). All treatments were given once daily for 21 days.
The results showed that the activities of mitochondrial superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase
(GSH-Px), and glutathione reductase (GR) in group II ducklings significantly decreased when compared with group I (P < 0.01). Furthermore, the content of hepatic mitochondrial malondialdehyde (MDA) significantly increased (P < 0.01). However, the activities of hepatic mitochondrial SOD, CAT, GSH-Px, and GR in group III ducklings significantly increased
when compared with group II (P < 0.05). In addition, the content of hepatic mitochondrial MDA significantly decreased (P < 0.01). These results revealed that AFB1 significantly induced hepatic mitochondrial antioxidant dysfunction. However, sodium selenite could significantly ameliorate
the negative effect induced by AFB1. 相似文献
4.
Atmaca M Bilgin HM Obay BD Diken H Kelle M Kale E 《Journal of physiology and biochemistry》2011,67(4):569-576
Coumarins are a vast group of natural compounds and some of them possess antioxidant activities. The comparison of the antioxidant
activity of some coumarins with various chemical molecular structure has not been investigated in previous studies. Therefore,
this study was aimed to investigate the hepatoprotective effect against carbon tetrachloride (CCl4) -induced hepatic injury by coumarin (1,2-benzopyrone) and coumarin derivatives, esculetin (6,7-dihydroxycoumarin), scoparone
(6,7-dimethoxycoumarin), and 4-methylumbelliferone (7-hyroxy-4-methyl) in male Sprague–Dawley rats. Product of lipid peroxidation,
malondialdehyde (MDA), activities of antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) were evaluated for oxidative
stress in hepatic injury. Gamma glutamyl transpeptidase (GGT), lactate dehydrogenase (LDH) were detected in plasma as a biomarker
of hepatic injury. Significantly elevated levels of MDA and lowered levels of SOD and CAT activities were observed in liver
of rats exposed to CCl4, when compared to control values. Similarly, administration of CCl4 increased LDH and GGT levels in serum. Pre-treatment of rats with esculetin (35 mg kg−1, orally) and scoparone (35 mg kg−1, orally) significantly prevented CCl4-induced decrease in MDA levels and increase in SOD and CAT, whereas 4-methylumbelliferone (35 mg kg−1) and coumarin (30 mg kg−1) had no effect against CCl4-induced rise in serum enzymes. Esculetin and scoparone also showed protective properties as was evidenced in reduced LDH
and GGT levels in serum. The results of this study indicate that the chemical structures of coumarins play an important role
in the prevention of oxidative stress. 相似文献
5.
Ononitol monohydrate, structurally similar to glycoside was isolated from Cassia tora L. leaves. Fifty Male rats were divided into five groups. Group I served as normal control. Group II, III and IV rats were induced hepatotoxicity by CCl4 administering single dose of CCl4 on 8th day only. Group III was treated with ononitol monohydrate (20 mg/kg body weight) and group IV was treated with reference drug silymarin (20 mg/kg body weight) both dissolved in corn oil and administering for 8 days. Ononitol monohydrate with corn oil alone was given for 8 days (group V). At the end of the experimental period all the animals were sacrificed and analyzed for biochemical parameters to assess the effect of ononitol monohydrate treatment in CCl4 induced hepatotoxicity. In in vivo study, ononitol monohydrate decreased the levels of serum transaminase, lipid peroxidation and TNF-α but increased the levels of antioxidant and hepatic glutathione enzyme activities. Compared with reference drug silymarin ononitol monohydrate possessesed high hepatoprotective activity. Histopathological results also suggested the hepatoprotective activity of ononitol monohydrate with no adverse effect. Hence we conclude that ononitol monohydrate is a potent hepatoprotective agent. 相似文献
6.
Mohamed A. Haidara Mohamed D. Morsy Hesham A. Abdel-Razek Dimitri P. Mikhailidis Esma R. Isenovic 《Journal of physiology and biochemistry》2010,66(3):255-264
Septicemia leads to oxidative stress with overproduction of reactive-oxygen species (ROS) and consumption of endogenous antioxidant
enzymes. We tested a twofold hypothesis: (1) does oxidative stress (OxS) induced by sepsis acting alone or in concert with
augmented inflammatory processes contributes to sepsis-related vascular dysfunction, and, (2) whether ozone (O3) and l-canavanine (CAV) mitigate the negative impact of the aforementioned phenomena. We investigated the relative impact of treatment
with CAV and/or O3 on vascular OxS associated vascular functional changes in septicemic rats. For this study, 60 male Sprague–Dawley rats were
used and divided into six experimental groups (n = 10): control group (C), sham-operated (Sham), septicemic rats (S), S rats treated with CAV (100 mg/kg. i.p; S + CAV), S
rats treated with O3 (1.2 mg/kg, i.p.; S + O3) and S rats treated with both O3 and CAV (S + O3 + CAV). After 22 h, the mean arterial blood pressure (MAP), the aortic ring vascular reactivity to phenylephrine, abdominal
aortic blood flow (AABF), serum tumor necrosis factor-α (TNF-α) and plasma nitrite/nitrate (NOx) concentration were measured.
In addition, hepatic antioxidant enzyme activities sodium dismutase (SOD) and glutathione peroxidase (GSH-Px) were estimated.
Septicemia caused significant elevation of serum TNF-α (p < 0.001) and plasma NOx (p < 0.001) and significant (p < 0.001) reduction of AABF (p < 0.001), aortic vascular response to phenylephrine (p < 0.001), MAP (p < 0.001) and hepatic SOD and GSH-Px activity (p < 0.001) compared with the C group, while treatment with O3 and/or CAV induced significant amelioration of all those increases. Abnormalities were attenuated to a similar extent with
treatment with both O3 and CAV. These results suggested that concomitant administration of O3 and CAV alleviated the compromised vascular reactivity in septicemic conditions and prevent its progression into septic shock
compared with each alone. 相似文献
7.
The protective effect of taurine pretreatment on carbon tetrachloride-induced hepatic damage--a light and electron microscopic study 总被引:1,自引:0,他引:1
Summary. The results regarding taurine pretreatment on CCl4-induced hepatic injury are controversial. To assess the therapeutic efficacy of taurine on rat liver injury, hepatic malondialdehyde,
glutathione, and hydroxyproline levels together with morphologic alterations in the liver following CCl4 administration were investigated. The rats were divided into three groups. Taurine-treated animals received 15 ml/kg/day
of a 5% taurine solution by a gastric tube for 5 days before administering CCl4 (2 ml/kg, intraperitoneally, in a single dose). CCl4-treated rats received the same amount of saline solution. Control animals received no treatment. The increase of hepatic
malondialdehyde formation in the CCl4-treated group was partially prevented by taurine pretreatment, but taurine had no significant effect on the glutathione and
hydroxyproline content in the CCl4-treated rats. Taurine pretreatment induced a marked beneficial effect regarding the prevention of hepatocellular necrosis
and atrophy as demonstrated morphologically. In conclusion, these results suggest that taurine pretreatment might not significantly
change the biochemical parameters, but prevents the morphologic damage caused by CCl4 in the early stages.
Received March 17, 2001 Accepted July 18, 2001 相似文献
8.
Souvik Roy Sudheer Kumar Dontamalla Anil Kumar Mondru Santanu Sannigrahi Prabhakar Reddy Veerareddy 《Biological trace element research》2011,139(1):55-71
To investigate whether sodium selenate treatment would impact on the onset of diabetic nephropathy, we examined blood glucose,
serum biochemical components, and interrelationship between oxidative stress, TGF-β1, and apoptosis in streptozotocin (STZ)
induced diabetic rats. Sixty male Wistar rats were divided into six groups. Group I (n = 10), normal control; Group II (n = 10), diabetic control; Group III (n = 10), sodium selenate (16 μmoles/kg) + diabetic; Group IV (n = 10), sodium selenate (32 μmoles/kg) + diabetic; Group V (n = 10), sodium selenate (16 μmoles/kg) control; and Group VI (n = 10), sodium selenate (32 μmoles/kg) control. Sodium selenate was administered via orogastric route for 10 weeks. In the
diabetic group, diabetes was induced by single intraperitoneal injection of STZ (50 mg/kg). The levels of blood glucose were
estimated and total cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides, creatinine, urea, and albumin
were detected in serum. Antioxidant status was examined by measuring the superoxide dismutase (SOD), catalase, glutathione,
and lipid peroxidation in kidney tissues. Histopathological studies were performed in the kidney tissue sections. The expression
of TGF-β1 was estimated by the immunohistochemical analysis in kidneys. Apoptotic study in kidney was performed using the
TdT-mediated dUTP nick end labeling technique. It was observed that blood glucose, serum, total cholesterol, HDL cholesterol,
triglycerides, creatinine, urea, and albumin were significantly higher in diabetic control groups. Diabetic + sodium selenate
(16 and 32 μmoles/kg) significantly reduced blood glucose, serum, total cholesterol, HDL cholesterol, triglycerides, creatinine,
urea, and albumin levels. Selenium-treated groups significantly increased antioxidant enzyme activities (SOD, catalase, and
glutathione) in kidneys of diabetic rats. All enzyme activities of selenium control groups did not differ compared with the
normal control. Sodium selenate reduces significantly lipid peroxidation in diabetic rats. Cellular architecture of the diabetic
rats was altered whereas sodium selenate administration rectifies the degenerative changes of the kidney. Profound immunopositivity
of TGF-β1 was observed in the glomerular and tubulointerstitial cells of diabetic rat kidney. Immunopositivity of TGF-β1 was
significantly reduced in both low and high dose of sodium-selenate-treated rats (P < 0.05, P < 0.01). High numbers of apoptotic cells were observed in diabetic rats whereas sodium selenate in both doses significantly
reduces the incidence of apoptosis (P < 0.05, P < 0.01). We conclude herein that sodium selenate has the potential to play a significant role in limiting the renal impairment
by altering the apoptosis and TGF-β1 in experimental diabetic rats. 相似文献
9.
Mohamed Ali Medali Boujbiha Khaled Hamden Fadhel Guermazi Ali Bouslama Asma Omezzine Abdelfattah El Feki 《Biological trace element research》2011,142(3):598-610
Mercuric chloride (HgCl2) has been shown to affect the male reproductive organs, and oxidative stress has been linked with hypospermatogenesis and
with male infertility. However, the specific mode of impairment of spermatogenesis during HgCl2 exposure has not yet been clarified fully. Because of the involvement of 17β-estradiol (E2) in the male reproductive tract
and its putative role on spermatogenesis, the present study aimed to investigate the possibility that HgCl2-induced oxidative stress-mediated modulation of the E2 level exerts adverse effects on testicular steroidogenic and gametogenic
activities. HgCl2 treatment at 50 and 100 ppm for 90 days by continuous oral administration in the drink water resulted in significant dose-dependent
fashion decrease in serum and testicular E2 levels and an increase in testicular testosterone levels in dose-dependent manner, without statistical alteration in serum
testosterone level among HgCl2 exposed groups compared to the control. Cauda epididymal sperm count and motility were decreased significantly (p < 0.01), in a dose-dependent manner, in the HgCl2-treated groups, and qualitative examination revealed inhibition of spermatogenesis and the preferential loss of maturing
and elongated spermatids. The seminiferous tubules were dilated in treated animals. When compared to the control, increase
in lipid peroxidation due to toxic effects of HgCl2 was accompanied by significant reduction (p < 0.01) in antioxidant enzymes activities, superoxide dismutase, catalase, and glutathione peroxidase of testes, implicating
the presence of oxidative tissue damage. Furthermore, these tissue injuries caused functional impairment as evidenced with
testicular elevated activity of lactate dehydrogenase. Unless oxidative stress can lead to cancer development, testis’ tumor
markers as beta human chorionic gonadotropin and alpha-fetoprotein levels have shown no significant differences in the HgCl2-exposed group compared with respect to the control. Large quantities of metal accumulated in the testis tissue are in agreement
with the testis-activity failure verified in this tissue. These findings suggest that a decrease in E2 level after mercury
exposure may render testis more susceptible to oxidative damage leading to its functional inactivation, thus providing new
dimension to mechanisms underlying heavy metal-induced male infertility. 相似文献
10.
Arsenic (As) toxicity through induction of oxidative stress is a well-known mechanism of organ toxicity. To address this problem,
buffalo epiphyseal proteins (BEP, at 100 μg/kg BW, i.p. for 28 days) were administered intraperitoneally to female Wistar
rats exposed to As (100 ppm sodium arsenite via drinking water for 28 days). Arsenic exposure resulted in marked elevation
in lipid peroxidation in brain, cardiac, and hepatic tissues, whereas significant (p < 0.05) adverse change in catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase, and reduced glutathione
level were observed in cardiac, hepatic, and brain tissues of As-administered animals. BEP significantly (p < 0.05) counteracted all the adverse changes in antioxidant defense system brought about by As administration. Based on these
results, we consider BEP as a potent antioxidant to be used for protection from arsenic-induced oxidative stress related damage
of vital organs. 相似文献
11.
Maja Lazarus Tatjana Orct Jasna Aladrović Blanka Beer Ljubić Jasna Jurasović Maja Blanuša 《Biological trace element research》2011,142(3):611-622
Since there are no data about the protective role of selenium (Se) against cadmium (Cd)-induced oxidative damage in early
life, we studied the effect of Se supplementation on antioxidative enzyme activity and lipid peroxidation (through thiobarbituric
acid reactive substances; TBARS) in suckling Wistar rats exposed to Cd. Treated animals received either Se alone for 9 days
(8 μmol, i.e., 0.6 mg Se as Na2SeO3 kg−1 b.w., daily, orally; Se group), Cd alone for 5 days (8 μmol, i.e., 0.9 mg Cd as CdCl2 kg−1 b.w., daily, orally; Cd group), or pre-treatment with Se for 4 days and then co-treatment with Cd for the following 5 days
(Se + Cd group). Our results showed that selenium supplementation, with and without Cd, increased SOD activity in the brain
and kidney, but not in the liver and GSH-Px activity across all tissues compared to control rats receiving distilled water.
Relative to the Cd group, Se + Cd group had higher kidney and brain SOD and GSH-Px activity (but not the liver), while in
the liver caused increased and in the brain decreased TBARS level. These results suggest that Se stimulates antioxidative
enzymes in immature kidney and brain of Cd-exposed rats and could protect against oxidative damage. 相似文献
12.
Kun Yan Wei Chen Guoyou Zhang Sheng Xu Zhouli Liu Xingyuan He Lanlan Wang 《Acta Physiologiae Plantarum》2010,32(2):375-385
Using open top chambers, the effects of elevated O3 (80 nmol mol−1) and elevated CO2 (700 μmol mol−1), alone and in combination, were studied on young trees of Quercus mongolica. The results showed that elevated O3 increased malondialdehyde content and decreased photosynthetic rate after 45 days of exposure, and prolonged exposure (105 days)
induced significant increase in electrolyte leakage and reduction of chlorophyll content. All these changes were alleviated
by elevated CO2, indicating that oxidative stress on cell membrane and photosynthesis was ameliorated. After 45 days of exposure, elevated
O3 stimulated activities of superoxide dismutase (SOD, EC 1.15.1.1) and ascorbate peroxidase (APX, EC 1.11.1.11), but the stimulation
was dampened under elevated CO2 exposure. Furthermore, ascorbate (AsA) and total phenolics contents were not higher in the combined gas treatment than those
in elevated O3 treatment. It indicates that the protective effect of elevated CO2 against O3 stress was achieved hardly by enhancing ROS scavenging ability after 45 days of exposure. After 105 days of exposure, elevated
O3 significantly decreased activities of SOD, catalase (CAT, EC 1.11.1.6) and APX and AsA content. Elevated CO2 suppressed the O3-induced decrease, which could ameliorate the oxidative stress in some extent. In addition, elevated CO2 increased total phenolics content in the leaves both under ambient O3 and elevated O3 exposure, which might contribute to the protection against O3-induced oxidative stress as well. 相似文献
13.
Kum Suk Kang In Deok Kim Ryun Hee Kwon Bae Jin Ha 《Biotechnology and Bioprocess Engineering》2008,13(2):168-173
This study was performed to elucidate the effects of Undaria pinnatifida fucoidan extract (UPFE) in preventing CCl4-induced oxidative stress. UPFE (100 mg/kg) was intraperitoneally administered to rats for 14 days. On day 15, CCl4 dissolved in olive oil (50% CCl4) was injected 12 h before they were anesthetized and dissected. To measure UPFE-mediated antioxidation, we examined the levels
of glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), alkaline phosphatase (ALP), and lactate
dehydrogenase (LDH) in serum, as well as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione
peroxidase (GPx) in liver homogenates. CCl4 treatment markedly increased the levels of GOT, GPT, ALP, LDH, and MDA and significantly decreased levels of SOD, CAT, and
GPx. UPFE pretreatment decreased levels of GOT, GPT, ALP, LDH, and MDA, by 62.8, 68.5, 41.9, 72.7, and 122%, respectively
and increased those of SOD, CAT, and GPx by 111.1, 15.9, and 52.6%, respectively. These results showed that UPFE has antioxidant
effects against CCl4-induced oxidative stress. 相似文献
14.
M. E. Shaker M. E. Houssen E. M. Abo-Hashem T. M. Ibrahim 《Journal of physiology and biochemistry》2009,65(3):225-233
This study aimed to investigate whether treatments with vitamin E, L-carnitine and melatonin can protect against CCl4 and diabetes-induced hepatic oxidative stress. Hepatic oxidative stress was performed in rats through 50% v/v carbon tetrachloride
(CCl4) (1 ml/kg/3days, i.p.), and through diabetes mellitus induced by streptozotocin (STZ) (40 mg/kg, i.p.). Vitamin E (100 mg/kg/day,
i.p), L-carnitine (300 mg/kg/day, i.p.) and melatonin (10 mg/kg/day, i.p.) were injected for a period of 6 weeks. Thereafter,
changes in serum glucose level, liver function tests, hepatic malondialdehyde (MDA) content, hepatic reduced glutathione (GSH)
content, hepatic superoxide dismutase (SOD) activity, and serum total antioxidant capacity (TAC) level were evaluated. In
CCl4-induced liver fibrosis, the efficacy order was melatonin > L-carnitine > vitamin E, while in STZ-induced diabetes, the efficacy
order was vitamin E ≥ melatonin > L-carnitine. In conclusion, these data indicate that low dose of melatonin is more effective
than high doses of vitamin E and L-carnitine in reducing hepatic oxidative stress induced by CCl4 and diabetes. Moreover, the potent effect of vitamin E in ameliorating diabetes can be linked not only to the antioxidant
actions, but also to the superior effect in reducing diabetes-induced hyperglycaemia. Meanwhile, potency of L-carnitine was
nearly the same in CCl4 and diabetes-induced liver damage. 相似文献
15.
Ayhan Dogukan Nurhan Sahin Mehmet Tuzcu Vijaya Juturu Cemal Orhan Muhittin Onderci James Komorowski Kazim Sahin 《Biological trace element research》2009,131(2):124-132
The present study was conducted to investigate the effects of chromium histidinate (CrHis) against experimentally induced
type II diabetes and on chromium (Cr), zinc (Zn), selenium (Se), manganese (Mn), iron (Fe), and copper (Cu) in serum, liver,
and kidney of diabetic rats. The male Wistar rats (n = 60, 8 weeks old) were divided into four groups. Group I received a standard diet (12% of calories as fat); group II were
fed standard diet and received CrHis (110 mcg CrHis/kg body weight per day); group III received a high-fat diet (HFD; 40% of calories as fat) for 2 weeks and then
were injected with streptozotocin (STZ) on day 14 (STZ, 40 mg/kg i.p.; HFD/STZ); group IV were treated as group III (HFD/STZ)
but supplemented with 110 mcg CrHis/kg body weight per day. The mineral concentrations in the serum and tissue were determined
by atomic absorption spectrometry. Compared to the HFD/STZ group, CrHis significantly increased body weight and reduced blood
glucose in diabetic rats (p < 0.001). Concentrations of Cr, Zn, Se, and Mn in serum, liver, and kidney of the diabetic rats were significantly lower
than in the control rats (p < 0.0001). In contrast, higher Fe and Cu levels were found in serum and tissues from diabetic versus the non-diabetic rats
(p < 0.001). Chromium histidinate supplementation increased serum, liver, and kidney concentrations of Cr and Zn both in diabetic
and non-diabetic rats (p < 0.001). Chromium supplementation increased Mn and Se levels in diabetic rats (p < 0.001); however, it decreased Cu levels in STZ-treated group (p < 0.001). Chromium histidinate supplementation did not affect Fe levels in both groups (p > 0.05). The results of the present study conclude that supplementing Cr to the diet of diabetic rats influences serum and
tissue Cr, Zn, Se, Mn, and Cu concentrations. 相似文献
16.
The present study investigates the antioxidative effects of vitamin E and curcumin against l-thyroxine (T4)-induced oxidative stress in renal cortex of adult male rats. Rats were made hyperthyroid by administration of l-thyroxine (0.0012%) in their drinking water for 30 days. Vitamin E (200 mg/kg body weight/day) and curcumin (30 mg/kg body
weight/day) were supplemented singly or in combination orally for 30 days along with l-thyroxine treatment. The elevated level of oxidative stress parameters (lipid peroxidation and protein carbonylation) and
decline level of small antioxidant molecules (reduced glutathione and ascorbic acid) in renal cortex of T4-treated rats were restored back by supplementation of vitamin E or/and curcumin. Increased superoxide dismutase and catalase
activities in kidney cortex of T4-treated rats were ameliorated in response to vitamin E or/and curcumin treatment. The elevated translated product of Cu/Zn-SOD,
Mn-SOD and catalase in T4-treated rats were differentially reduced by the administration of vitamin E and curcumin independently or in combination.
Cu/Zn-SOD expression was ameliorated by both vitamin E and curcumin independently or in combination, whereas Mn-SOD expression
was ameliorated by the supplementation of vitamin E or curcumin independently. However, the expression of catalase was alleviated
by only supplementation of vitamin E to T4-treated rats. The results suggest that both vitamin E and curcumin may play an important role in protecting T4-induced oxidative stress in rat renal cortex by differentially modulating the activities of antioxidant enzymes and oxidative
stress parameters. 相似文献
17.
Alireza Nakhaee Mohammad Bokaeian Azim Akbarzadeh Mohammad Hashemi 《Biological trace element research》2010,136(2):221-231
High blood glucose concentration in diabetes induces free radical production and, thus, causes oxidative stress. Damage of
cellular structures by free radicals play an important role in development of diabetic complications. In this study, we evaluated
effects of sodium tungstate on enzymatic and nonenzymatic markers of oxidative stress in brain of streptozotocin (STZ)-induced
diabetic rats. Rats were divided into four groups (ten rats in each group): untreated control, sodium tungstate-treated control,
untreated diabetic, and sodium tungstate-treated diabetic. Diabetes was induced with an intraperitoneal STZ injection (65 mg/kg
body weight), and sodium tungstate with concentration of 2 g/L was added to drinking water of treated animals for 4 weeks.
Diabetes caused a significant increase in the brain thiobarbituric acid reactive substances (P < 0.01) and protein carbonyl levels (P < 0.01) and a decrease in ferric reducing antioxidant power (P < 0.01). Moreover, diabetic rats presented a reduction in brain glucose-6-phosphate dehydrogenase (21%), superoxide dismutase
(41%), glutathione peroxidase (19%), and glutathione reductase (36%) activities. Sodium tungstate reduced the hyperglycemia
and restored the diabetes-induced changes in all mentioned markers of oxidative stress. However, catalase activity was not
significantly affected by diabetes (P = 0.4), while sodium tungstate caused a significant increase in enzyme activity of treated animals (P < 0.05). Data of present study indicated that sodium tungstate can ameliorate brain oxidative stress in STZ-induced diabetic
rats, probably by reducing of the high glucose-induced oxidative stress and/or increasing of the antioxidant defense mechanisms. 相似文献
18.
Abdulkerim Kasim Baltaci Hakki Gokbel Rasim Mogulkoc Nilsel Okudan Kagan Ucok Ihsan Halifeoglu 《Biological trace element research》2010,134(1):79-83
The objective of the present study was to determine the effects of exercise and zinc deficiency on some elements in rats.
Forty adult male Sprague–Dawley species male rats were allocated to four groups as follows: Group 1: control, Group 2: zinc-deficient,
Group 3: exercise in which exercise group fed with a normal diet, Group 4: zinc-deficient exercise, exercise group fed by
a zinc-deficient diet for 15 days. After the procedure ended, rats in groups 3 and 4 were exercised on the treadmill for 60 min
at a speed of 6 m/min until the exhaustion. The rats were decapitated 48 h after exercise together with their controls, and
blood samples were collected to determine copper (Cu), iron (Fe), magnesium (Mg), calcium (Ca), and phosphorus (P) levels.
The highest Cu and Fe values in the serum were obtained in group 2 (p < 0.01). The levels of these elements in group 4 were lower than those in group 2 and higher than the levels in groups 1
and 3 (p < 0.01). Serum Mg levels did not differ significantly between groups. Group 4 had the lowest serum Ca and P levels (p < 0.01). These same parameters in Group 2 were higher than those in group 4 but significantly lower than those in groups
1 and 3 (p < 0.01). There was no significant difference between Ca and P levels of groups 1 and 3. The results of the study indicate
that zinc deficiency adversely affects copper, iron, calcium, and phosphorus mechanisms and that these adverse effects much
more marked after an effort exercise. 相似文献
19.
Ethel Antunes Wilhelm Cristiano Ricardo Jesse Marina Prigol Diego Alves Ricardo Frederico Schumacher Cristina Wayne Nogueira 《Cell biology and toxicology》2010,26(6):569-577
The aim of this study was to investigate the protective effect of 3-alkynyl selenophene (3-ASP) on acute liver injury induced
by carbon tetrachloride (CCl4) and 2-nitropropane (2-NP) in rats. On the first day of treatment, the animals received 3-ASP (25 mg/kg, p.o.). On the second
day, the rats received CCl4 (1 mg/kg, i.p.) or 2-NP (100 mg/kg, p.o.). Twenty-four hours after CCl4 or 2-NP administration, the animals were euthanized, and their plasma and liver were removed for biochemical and histological
analyses. The histological analysis revealed extensive injury in the liver of CCl4-exposed and 2-NP-exposed rats, which was attenuated by 3-ASP. 3-ASP significantly attenuated (1) the increase in plasmatic
aspartate and alanine aminotransferase activities and lipid peroxidation levels induced by CCl4 and 2-NP; (2) the inhibition of δ-aminolevulinic dehydratase activity caused by 2-NP; and (3) the decrease in ascorbic acid
(AA) levels and catalase (CAT) activity caused by CCl4. AA levels and CAT activity remained unaltered in the liver of rats exposed to 2-NP. The protective effect of 3-ASP on acute
liver injury induced by CCl4 and 2-NP in rats was demonstrated. 相似文献
20.
Mervi T. Hyvönen Riitta Sinervirta Nikolay Grigorenko Alex R. Khomutov Jouko Vepsäläinen Tuomo A. Keinänen Leena Alhonen 《Amino acids》2010,38(2):575-581
The role of polyamines in carbon tetrachloride (CCl4)-induced organ injury was studied in syngenic rats and transgenic rats with activated polyamine catabolism. In syngenic rats,
administration of CCl4 resulted in the induction of hepatic spermidine/spermine N
1-acetyltransferase (SSAT), accumulation of putrescine, reduction in spermine level and appearance of moderate hepatic injury
within 24 h. Upon treatment with CCl4, transgenic rats overexpressing SSAT displayed induction of both hepatic and pancreatic SSAT, with subsequent accumulation
of putrescine and decrease of both spermidine and spermine pools. Administration of CCl4 in SSAT transgenic rats induced not only massive hepatic injury, but also severe acute necrotizing pancreatitis. Pretreatment
of the animals with catabolically stable functional polyamine mimetic, α-methylspermidine (MeSpd) prevented pancreatic and
hepatic injury in SSAT rats and markedly reduced liver damage in syngenic animals. As assessed by immunostaining of proliferating
cell nuclear antigen, MeSpd increased the amount of regenerating hepatocytes in both genotypes. These results show that CCl4 induces hepatic and pancreatic polyamine catabolism, and the extent of organ damage correlates with the degree of polyamine
depletion. Furthermore, MeSpd protects against CCl4-induced hepatic and pancreatic damage and promotes tissue regeneration. 相似文献