共查询到20条相似文献,搜索用时 9 毫秒
1.
The present study was carried to evaluate the protective effects of melatonin alone and vitamin E with selenium combination
against high dose cadmium-induced oxidative stress in rats. The control group received subcutanous physiological saline. The
first study group administered cadmium chloride (CdCl2) by subcutaneous injection of dose of 1 mg/kg. The second study group administered cadmium plus vitamin E with selenium (1 mg/kg
sodium selenite with 60 mg/kg vitamin E); the third study group administered cadmium plus 10 mg/kg melatonin (MLT); the fourth
study group administered CdCl2 plus a combination of melatonin in addition to vitamin E and selenium for a month. Determination levels of plasma malondialdehyde
(MDA), glutathione peroxidase (GSH-Px), blood superoxide dismutase (SOD), creatinine alanine transaminase (ALT), aspartate
aminotransferase (AST), alkaline phosphatase (ALP), blood urea nitrogen (BUN), and urea were measured in serum. In only CdCl2 administered group, the MDA, creatinine, ALT, AST, ALP, and urea levels in the serum were significantly higher than the control
group (p < 0.05). Whereas in all other groups, this values were significantly lower than the only CdCl2 administered group (p < 0.05). Erythrocytes GSH-Px, serum SOD activities of only CdCl2 received group were significantly lower than the control group (p < 0.05). In conclusion, vitamin E + Se, melatonin and vitamin E, and Se, in addition to MLT combinations, had protective
effects against high dose cadmium-induced oxidative damage. 相似文献
2.
The aim of this study was to investigate the effects of vitamin E (alpha-tocopherol) and 17β-estradiol (E(2)) supplementation on malondialdehyde (MDA), glutathione (GSH), vitamin A, beta carotene, selenium-dependent glutathione peroxidase (GSH-Px), zinc-dependent superoxide dismutase (SOD), and copper/zinc-dependent catalase (CAT) values in the kidney of ovariectomized (OVX) diabetic rats. Forty-two female rats were randomly divided into seven equal groups as follows: group I, control; group II, OVX; group III, OVX+E(2); group IV, OVX+E(2)+alpha-tocopherol; group V, OVX+diabetic; group VI, OVX+diabetic+E(2); and group VII, OVX+diabetic+E(2)+alpha-tocopherol. E(2) (40?μg?kg(-1)/day) and alpha-tocopherol (100?μg?kg(-1)/day) were given. Bilateral ovariectomy was performed in all groups except group I. After 4?weeks, antioxidant and MDA levels in the kidney for all groups were analyzed. GSH-Px, CAT, SOD, GSH levels, vitamin A, and beta carotene levels were decreased in OVX group compared to those in the control group but MDA level was elevated via ovariectomy. However, E(2) and E(2)+alpha-tocopherol supplementations in OVX group was associated with an increase in the GSH-Px, GSH, CAT and Zn-SOD values, vitamin A, and beta carotene levels but a decrease in MDA levels in kidney. The MDA levels in the kidney of diabetic OVX rats were found higher than those in the control and OVX groups. However, GSH, GSH-Px, CAT, SOD, vitamin A, and beta carotene levels in kidney were lower in OVX diabetic rats. On the other hand, E(2) and E(2)+alpha-tocopherol supplementations to OVX diabetic rats have caused an increase in GSH-Px, CAT and SOD, GSH, vitamin A, and beta carotene levels but a decrease in MDA levels. In conclusion, the E(2) and E(2)+alpha-tocopherol supplementations to diabetic OVX and OVX rats may strengthen the antioxidant defense system by reducing lipid peroxidation, and therefore they may play a role in preventing renal disorders. 相似文献
3.
We investigated the effect of 17β-estradiol (E2) alone and separately vitamin E treatment on trace element status of rats following an ovariectomic operation. Forty rats
were equally divided into four groups: Group 1, control, non-ovariectomized rats; Group 2, (OVX) rats, ovariectomized under
general anesthesia; Group 3, (OVX+E2) rats, the group received a 40 μg kg−1 subcutan dose of E2 per day after ovariectomy; and Group 4, (OVX + E2 + vitamin E) rats, received the same E2 treatment, but with an additional 100 mg kg−1 intraperitoneal dose of vitamin E per day after ovariectomy. At the end of the 30-day experiment, the rats were sacrificed
and their blood was collected for the measurement of zinc, copper, iron, phosphorus, selenium, magnesium, calcium, manganese,
and chromium; copper–zinc superoxide dismutase (SOD); manganese-superoxide dismutase (Mn-SOD); glutathione peroxidase (Se-GSH-Px);
and catalase (CAT). The levels of zinc, copper, iron, phosphorus, selenium, calcium, chromium, and manganese and activities
of SOD, Mn-SOD, Se-GSH-Px, and CAT were lower in the OVX than in the control group, but magnesium level was unaffected. However,
zinc, copper, iron, phosphorus, selenium, calcium, chromium, and manganese levels and SOD, Mn-SOD, Se-GSH-Px, and CAT activities
were higher under separate E2 and E2 + vitamin E treatments. The level of magnesium in the treated-OVX groups was not different than in the OVX group. In conclusion,
E2 treatment has an ameliorating effect on the trace element status in OVX, and this effect may be enhanced with the addition
of vitamin E. 相似文献
4.
Katerina Apostolopoulou Dimitris Konstantinou Rodoula Alataki Ioannis Papapostolou Dimitrios Zisimopoulos Electra Kalaitzopoulou Vasiliki Bravou Ioannis Lilis Fevronia Angelatou Helen Papadaki Christos D. Georgiou Elisabeth Chroni 《Neurochemical research》2018,43(3):650-658
An ischemia/reperfusion injury of rat’s sciatic nerve was experimentally developed. In this model, we measured the in vivo production of superoxide radical, as a marker of oxidative stress and the occludin expression as an indicator of blood-nerve barrier function and we examined potential protective innervations against these abnormalities. Right sciatic nerves of the animals underwent 3 h of ischemia followed by 7 days of reperfusion and were divided into three groups: ischemic, pretreated with vitamin C in conjunction with vitamin E and treated with tissue plasminogen activator. Compared to measurements from left sciatic nerves used as sham, the ischemic group showed significantly increased superoxide radical and reduced expression of occludin in western blot and immunohistochemistry. No such differences were detected between sham and nerves in the vitamin or tissue plasminogen activator groups. It is suggested that the experimental ischemia/reperfusion model was suitable for studying the relationship between oxidative state and blood-nerve barrier. The reversion of abnormalities by the applied neuroprotective agents might prove to be a clinically important finding in view of the implication of vascular supply derangement in various neuropathies in humans. 相似文献
5.
The effect of amyloid (A), the major constituent of the Alzheimer's (AD) brain on lipid metabolism was investigated in cultured nerve cells and in a fetal rat brain model. Differentiated (NGF) and undifferentiated PC12 cells or primary cerebral cell cultures were incubated with [14C]acetate in the absence or presence of A1–40. Incorporation of label into lipid species was determined after lipid extraction and TLC separation. Phosphatidylcholine (PC) and phosphatidylserine (PS) synthesis was increased by A1–40, in a dose dependent manner, an effect which was more pronounced in differentiated PC12 cells. A significant proportion of radioactivity (5–6%) was released into the medium with a radioactivity distribution similar to that of the cellular lipids. Cholesterol and PC were the highest labeled medium lipids. Increasing A1–40 concentration up to 0.1 g/ml in cerebral cells but not in PC12 cells, caused a relative increase (1.5 fold) in release of PS, while that of PE decreased. Stimulation of PS release may possibly be associated with apoptotic cell death. A1–40 peptide (5 g) was administered intraperitonealy into rat fetuses (18 days gestation) along with [14C]acetate (2Ci/fetus). After 24 h, the maternal-fetal blood supply was occluded for 20 min (ischemia) followed by 15 min reperfusion. Fetuses were killed and liver and brain tissue subjected to lipid extraction and radioactivity determination after TLC. A1–40 peptide increased synthesis of different classes of lipids up to 20–40% in brain tissue compared to controls. Labeling of liver lipids was decreased by A1–40 by 20–30%. A general decrease in synthesis of lipids was observed after ischemia/reperfusion. Our data suggest that A1–40 peptide regulates normal lipid biosynthesis but under ischemia it compromises it. The latter finding may confirm the oxidative stress etiology in AD and suggests that A1–40 modulation of lipid metabolism may have Alzheimer's pathological relevance, particularly at high peptide concentrations. 相似文献
6.
Selenium–Mercury Interactions in Man and Animals 总被引:4,自引:0,他引:4
Selenium–mercury interactions were most extensively studied in relation to alleviation of Hg toxicity by added selenium. This
presentation considers the influence of mercury on endogenous selenium, on its tissue and cellular “status” after lifelong
or acute exposure to mercury vapor (Hgo). Discussed are data obtained from (1) humans living near or working in a mercury mine, and (2) rats experimentally exposed
in the mine. Mercury vapor is unique—or similar to methylmercury—because of its ability to penetrate cell membranes and so
invade all cells, where it is oxidized in the biologically active form (Hg++) by catalase. Such in situ-generated ions can react with endogenously generated highly reactive Se metabolites, like HSe−,
and render a part of the selenium unavailable for selenoprotein synthesis. Data on human populations indicate that in moderate
Hg exposure combined with an adequate selenium supply through diet, Se bioavailability can be preserved. On the other hand,
the results of an acute exposure study emphasize the dual role of selenium in mercury detoxification. Besides the well-known
Se coaccumulation through formation of nontoxic Hg–Se complexes, we observed noticeable Se (co)excretion, at least at the
beginning of exposure. The higher Hg accumulation rate in the group of animals with lower basal selenium levels can also point
to selenium involvement in mercury excretion. In such conditions there is a higher probability for decreased selenoprotein
levels (synthesis) in some tissues or organs, depending on the synthesis hierarchy. 相似文献
7.
Shirin Hasan Nayeem Bilal Shoa Naqvi Ghulam Md Ashraf Nida Suhail Sadhana Sharma Naheed Banu 《Biological trace element research》2011,142(3):589-597
Brain is a target of stress along with the immune, metabolic, and cardiovascular systems of the body. In the present work,
the preventive roles of a multivitamin–mineral supplement and vitamins (E + C) in chronic unpredictable stress (CUS)-induced
oxidative damage were studied in the brain and heart of Swiss albino mice. Thirty-two mice were randomized to one of the following
groups: control + vehicle, CUS + vehicle, CUS + multivitamin–mineral, and CUS + vitamins (E + C). CUS was applied for 4 weeks,
and multivitamin–mineral and vitamins (E + C) were administered orally for the same period. CUS led to a negative impact on
all the biochemical parameters analyzed. Elevation in malondialdehyde and reduction in glutathione levels were found. The
activities of superoxide dismutase, catalase, glutathione S-transferase, and glutathione reductase were decreased. Treatment with multivitamin–mineral and vitamins (E + C) brought these
parameters to near normal levels. Multivitamin–mineral was found more restitutive than combined vitamins (E + C) doses. The
present study hypothesizes that supplementation with a multivitamin–mineral may prove more effective than vitamin treatment
alone in the alleviation of oxidative damage in brain and heart during periods of chronic stress. 相似文献
8.
9.
The aim of our study is to evaluate the possible biological effects of whole-body 1800 MHz GSM-like radiofrequency (RF) radiation
exposure on liver oxidative DNA damage and lipid peroxidation levels in nonpregnant, pregnant New Zealand White rabbits, and
in their newly borns. Eighteen nonpregnant and pregnant rabbits were used and randomly divided into four groups which were
composed of nine rabbits: (i) Group I (nonpregnant control), (ii) Group II (nonpregnant-RF exposed), (iii) Group III (pregnant
control), (iv) Group IV (pregnant-RF exposed). Newborns of the pregnant rabbits were also divided into two groups: (v) Group
V (newborns of Group III) and (vi) Group VI (newborns of Group III). 1800 MHz GSM-like RF radiation whole-body exposure (15 min/day
for a week) was applied to Group II and Group IV. No significant differences were found in liver 8 OHdG/106 dG levels of exposure groups (Group II and Group IV) compared to controls (Group I and Group III). However, in Group II and
Group IV malondialdehyde (MDA) and ferrous oxidation in xylenol orange (FOX) levels were increased compared to Group I (P < 0.05, Mann–Whitney). No significant differences were found in liver tissue of 8 OHdG/106 dG and MDA levels between Group VI and Group V (P > 0.05, Mann–Whitney) while liver FOX levels were found significantly increased in Group VI with respect to Group V (P < 0.05, Mann–Whitney). Consequently, the whole-body 1800 MHz GSM-like RF radiation exposure may lead to oxidative destruction
as being indicators of subsequent reactions that occur to form oxygen toxicity in tissues. 相似文献
10.
Atilla Semercioz Abdulkerim Kasim Baltaci Rasim Mogulkoc Mustafa Cihat Avunduk 《Biochemical genetics》2017,55(5-6):395-409
The present study was aimed to examine the effects of 3-week zinc and melatonin administration on testicular tissue injury and serum Inhibin-B levels caused by unilateral testicular torsion–detorsion in rats. The study was performed on 60 Wistar Albino-type adult male rats. The animals were allocated to 6 groups in equal numbers. 1. Control; 2. Sham; 3. Ischemia–reperfusion; 4. Zinc + ischemia–reperfusion; 5. Melatonin + ischemia–reperfusion; 6. Zinc + melatonin + ischemia–reperfusion. Zinc and melatonin were administered before ischemia–reperfusion at doses of 5 and 3 mg/kg respectively, by intraperitoneal route for a period of 3 weeks. Testicular torsion–detorsion procedures consisted of ischemia for 1 h and then reperfusion for another hour of the left testis. Blood and testicular tissue samples were collected to analyze erythrocyte and tissue GSH and plasma and tissue MDA, Inhibin-B levels. The highest erythrocyte and testis GSH values were found in zinc, melatonin, and zinc + melatonin groups (p < 0.001). Torsion–detorsion group has significantly lower erythrocyte GSH levels and higher plasma MDA values (p < 0.001). Serum inhibin-B and spermatogenic activity levels in the torsion–detorsion group were also significantly lower than those in the other groups (p < 0.001). However, zinc-, melatonin-, and melatonin + zinc-supplemented groups have higher inhibin-B and spermatogenetic activity (p < 0.001). The results of the study show that zinc, melatonin, and melatonin + zinc administration partially restores the increased oxidative stress, as well as the reduced inhibin-B and spermatogenic activity levels in testes ischemia–reperfusion in rats. Suppressed inhibin-B levels in the testicular tissue may be a marker of oxidative stress. 相似文献
11.
Yao YF Pei FX Li XB Yang J Shen B Zhou ZK Li L Kang PD 《Biological trace element research》2012,146(2):199-206
The purpose of this study was to investigate the effects of supplemental selenium and selenium plus iodine on bone and growth
plate cartilage histology and serum biochemistic parameters in rats. Ninety-six Wistar rats were randomly divided into the
following four groups: group A, the rats fed with normal diet; group B, fed with diet from Kashin–Beck disease (KBD) endemic
area; group C, fed with diet from KBD endemic area supplemented with selenium; and group D, fed with diet from KBD endemic
area supplemented with selenium and iodine. After 4, 8, and 12 weeks, bone and cartilage samples were collected from the rats
and were examined for morphological changes in the tibial growth zone and for changes in the plate cartilage and metaphysic.
Compared to the rats fed with diet from the KBD endemic area, the rats fed with the supplemental selenium or selenium plus
iodine exhibited diminished necrosis of the chondrocytes in the growth plate. In the groups of rats receiving supplemental
selenium and selenium plus iodine, the bone volume/tissue volume ratio (BV/TV), the trabecular thickness (Tb.Th), and the
trabecular number were increased, while the trabecular separation was decreased. In the 12th week of the experiment, BV/TV
and Tb.Th were significantly increased in the selenium plus iodine group compared to the selenium group. It is concluded that
feeding the diet from the KBD endemic area caused necrosis of chondrocytes and dysfunctions of bone development similar to
the pathological changes that are seen in KBD. Selenium and iodine protected chondrocytes in growth plate and promoted the
formation of trabecular bone. The effects of selenium plus iodine on bone formation were more obvious than those of selenium
alone 相似文献
12.
M Boyko D Stepensky BF Gruenbaum SE Gruenbaum I Melamed S Ohayon M Glazer Y Shapira A Zlotnik 《Neurochemical research》2012,37(10):2198-2205
Traumatic brain injury (TBI) and stroke lead to elevated levels of glutamate in the brain that negatively affect the neurological outcomes in both animals and humans. Intravenous administration of glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT) enzymes can be used to lower the blood glutamate levels and to improve the neurological outcome following TBI and stroke. The objective of this study was to analyze the pharmacokinetics and to determine the glutamate-lowering effects of GOT and GPT enzymes in na?ve rats. We determined the time course of serum GOT, GPT, and glutamate levels following a single intravenous administration of two different doses of each one of the studied enzymes. Forty-six male rats were randomly assigned into one of 5 treatment groups: saline (control), human GOT at dose 0.03 and 0.06?mg/kg and porcine GPT at dose 0.6 and 1.2?mg/kg. Blood samples were collected at baseline, 5?min, and 2, 4, 8, 12, and 24?h after the drug injection and GOT, GPT and glutamate levels were determined. The pharmacokinetics of both GOT and GPT followed one-compartment model, and both enzymes exhibited substantial glutamate-lowering effects following intravenous administration. Analysis of the pharmacokinetic data indicated that both enzymes were distributed predominantly in the blood (central circulation) and did not permeate to the peripheral organs and tissues. Several-hour delay was present between the time course of the enzyme levels and the glutamate-lowering effects (leading to clock-wise hysteresis on concentration-effect curves), apparently due to the time that is required to affect the pool of serum glutamate. We conclude that the interaction between the systemically-administered enzymes (GOT and GPT) and the glutamate takes place in the central circulation. Thus, glutamate-lowering effects of GOT and GPT apparently lead to redistribution of the excess glutamate from the brain's extracellular fluid into the blood and can reduce secondary brain injury due to glutamate neurotoxicity. The outcomes of this study regarding the pharmacokinetic and pharmacodynamic properties of the GOT and GPT enzymes will be subsequently verified in clinical studies that can lead to design of effective neuroprotective treatment strategies in patients with traumatic brain diseases and stroke. 相似文献
13.
Sirmali M Uz E Sirmali R Kilbaş A Yilmaz HR Altuntaş I Naziroğlu M Delibaş N Vural H 《Biological trace element research》2007,118(1):43-52
The aim of this study was to investigate the protective effects of erdosteine and vitamins C and E (VCE) on the lungs after
performing hind limb ischemia–reperfusion (I/R) by assessing oxidative stress, plasma copper (Cu), and zinc (Zn) analysis.
The animals were divided randomly into four groups as nine rats each as follows: control, I/R, I/R plus erdosteine, and I/R
plus VCE combination. I/R period for 60 min was performed on the both hind limbs of all the rats in the groups of I/R, erdosteine
with I/R, VCE with I/R allowing 120 min of reperfusion. The animals received orally erdosteine one time in a day and 3 days
before I/R in the erdosteine group. In the VCE group, the animals VCE combination received one time in a day and 3 days before
I/R, although placebo was given to control and I/R group animals. Lung lipid peroxidation (malondialdehyde [MDA]) level, superoxide
dismutase (SOD), and catalase activities were increased, although lung glutathione (GSH) and plasma Zn levels decreased in
I/R group in lung tissue compared with the control group. Serum MDA level, creatine kinase, and lactate dehydrogenase activities
were increased in I/R group compared with the control. Lung MDA and plasma Zn levels and lung SOD activity were decreased
by erdosteine administration, whereas lung GSH levels after I/R increased. The plasma Zn levels and lung SOD activity were
decreased by VCE administration, although the plasma Cu and lung GSH levels increased after I/R. In conclusion, erdosteine
has an antioxidant role on the values in the rat model, and it has more protective affect than in VCE in attenuating I/R-induced
lung injury in rats. 相似文献
14.
Ying Han Hai-Jian Sun Peng Li Qing Gao Ye-bo Zhou Feng Zhang Xing-Ya Gao Guo-Qing Zhu 《PloS one》2012,7(11)
Background
Excessive sympathetic activity contributes to the pathogenesis and progression of hypertension. Enhanced cardiac sympathetic afferent reflex (CSAR) is involved in sympathetic activation. This study was designed to determine the roles of angiotensin (Ang)-(1–7) in paraventricular nucleus (PVN) in modulating sympathetic activity and CSAR and its signal pathway in renovascular hypertension.Methodology/Principal Findings
Renovascular hypertension was induced with two-kidney, one-clip method. Renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded in sinoaortic-denervated and cervical-vagotomized rats with anesthesia. CSAR was evaluated with the RSNA and MAP responses to epicardial application of capsaicin. PVN microinjection of Ang-(1–7) and cAMP analogue db-cAMP caused greater increases in RSNA and MAP, and enhancement in CSAR in hypertensive rats than in sham-operated rats, while Mas receptor antagonist A-779 produced opposite effects. There was no significant difference in the angiotensin-converting enzyme 2 (ACE2) activity and Ang-(1–7) level in the PVN between sham-operated rats and hypertensive rats, but the Mas receptor protein expression in the PVN was increased in hypertensive rats. The effects of Ang-(1–7) were abolished by A-779, adenylyl cyclase inhibitor SQ22536 or protein kinase A (PKA) inhibitor Rp-cAMP. SQ22536 or Rp-cAMP reduced RSNA and MAP in hypertensive rats, and attenuated the CSAR in both sham-operated and hypertensive rats.Conclusions
Ang-(1–7) in the PVN increases RSNA and MAP and enhances the CSAR, which is mediated by Mas receptors. Endogenous Ang-(1–7) and Mas receptors contribute to the enhanced sympathetic outflow and CSAR in renovascular hypertension. A cAMP-PKA pathway is involved in the effects of Ang-(1–7) in the PVN. 相似文献15.
16.
Seyede Zahra Ghaemi Sedighe Forouhari Mohammad Hossein Dabbaghmanesh Mehrab Sayadi Marzieh Bakhshayeshkaram Faride Vaziri Zohreh Tavana 《Biological trace element research》2013,152(2):174-179
Preeclampsia remains a leading cause of maternal and perinatal mortality and morbidity worldwide; however, its specific etiology still remains obscure. Some studies implicate poor maternal selenium status predisposing the mother to preeclampsia. This study was designed to determine changes in plasma selenium levels in women having preeclampsia as compared with those with normal pregnancy. In a nested case–control study, 650 normal primigravida in their first 24–28 weeks participated in the study. After 3 months of follow-up of all subjects, blood selenium levels were measured in 38 women presenting consecutively with preeclampsia and in 38 women having a normal pregnancy by atomic absorption spectrophotometry. Birth outcomes were recorded, such as gestational age at delivery, height, weight, birth head circumflex and 1-min Apgar score. Preeclampsia affects about 5.84 % of pregnancies, and in our study, there were no significant differences in age, anthropometric indices, and family history of preeclampsia between the preeclamptic and control groups. The selenium concentrations in plasma in women with preeclampsia were significantly lower as compared with those in women with normal pregnancy (70.63?±?21.41 versus 82.03?±?15.54 μg/L, p?<?0.05). Being in the bottom tertile of selenium concentration (less than 62.2 μg/L) was associated with greater risk of preeclampsia in pregnant women. The reduced selenium in the maternal circulations observed in the preeclamptic mothers support the hypothesis that insufficient selenium concentration may be a contributing factor to the pathophysiological mechanisms associated with preeclampsia, and optimizing the dietary selenium intake through supplementation could produce demonstrable clinical benefits. 相似文献
17.
Guerrero-Encinas Ildefonso González-González Javier Nicolás Santiago-López Lourdes Muhlia-Almazán Adriana Garcia Hugo Sergio Mazorra-Manzano Miguel Angel Vallejo-Cordoba Belinda González-Córdova Aarón F Hernández-Mendoza Adrián 《Probiotics and antimicrobial proteins》2021,13(4):1033-1043
Probiotics and Antimicrobial Proteins - Studies have shown that the intracellular content of probiotic (postbiotics) has antioxidant properties, which can improve the antioxidant status in vivo.... 相似文献
18.
Murri M García-Delgado R Alcázar-Ramírez J Fernández de Rota L Fernández-Ramos A Cardona F Tinahones FJ 《Biological trace element research》2011,143(3):1289-1301
Sleep apnea-hypopnea syndrome (SAHS) is characterized by recurrent episodes of hypoxia/reoxygenation, which seems to promote oxidative stress. SAHS patients experience increases in hypertension, obesity and insulin resistance (IR). The purpose was to evaluate in SAHS patients the effects of 1?month of treatment with continuous positive airway pressure (CPAP) on oxidative stress and the association between oxidative stress and insulin resistance and blood pressure (BP). Twenty-six SAHS patients requiring CPAP were enrolled. Measurements were recorded before and 1?month after treatment. Cellular oxidative stress parameters were notably decreased after CPAP. Intracellular glutathione and mitochondrial membrane potential increased significantly. Also, total antioxidant capacity and most of the plasma antioxidant activities increased significantly. Significant decreases were seen in BP. Negative correlations were observed between SAHS severity and markers of protection against oxidative stress. BP correlated with oxidative stress markers. In conclusion, we observed an obvious improvement in oxidative stress and found that it was accompanied by an evident decrease in BP with no modification in IR. Consequently, we believe that the decrease in oxidative stress after 1?month of CPAP treatment in these patients is not contributing much to IR genesis, though it could be related to the hypertension etiology. 相似文献
19.
Tan GY Zheng SS Zhang MH Feng JH Xie P Bi JM 《Biological trace element research》2008,126(1-3):129-140
Chromium picolinate (CrPic) is a popular nutritional supplement; however, its safety has been questioned as it may be a source of oxidative stress that induces genotoxicity. The current work investigated the effect of excessive CrPic intake on oxidative damage in growing-finishing pigs. Thirty castrated male pigs, weighing approximately 30 kg each, were randomly divided into five groups and fed a diet with 0, 200, 800, 1,600, 3,200 microg of Cr/kg feed as CrPic for 80 days (approximately the entire growing-finishing period). High CrPic dose significantly decreased superoxide dismutase activity in serum at 80 days as well as the catalase activity in kidney (p < 0.05); however, compared to controls, malondialdehyde in tissue and serum, urinary 8-hydroxydeoxyguanosine level, and DNA strand breaks in liver and kidney had no notable differences (p > 0.05). These results suggested that long-term exposure to different doses of CrPic in feed did not increase the formation of biomarkers of oxidative damage in growing-finishing pigs. However, taking into account the changes of antioxidant enzymes activity, excessive dietary CrPic intake was not recommended in this study. 相似文献
20.
Jae Hoon Lee Hui Song Cui Seo Kyung Shin Jeong Min Kim So Yeon Kim Jong Eun Lee Bon-Nyeo Koo 《Neurochemical research》2013,38(11):2276-2286
Although propofol has been reported to offer neuroprotection against cerebral ischemia injury, its impact on cerebral edema following ischemia is not clear. The objective of this investigation is to evaluate the effects of propofol post-treatment on blood–brain barrier (BBB) integrity and cerebral edema after transient cerebral ischemia and its mechanism of action, focusing on modulation of aquaporins (AQPs), matrix metalloproteinases (MMPs), and hypoxia inducible factor (HIF)-1α. Cerebral ischemia was induced in male Sprague–Dawley rats (n = 78) by occlusion of the right middle cerebral artery for 1 h. For post-treatment with propofol, 1 mg kg?1 min?1 of propofol was administered for 1 h from the start of reperfusion. Nineteen rats undergoing sham surgery were also included in the investigation. Edema and BBB integrity were assessed by quantification of cerebral water content and extravasation of Evans blue, respectively, following 24 h of reperfusion. In addition, the expression of AQP-1, AQP-4, MMP-2, and MMP-9 was determined 24 h after reperfusion and the expression of HIF-1α was determined 8 h after reperfusion. Propofol post-treatment significantly reduced cerebral edema (P < 0.05) and BBB disruption (P < 0.05) compared with the saline-treated control. The expression of AQP-1, AQP-4, MMP-2, and MMP-9 at 24 h and of HIF-1α at 8 h following ischemia/reperfusion was significantly suppressed in the propofol post-treatment group (P < 0.05). Propofol post-treatment attenuated cerebral edema after transient cerebral ischemia, in association with reduced expression of AQP-1, AQP-4, MMP-2, and MMP-9. The decreased expression of AQPs and MMPs after propofol post-treatment might result from suppression of HIF-1α expression. 相似文献