The effects of long-term exposure of magnetic field via 900-MHz GSM radiation on some biochemical parameters and brain histology in rats

The aim of this study is to determine the effects of magnetic field via cell phones on some blood parameters and neurons in the brain of rats. Animals have been classified into three groups: control, Magnetic Field (MF), and F2 groups. Throughout this study, cell phones were placed on the wall of the cages. Rats were exposed to the effects of cell phones during prenatal and postnatal periods until they were 80 days old. During the study, the exposure procedure of rats was that the phone was in standby mode for a whole day and in talking mode for 30 min per day. The waves of cell phones caused an increased blood glucose level from 96.52 ± 5.64 mg/dl to 132.14 ± 5.93 mg/dl and an increased serum protein level from 131.14 ± 6.19 mg/dl to 319.29 ± 6.73 mg/dl compared to control. Statistically, significant differences wasn't observed in the blood cholesterol concentration between the groups compared to the control. Weekly weight gain decreased in all groups compared to the control. MF exposure decreased pyramidal neuron numbers 51.15% and increased ischemic neuron numbers 73% at cortex region of brain. In addition, vascular dilatations have increased clearly in group F2.Whereas the procedure of MF did not have any effects on hippocampal pyramidal cell numbers, magnetic fields increased the amount of ischemic neurons three-fold compared to the control. In conclusion, MF affected some biochemical parameters, especially the cortex region of the brain.     

Effect of 900 MHz radiofrequency radiation on oxidative stress in rat brain and serum

The increasing use of mobile telephones raises the question of possible adverse effects of the electromagnetic fields (EMF) that these phones produce. In this study, we examined the oxidative stress in the brain tissue and serum of rats that resulted from exposure to a 900-MHz EMF at a whole body average specific absorption rate (SAR) of 1.08 W/kg for 1 h/day for 3 weeks. We also examined the antioxidant effect of garlic powder (500 mg/kg/day) given orally to EMF-exposed rats. We found that malondialdehyde (MDA) (p < 0.001) and advanced oxidation protein product (AOPP) (p < 0.05) increased in rat brain tissue exposed to the EMF and that garlic reduced these effects (p < 0.05). There was no significant difference in the nitric oxide (NO) levels in the brain. Paraoxonase (PON) was not detected in the brain. There was a significant increase in the levels of NO (p < 0.001) detected in the serum after EMF exposure, and garlic intake did not affect this increase in NO. Our results suggest that there is a significant increase in brain lipid and protein oxidation after electromagnetic radiation (EMR) exposure and that garlic has a protective effect against this oxidative stress.     

Effect of selenium supplementation on some blood biochemical parameters in male rats

The long-term effect of selenium supplementation on blood glutathione peroxidase (GSH-Px) activity and plasma TBARS’ production (as an index of peroxidation) was evaluated in 15-mo-old male rats fed a diet supplemented with 0.25 or 0.50 ppm selenium, for 12 mo. A group of nonsupplemented age-matched rats was the control. In addition, triglycerides, phospholipids, total and free cholesterol, HDL-cholesterol, and HDL-phospholipid levels were measured in plasma. Plasma testosterone levels were also determined in order to control the aging process in these animals. The GSH-Px activity and the peroxidation level were unchanged in all the groups. However, concerning the lipid parameters, a decrease in triglycerides concentration was observed in both treated groups (p<0.05). Therefore, in these experimental conditions, despite no observed changes in parameters related to lipid peroxidation, selenium seems to be involved with triglycerides metabolism, eventually improving the triglycerides status of aged animals.     

Effect of Terminalia chebula aqueous extract on oxidative stress and antioxidant status in the liver and kidney of young and aged rats

We evaluated the preventive effects of Terminalia chebula (T. chebula) aqueous extract on oxidative and antioxidative status in liver and kidney of aged rats compared to young albino rats. The concentrations of malondialdehyde (MDA), lipofuscin (LF), protein carbonyls (PCO), activities of xantione oxidase (XO), manganese‐superoxide dismutase (MnSOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione‐S‐transferase (GST), and glucose‐6‐phosphate dehydrogenase (G6PDH), levels of glutathione (GSH), vitamin C and vitamin E were used as biomarkers. In the liver and kidney of aged animals, enhanced oxidative stress was accompanied by compromised antioxidant defences. Administration of aqueous extract of T. cheubla effectively modulated oxidative stress and enhanced antioxidant status in the liver and kidney of aged rats. The results of the present study demonstrate that aqueous extract of T. cheubla inhibits the development of age‐induced damages by protecting against oxidative stress. Copyright © 2009 John Wiley & Sons, Ltd.     

Dietary vitamin C supplementation decreases blood pressure in DOCA-salt hypertensive male Sprague Dawley rats and this is associated with increased liver oxidative stress

The effects of a vitamin C supplemented diet on blood pressure, body and liver weights, liver antioxidant status, iron and copper levels were investigated in DOCA-salt treated and untreated Sprague-Dawley (SD) male rats after 8 weeks of treatment. Vitamin C supplementation had no effect on blood pressure in SD rats but induced a significant decrease in blood pressure in DOCA-salt treated rats, the decrease being more efficient at 50 mg/kg of vitamin C than at 500 mg/kg. Hepatic lipid peroxidation and iron levels were significantly increased in DOCA-salt hypertensive rats whereas total hepatic antioxidant capacity (HAC), glutathione peroxidase (GSH-Px) and catalase (CAT) activities were decreased. Vitamin C supplementation did not affect the overall antioxidant defences of control SD rat livers. In contrast, vitamin C supplementation accentuated the DOCA-salt induced accumulation of liver iron and lipid peroxidation. This occurred without any notable aggravation in the antioxidant deficiency of vitamin C supplemented DOCA-salt treated rat livers. Our data suggest that DOCA-salt treatment induces an accumulation of iron in rat livers which is responsible for the prooxidant effect of vitamin C. The normalization of blood pressure in DOCA-salt treated rats by vitamin C supplementation appears thus independent from liver antioxidant status.     

The comparison of the effects of ketamine and etomidate on cardiodynamics,biochemical and oxidative stress parameters in Wistar male rats

Molecular and Cellular Biochemistry - Our previous studies have confirmed that proline/serine-rich coiled-coil 1 (PSRC1) overexpression can regulate blood lipid levels and inhibit atherosclerosis...     

Effect of 900-, 1800-, and 2100-MHz radiofrequency radiation on DNA and oxidative stress in brain

Ubiquitous and ever increasing use of mobile phones led to the growing concern about the effects of radiofrequency radiation (RFR) emitted by cell phones on biological systems. The aim of this study is to explore whether long-term RFR exposure at different frequencies affects DNA damage and oxidant-antioxidant parameters in the blood and brain tissue of rats. 28 male Sprague Dawley rats were randomly divided into four equal groups (n = 7). They were identified as Group 1: sham-control, Group 2: 900 MHz, Group 3: 1800 MHz, and Group 4: 2100 MHz. Experimental groups of rats were exposed to RFR 2 h/day for 6 months. The sham-control group of rats was subjected to the same experimental condition but generator was turned off. Specific absorption rates (SARs) at brain with 1 g average were calculated as 0.0845 W/kg, 0.04563 W/kg, and 0.03957, at 900 MHz, 1800 MHz, and 2100 MHz, respectively. Additionally, malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), total antioxidant status (TAS), and total oxidant status (TOS) analyses were conducted in the brain tissue samples. Results of the study showed that DNA damage and oxidative stress indicators were found higher in the RFR exposure groups than in the sham-control group. In conclusion, 900-, 1800-, and 2100-MHz RFR emitted from mobile phones may cause oxidative damage, induce increase in lipid peroxidation, and increase oxidative DNA damage formation in the frontal lobe of the rat brain tissues. Furthermore, 2100-MHz RFR may cause formation of DNA single-strand breaks.     

The effect of age and selenium on some biochemical parameters in rat liver

Two age groups, 3 and 15 mo, were used to investigate whether age-associated changes in some parameters related to lipid peroxidation occur in the liver of male Wistar rats and to observe possible effects of dietary selenium supplementation (0.25 and 0.50 ppm) for 12 mo on the same parameters. At these experimental conditions, the most important observation was that peroxidation did not change by aging, at least until 15 mo of age. In addition, the activity of Sedependent glutathione peroxidase (GSH-Px, EC 1.11.1.9) was higher in the liver of the older animals. It is suggested that the enzyme could have a role in the unchanged hepatic peroxidation observed in aged male rats. On the other hand, an effect of dietary selenium supplementation on those parameters was not observed, probably because the selenium levels were still at an adequate plateau.     

Effect of melatonin on oxidative status of rat brain, liver and kidney tissues under constant light exposure

An enormous amount of data has been published in recent years demonstrating melatonin's defensive role against toxic free radicals. In the present study, we examined the role of melatonin as an antioxidant against the effect of continuous light exposure. Rats were divided into three groups. Control rats (group A) were kept under natural conditions whereas other group of rats (group B and C) were exposed to constant light for inhibition of melatonin secretion by the pineal gland. Group C rats also received melatonin via s.c. injection (1 mg x kg(- 1) body weight x day(- 1)). At the end of experiment, all animals were sacrificied by decapitation, serum and tissue samples were removed for determination of malondialdehyde (MDA), a product of lipid peroxidation, conjugated dienes levels and glutathione peroxidase (GSH-Px) activity levels. It was found that lipid peroxidation was increased in the rats which were exposed to constant light. Melatonin injection caused a decrease in lipid peroxidation, especially in the brain. In addition, melatonin application resulted in increased GSH-Px activity, which has an antioxidant effect. Thus, melatonin is not only a direct scavenger of toxic radicals, but also stimulates the antioxidative enzyme GSH-Px activity to detoxify hydroxyl radical produced by constant light exposure.     

Direct and indirect effects of kisspeptin on liver oxidant and antioxidant systems in young male rats

Kisspeptin is a recently discovered hypothalamic peptide which plays an important role in the central control of reproductive functions. We have investigated direct and indirect effects of kisspeptin on the liver oxidative stress in young male rats. Twenty‐four rats were divided into four groups (n = 6/group). First group served as control and received saline. Kisspeptin‐10 was administered to the animals in the second group (20 nmol/rat/day), for a period of 7 days. Rats were given only one dose gosereline (0.9 mg/rat), a GnRH agonist in the third group. The last group received kisspeptin‐10 with gosereline. The activities of catalase, superoxide dismutase (SOD), xanthine oxidase (XO), adenosine deaminase (AD) and level of malondialdehyde were studied in liver tissue. Serum samples were separated for total antioxidant capacity (TAC), total oxidant status (TOS), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, blood urea nitrogen (BUN), colesterol, high‐density lipoprotein (HDL) and triglyceride. Kisspeptin increased the activities of SOD and catalase (p < 0.05). When compared to the control group, the levels of malondialdehyde, TOS and AST were lower, but levels of BUN, cholesterole, HDL and AD were higher in the other three groups (p < 0.05). In conclusion, our findings suggest that kisspeptin may have antioxidant and thus protective effects on the liver tissue. Copyright © 2010 John Wiley & Sons, Ltd.     

楮实子对药物性肝损伤大鼠氧化应激因子的影响

为了探讨楮实子对对乙酰氨基酚(APAP)诱导的药物性肝损伤大鼠的保护作用以及对过氧化物酶体增殖物激活受体γ(PPAR-γ)、过氧化物酶体增殖物激活受体α(PPAR-α)、C-Ros癌基因1(ROS1)的调控作用。实验将50只SD大鼠随机分为正常组、模型组、水飞蓟宾组(44mg/kg)和楮实子高、低剂量组(4.2、1.05g生药/kg),每组10只。灌胃给予对乙酰氨基酚(1.2kg/kg)制备肝损伤模型,给药组造模的同时给予相应药物治疗,连续30天。实验结束,收集血清、肝组织标本进行指标检测。结果显示,楮实子各剂量均能降低药物性肝损伤大鼠血清中谷丙转氨酶(ALT)和谷草转氨酶(AST)活性,降低总胆红素(TBIL)和直接胆红素(TBIL)的含量,升高血清中谷胱甘肽(GSH)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性,降低丙二醛(MDA)含量以及ROS1的表达,上调PPAR-αmRNA的表达,下调PPAR-γmRNA的表达。以上研究结果表明,楮实子能防治对乙酰氨基酚所致肝损伤,其作用机制可能是通过降低ROS1的表达、调节转录因子PPAR-α和PPAR-γ的基因表达,从而缓解氧化应激损伤来实现的。     

Co-administration of zinc and n-acetylcysteine prevents arsenic-induced tissue oxidative stress in male rats

Arsenic is a widespread environmental toxicant that may cause neuropathy, skin lesions, vascular lesions and cancer upon prolonged exposure. Improving nourishment like supplementation of micronutrients, antioxidants, vitamins and amino acids could be able to halve the risk in those who were previously the poor nourished. The present study was planned to investigate the preventive effects of zinc and n-acetylcysteine (NAC) supplementation either alone or in combination with arsenic on selected biochemical variables indicative of oxidative stress and liver injury in male rats. For 3 weeks 25 male wistar rats were exposed to arsenic as sodium arsenite (2 mg/kg, orally through gastric intubation) either alone or in combination with NAC (10 mg/kg, intraperitoneally), zinc (5 mg/kg, orally) or zinc plus NAC. Animals were sacrificed 24h after the last dosing for various biochemical parameters. Concomitant administration of zinc with arsenic showed remarkable protection against blood delta-aminolevulinic acid dehydratase (ALAD) activity as well as providing protection to hepatic biochemical variables indicative of oxidative stress (like thiobarbituric acid reactive substances (TBARS) level, catalase) and tissue injury. NAC supplementation on the other hand, was moderately effective in protecting animals from the toxic effects of arsenic. Interestingly, concomitant administration of zinc and NAC was most effective compared to zinc or NAC in eliciting above-mentioned protective effects. The above results suggest significant protective value of combined zinc and NAC administration in acute arsenic exposure.     

Efficacy of some antioxidants supplementation in reducing oxidative stress post sodium tungstate exposure in male wistar rats

This study aimed to evaluate the protective efficacy of some antioxidants against sodium tungstate induced oxidative stress in male wistar rats. Animals were sub-chronically exposed to sodium tungstate (100 ppm in drinking water) for three months except for control group. In the same time, many rats were supplemented orally with different antioxidants (alpha-lipoic acid (ALA), n-acetylcysteine (NAC), quercetin or naringenin (0.30 mM)) for five consecutive days a week for the same mentioned period before. Exposure to sodium tungstate significantly (P < 0.05) inhibit blood δ-aminolevulinic acid dehydratase (ALAD) activity, liver and blood reduced glutathione (GSH) levels and an increase in oxidized glutathione (GSSG) and thiobarbituric acid reactive species (TBARS) levels in tissues. ALA acid and NAC supplementation post sodium tungstate exposure increased GSH and also, was beneficial in the recovery of altered superoxide dismutase and catalase activity, besides, significantly reducing blood and tissue reactive oxygen species and TBARS levels. The results suggest a more pronounced efficacy of ALA acid and NAC supplementation than quercetin or naringenin supplementation post sodium tungstate exposure in preventing induced oxidative stress in rats.     

Effect of Triphala on oxidative stress and on cell-mediated immune response against noise stress in rats

Stress is one of the basic factors in the etiology of number of diseases. The present study was aimed to investigate the effect of Triphala (Terminalia chebula, Terminalia belerica and Emblica officinalis) on noise-stress induced alterations in the antioxidant status and on the cell-mediated immune response in Wistar strain male albino rats. Noise-stress employed in this study was 100 dB for 4 h/d/15 days and Triphala was used at a dose of 1 g/kg/b.w/48 days. Eight different groups of rats namely, non-immunized: control, Triphala, noise-stress, Triphala with noise-stress, and corresponding immunized groups were used. Sheep red blood cells (5×10⁹ cells/ml) were used to immunize the animals. Biochemical indicators of oxidative stress namely lipid peroxidation, antioxidants superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), ascorbic acid in plasma and tissues (thymus and spleen) and SOD, GPx and corticosterone level in plasma were estimated. Cell-mediated immune response namely foot pad thickness (FPT) and leukocyte migration inhibition (LMI) test were performed only in immunized groups. Results showed that noise-stress significantly increased the lipid peroxidation and corticosterone level with concomitant depletion of antioxidants in plasma and tissues of both non-immunized and immunized rats. Noise-stress significantly suppressed the cell-mediated immune response by decreased FPT with an enhanced LMI test. The supplementation with Triphala prevents the noise-stress induced changes in the antioxidant as well as cell-mediated immune response in rats. This study concludes that Triphala restores the noise-stress induced changes may be due to its antioxidant properties.     

Effect of chronic exposure to aspartame on oxidative stress in brain discrete regions of albino rats

This study was aimed at investigating the chronic effect of the artificial sweetener aspartame on oxidative stress in brain regions of Wistar strain albino rats. Many controversial reports are available on the use of aspartame as it releases methanol as one of its metabolite during metabolism. The present study proposed to investigate whether chronic aspartame (75 mg/kg) administration could release methanol and induce oxidative stress in the rat brain. To mimic the human methanol metabolism, methotrexate (MTX)-treated rats were included to study the aspartame effects. Wistar strain male albino rats were administered with aspartame orally and studied along with controls and MTX-treated controls. The blood methanol level was estimated, the animal was sacrificed and the free radical changes were observed in brain discrete regions by assessing the scavenging enzymes, reduced glutathione, lipid peroxidation (LPO) and protein thiol levels. It was observed that there was a significant increase in LPO levels, superoxide dismutase (SOD) activity, GPx levels and CAT activity with a significant decrease in GSH and protein thiol. Moreover, the increases in some of these enzymes were region specific. Chronic exposure of aspartame resulted in detectable methanol in blood. Methanol per se and its metabolites may be responsible for the generation of oxidative stress in brain regions.     

基于抗炎及抗氧化作用探讨微生态制剂在非酒精性脂肪肝模型大鼠中的应用价值

目的研究基于抗炎及抗氧化作用探讨微生态制剂在非酒精性脂肪肝(NAFLD)模型大鼠中的应用价值。方法选择成年雄性SD大鼠并随机分为对照组、NAFLD组、蓝莓益生菌(BP)组。后2组采用复合高脂饲料建立NAFLD模型,BP组给予蓝莓联合益生菌干预。比较3组间血清肝功能指标、炎症指标、氧化应激指标含量及肝脏组织中炎症及氧化应激信号分子表达的差异。结果 NAFLD组大鼠血清中ALT、AST、TNF-α、IL-1、IL-6、IL-18、MDA的含量及肝脏中p-p38MAPK、NF-κB的表达量明显高于对照组,血清中SOD、GPX的含量及肝脏中p-AMPK、Nrf-2的表达量明显低于对照组;BP组大鼠血清中ALT、AST、TNF-α、IL-1、IL-6、IL-18、MDA的含量及肝脏中p-p38MAPK、NF-κB的表达量明显低于NALFD组,血清中SOD、GPX的含量及肝脏中p-AMPK、Nrf-2的表达量明显高于NALFD组。结论蓝莓益生菌用于NALFD模型大鼠的干预能够改善肝功能并抑制炎症反应、氧化应激反应。     

The effect of bisphenol A on some oxidative stress parameters and acetylcholinesterase activity in the heart of male albino rats

Bisphenol A (BPA) is an endocrine disrupting chemical used on a wide range in industry. Several studies reported that BPA may cause cardiovascular disorders in humans and animals. The present study aims to investigate the effect of BPA on the heart of adult male rats. The rats received a daily oral administration of BPA (25 mg/kg for 6 weeks and 10 mg/kg for 6 and 10 weeks). It was found that BPA at the two studied doses induced a significant increase in malondialdehyde, and a significant decrease in catalase after 6 weeks. Moreover, a significant decrease in reduced glutathione and acetylcholinesterase (AchE) activity was observed after treatment with the two doses of BPA throughout the studied time intervals. The two doses (25 and 10 mg/kg) resulted in a significant decrease in nitric oxide (NO) levels after 6 and 10 weeks, respectively. A significant increase in body weight gain occurred in all animals after BPA treatment. These results suggest that BPA has cardiotoxic effects which are mediated by the oxidative stress resulting from the overproduction of free radicals, the deficiency of NO and the inhibition of AchE leading to cholinergic activation. The obesity promoting effect of BPA may also participate in the observed cardiovascular disturbances.     

The effects of moderate-, strenuous- and over-training on oxidative stress markers, DNA repair, and memory, in rat brain

We have tested the hypothesis that training with moderate- (MT), strenuous- (ST), or over- (OT) load can cause alterations in memory, lipid peroxidation, protein oxidation, DNA damage, activity of 8-oxoG-DNA glycosylase (OGG1) and brain-derived neurotrophic factor (BDNF), in rat brain. Rat memory was assessed by a passive avoidance test and the ST and OT group demonstrated improved memory. The content of BDNF was increased only in the OT group. The oxidative damage of lipids and DNA, as measured by thiobarbituric acid reactive substances (TBARS), and 8-hydroxydeoxyguanosine (8-OHdG), did not change significantly with exercise. Similarly, the activity of DNA repair enzyme, 8-oxoguanine DNA glycosylase (OGG1), was not altered with exercise training. On the other hand, the content of reactive carbonyl derivatives (RCDs) decreased in all groups and the decrease reached significance levels in the ST and OT groups. The activity of the proteasome complex increased in the brain of OT. The findings of this study imply that over-training does not induce oxidative stress in the brain and does not cause loss of memory. The improved memory was associated with enhanced BDNF content.     

Effects of long-term exposure to 900 megahertz electromagnetic field on heart morphology and biochemistry of male adolescent rats

The pathological effects of exposure to an electromagnetic field (EMF) during adolescence may be greater than those in adulthood. We investigated the effects of exposure to 900 MHz EMF during adolescence on male adult rats. Twenty-four 21-day-old male rats were divided into three equal groups: control (Cont-Gr), sham (Shm-Gr) and EMF-exposed (EMF-Gr). EMF-Gr rats were placed in an EMF exposure cage (Plexiglas cage) for 1 h/day between postnatal days 21 and 59 and exposed to 900 MHz EMF. Shm-Gr rats were placed inside the Plexiglas cage under the same conditions and for the same duration, but were not exposed to EMF. All animals were sacrificed on postnatal day 60 and the hearts were extracted for microscopic and biochemical analyses. Biochemical analysis showed increased levels of malondialdehyde and superoxide dismutase, and reduced glutathione and catalase levels in EMF-Gr compared to Cont-Gr animals. Hematoxylin and eosin stained sections from EMF-Gr animals exhibited structural changes and capillary congestion in the myocardium. The percentage of apoptotic myocardial cells in EMF-Gr was higher than in either Shm-Gr or Cont-Gr animals. Transmission electron microscopy of myocardial cells of EMF-Gr animals showed altered structure of Z bands, decreased myofilaments and pronounced vacuolization. We found that exposure of male rats to 900 MHz EMF for 1 h/day during adolescence caused oxidative stress, which caused structural alteration of male adolescent rat heart tissue.