Neuroprotective effects of magnesium against stress induced by hydrogen peroxide in Wistar rat.

INTRODUCTION: Oxidative stress has been implicated in the pathogenesis of diverse disease states. The present study was designed to examine the effects of magnesium sulphate (MgSO4) against hydrogen peroxide (H2O2) induced behaviour impairment and oxidative damage in rats. MATERIAL AND METHODS: Eighteen rats were equally divided into three groups. The first group was kept as a control. In the second group, H2O2 was given in drinking water at 3% during 5 days. In the third group, rats were subjected to daily administration of H2O2 and MgSO4 (100 mg/kg; b.w) for 5 days. Animals were subjected to behavioural tests (elevated plus maze and open field). At the end of experiment, brains were extracted for oxidative stress biomarkers assessment including levels of malondialdéhyde and hydrogen peroxide and activities of superoxide dismutase and catalase. RESULTS: Our findings showed that H2O2 treated rat exhibited anxiogenic behaviour and the genesis of free radicals in the brain. Magnesium showed amelioration against oxidative stress and significant decrease in anxiety levels. DISCUSSION AND CONCLUSION: Stress is a powerful process that disrupts brain homeostasis by inducing oxidative stress and its appear that magnesium may have potential therapeutic benefits by reducing oxidative stress and inducing anxiolytic effect.

Prevention of neurotoxicity and cognitive impairment induced by zinc nanoparticles by oral administration of saffron extract.

The accumulation of relatively higher dose of zinc oxide nanoparticles in brain was reported to produce neurotoxicity. Indeed, nanoparticles have a high ability to penetrate biological membranes and be uptaken by cells, which may cause cell disorders and physiological dysfunctions. The aim of the current study was to evaluate, whether oral administration of saffron extract, in rats, can protect from neurotoxicity and behavioural disturbances induced by chronic administration of ZnO-NPs. Daily oral administration of ZnO-NPs was performed for 21 consecutive days to induce oxidative stress-like situation. Then after the saffron extract was concomitantly administrated in several rat groups to overcome the nanotoxicological effect induced by ZnO-NPs. In the frontal cortex, the hippocampus and the cerebellum, ZnO-NPs induced a H2 O2 -oxydative stress-like effect reflected in reduced enzymatic activities of catalase, superoxide dismutase and glutathione S-transferase, and decreased acetylcholinesterase activity. In addition, increased levels of proinflammatory interleukins IL-6 and IL-1-⍺ occurred in the hippocampus, reveal the existence of brain inflammation. The concomitant administration of saffron extract to animals exposed to ZnO-NPs prevented the enhanced anxiety-related to the behaviour in the elevated plus-maze test, the open field test and preserved spatial learning abilities in the Morris water maze. Moreover, animals exposed to ZnO-NPs and saffron showed abnormal activity of several antioxidant enzymes as well as acetylcholinesterase activity, an effect that may underly the preserved anxiety-like behaviour and spatial learning abilities observed in these animals. Saffron extract has a potential beneficial therapeutic effect: antioxidant, anti-inflammatory and neuroprotective agent.

Quercetin alleviates styrene oxide-induced cytotoxicity in cortical neurons in vitro via modulation of oxidative stress and apoptosis.

Styrene 7,8-oxide (SO) is the principal metabolite of styrene, an industrial neurotoxic compound which causes various neurodegenerative disorders. The present study aimed to explore the mechanisms of SO cytotoxicity (0.5 - 4 mM) in primary cortical neurons and to evaluate the neuroprotective potential of quercetin (QUER). Our results showed that exposure to SO decreased viability of cortical neurons in a concentration-dependent manner. In the presence of QUER, cell viability was increased significantly. The neuroprotective effects of QUER were associated with the reduction of intracellular Reactive Oxygen Species (ROS), the decrease in calcium overload and the restoration of mitochondrial membrane depolarization caused by SO. Additionally, to evaluate neuronal death mechanisms triggered by SO, cells were incubated with Ac-DEVD-CHO, Calpeptin and Necrostatin-1, pharmacological inhibitors of caspase-3, calpains and necroptosis respectively. The data showed that the three inhibitors reduced cell death induced by SO and suggested the implication of apoptotic, necrotic and necroptotic pathways. However, western blot analysis showed that QUER attenuated the activation of caspase-3 but did not prevent calpain activity. Taken together, these data indicated that the cytotoxicity of SO was mediated by oxidative stress and apoptosis, necrosis and necroptosis mechanisms, while the neuroprotection provided by QUER against SO depended mainly on its anti-apoptotic activity.

Exposure to 2.45 GHz Radiation Triggers Changes in HSP-70, Glucocorticoid Receptors and GFAP Biomarkers in Rat Brain.

Brain tissue may be especially sensitive to electromagnetic phenomena provoking signs of neural stress in cerebral activity. Fifty-four adult female Sprague-Dawley rats underwent ELISA and immunohistochemistry testing of four relevant anatomical areas of the cerebrum to measure biomarkers indicating induction of heat shock protein 70 (HSP-70), glucocorticoid receptors (GCR) or glial fibrillary acidic protein (GFAP) after single or repeated exposure to 2.45 GHz radiation in the experimental set-up. Neither radiation regime caused tissue heating, so thermal effects can be ruled out. A progressive decrease in GCR and HSP-70 was observed after acute or repeated irradiation in the somatosensory cortex, hypothalamus and hippocampus. In the limbic cortex; however, values for both biomarkers were significantly higher after repeated exposure to irradiation when compared to control animals. GFAP values in brain tissue after irradiation were not significantly different or were even lower than those of nonirradiated animals in all brain regions studied. Our results suggest that repeated exposure to 2.45 GHz elicited GCR/HSP-70 dysregulation in the brain, triggering a state of stress that could decrease tissue anti-inflammatory action without favoring glial proliferation and make the nervous system more vulnerable.

Effects of Iron Oxide Nanoparticles (γ-Fe2O3) on Liver, Lung and Brain Proteomes following Sub-Acute Intranasal Exposure: A New Toxicological Assessment in Rat Model Using iTRAQ-Based Quantitative Proteomics.

Iron Oxide Nanoparticles (IONPs) present unique properties making them one of the most used NPs in the biomedical field. Nevertheless, for many years, growing production and use of IONPs are associated with risks that can affect human and the environment. Thus, it is essential to study the effects of these nanoparticles to better understand their mechanism of action and the molecular perturbations induced in the organism. In the present study, we investigated the toxicological effects of IONPs (γ-Fe2O3) on liver, lung and brain proteomes in Wistar rats. Exposed rats received IONP solution during 7 consecutive days by intranasal instillation at a dose of 10 mg/kg body weight. An iTRAQ-based quantitative proteomics was used to study proteomic variations at the level of the three organs. Using this proteomic approach, we identified 1565; 1135 and 1161 proteins respectively in the brain, liver and lung. Amon them, we quantified 1541; 1125 and 1128 proteins respectively in the brain, liver and lung. Several proteins were dysregulated comparing treated samples to controls, particularly, proteins involved in cytoskeleton remodeling, cellular metabolism, immune system stimulation, inflammation process, response to oxidative stress, angiogenesis, and neurodegenerative diseases.

Dual-energy X-ray absorptiometry underestimates in vivo lumbar spine bone mineral density in overweight rats.

Dual-energy X-ray absorptiometry (DXA) is currently the most widely used technique for measuring areal bone mineral density (BMD). However, several studies have shown inaccuracy, with either overestimation or underestimation of DXA BMD measurements in the case of overweight or obese individuals. We have designed an overweight rat model based on junk food to compare the effect of obesity on in vivo and ex vivo BMD and bone mineral content measurements. Thirty-eight 6-month old male rats were given a chow diet (n = 13) or a high fat and sucrose diet (n = 25), with the calorie amount being kept the same in the two groups, for 19 weeks. L1 BMD, L1 bone mineral content, amount of abdominal fat, and amount of abdominal lean were obtained from in vivo DXA scan. Ex vivo L1 BMD was also measured. A difference between in vivo and ex vivo DXA BMD measurements (P < 0.0001) is evidenced with an underestimation of in vivo BMD by (8.47 ± 10.54)%. This difference was found for the chow and high fat, high sucrose diets (P = 0.008), and a significant interaction between in vivo measurements, ex vivo measurements, and diet was observed (P = 0.030). Also, the data show a positive significant correlation of ex vivo BMD with body weight, perirenal fat, abdominal fat, and abdominal lean. Multiple linear regression analysis shows that body weight, abdominal fat, and abdominal lean were independently related to ex vivo BMD. DXA underestimated lumbar in vivo BMD in overweight rats, and this measurement error is related to body weight and abdominal fat. Therefore, caution must be used when one is interpreting BMD among overweight and obese individuals.

Hepatotoxicity of vanadyl sulfate in nondiabetic and streptozotocin-induced diabetic rats.

This study examined the effects of vanadyl sulfate (VOSO4) on the livers of nondiabetic and streptozotocin-induced diabetic rats. Rats were divided into 6 groups. Groups 1, 2, and 3 consisted of nondiabetic rats that were, respectively, control animals or those receiving an intraperitoneal (i.p.) injection of either 5 or 10 mg·kg-1 (i.p.) VOSO4 for 30 days. Groups 4, 5, and 6 consisted of diabetic animals that were, respectively, control animals or those treated with 5 or 10 mg·kg-1 (i.p.) VOSO4 for 30 days. Results showed that VOSO4 reduced body mass in nondiabetic rats, whereas it increased body mass in diabetic groups. Plasma transaminases (aspartate aminotransferase, alanine aminotransferase), lactate dehydrogenase, and alkaline phosphatase activities and malondialdehyde levels were increased, while liver catalase and superoxide dismutase activities were profoundly decreased in diabetic animals in comparison with enzyme activities in the nondiabetic group. Rats in the diabetic group also showed notable oxidative damage to the liver. Treatment of diabetic rats with VOSO4 decreased the hepatotoxic markers, significantly restored the activities of antioxidant enzymes, and attenuated histopathological changes in liver tissue. In nondiabetic rats, VOSO4 treatment increased most of the hepatotoxic markers, reduced antioxidant enzyme activities, and induced pronounced oxidative damage in liver tissue. These data suggest that treatment with VOSO4 exerts toxic effects in healthy animals and significantly prevents liver oxidative damage in streptozotocin-induced diabetic rats, but without total safety. Further studies are needed to clarify its mechanism of action.

Positive Association of Obesity and Insulin Resistance With Bone Mineral Density in Tunisian Postmenopausal Women.

The association of bone mineral density (BMD) with obesity and insulin resistance remains unclear. This study aimed to explore these associations in Tunisian menopausal women. Eighty-one postmenopausal women were recruited. Data were analyzed for obese (N = 57) and non-obese women (N = 24) and for insulin-resistant (N = 43) and non insulin-resistant women (N = 36). Anthropometric and biochemical parameters were recorded. BMD in different sites and body composition were measured using dual-energy X-ray absorptiometry. Higher BMD was observed in obese women than those non-obese in the left femur (p = 0.0067), right femur (p = 0.0108), total hip (p = 0.0077), and the whole body (p = 0.0276). Also BMD was significantly greater in insulin-resistant women than in non-insulin-resistant women when measured in the left femur and total hip. Positive correlations were recorded between BMD and anthropometric parameters, body composition parameters, and glycemia (r = 0.249, p < 0.05). Multiple linear regression analysis shows that only trunk fat (p < 0.05) and lean mass (p < 0.05) were independently and positively related to BMD, and the waist circumference was the only anthropometric parameter independently and negatively associated to BMD. BMD is improved in obese and insulin-resistant women. Also, trunk fat and lean mass are likely to be key positive independent factors for BMD.

p,p'-DDT induces testicular oxidative stress-induced apoptosis in adult rats.

BACKGROUND: The 1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane (p,p'-DDT) is a known persistent organic pollutant and male reproductive toxicant. The present study is designed to test the hypothesis that oxidative stress mediates p,p'-DDT-induced apoptosis in testis. METHODS: Male Wistar rats received an intraperitoneal (ip) injection of the pesticide at doses of 50 and 100mg/kg for 10 consecutive days. The oxidative stress was evaluated by biomarkers such lipid peroxidation (LPO) and metallothioneins (MTs) levels. Antioxidant enzymes activities was assessed by determination of superoxide dismutase (SOD), catalase (CAT) and hydrogen peroxide (H2O2) production. In addition, glutathione-dependent enzymes and reducing power in testis was evaluated by glutathione peroxidase (Gpx), glutathione reductase (GR), glutathione S-transferase (GST) activities and reduced and oxidized glutathione (GSH - GSSG) levels. Apoptosis was evaluated by DNA fragmentation detected by agarose gel electrophoresis. Germinal cells apoptosis and the apoptotic index was assessed through the TUNEL assay. RESULTS: After 10 days of treatment, an increase in LPO level and H2O2 production occurred, while MTs level, SOD and CAT activities were decreased. Also, the Gpx, GR, GST, and GSH activities were decreased, whereas GSSG activity was increased. Testicular tissues of treated rats showed pronounced degradation of the DNA into oligonucleotides as seen in the typical electrophoretic DNA ladder pattern. Intense apoptosis was observed in germinal cells of DDT-exposed rats. In addition, the apoptotic index was significantly increased in testis of DDT-treated rats. CONCLUSIONS: These results clearly suggest that DDT sub-acute treatment causes oxidative stress in rat testis leading to apoptosis.

Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue from northern Tunisia: Current extent of contamination and contributions of socio-demographic characteristics and dietary habits.

The aims of the present study were to investigate the current exposure levels of persistent organochlorine compounds (OCs) in adipose tissues intraoperatively collected from 40 patients over 20 years undergoing non-cancer-related surgery residing in Northern region of Tunisia (Bizerte), which constitutes an exemplary case, and examined association between levels of contamination and both socio-demographic characteristics and dietary habits. Concentration of hexachlorobenzene (HCB), hexachlorocyclohexane isomers (α-HCH, ß-HCH, γ-HCH and δ-HCH), dichlorodiphenyltrichloroethane isomers (p,p'-DDT and o,p'-DDT) and metabolites (p,p'-DDE, o,p'-DDE, p,p'-DDD and o,p'-DDD) and 12 polychlorinated biphenyls (PCBs) congeners were measured using capillary gas chromatography with electron capture detector. Overall, residue levels of OCs followed the decreasing order of DDTs > PCBs > HCB > HCHs. DDTs levels ranged from 74.49 to 1834.76ngg-1 lipid and contributing to more than 90% to the sum of organochlorine pesticides (OCPs). p,p'-DDE was the most abundant in all samples and the p,p'-DDT/p,p'-DDE ratio (range between 1.85% and 58.45%) suggesting recent and ongoing exposure to banned commercial DDT products. PCB concentrations varied from 29.27 to 322.58ngg-1 lipid and PCB-180, PCB-153 and PCB-138 were the dominant congeners accounting for 70% of total PCBs. We did not find significant correlations between OC exposure levels and sex, parity, habitat areas and smoking habits. In females, the adipose tissue concentrations of DDTs, HCB and PCB-118 were positively correlated with age. There was statistically significant relationship between body mass index (BMI) changes and the adipose tissue levels of HCB and HCHs. No association was found between OCPs levels and dietary factors. However, our study suggests that fish consumption may be an important contributor of PCBs adipose tissue content of PCBs in Tunisian people. The presented work is highly significant, being the first study pointing out the chronic exposure to OCs in Bizerte.

Fatty acid composition and mechanisms of the protective effects of myrtle berry seed aqueous extract in alcohol-induced peptic ulcer in rat.

This study aimed to investigate the antiulcer and antioxidant activities of myrtle berry seed aqueous extract (MBSAE) in a peptic ulcer model induced by ethanol in male Wistar rats. MBSAE is rich in total polyphenols, total flavonoids, and unsaturated fatty acids, particularly linoleic (18:2) and oleic (18:1) acids. MBSAE also exhibited in vitro antioxidant activity using 2,2-diphenyl-1-picrylhydrazyl (DPPH) (IC50 = 172.1 µg/mL) and superoxide anion (IC50 = 200.24 µg/mL) scavenging activities. In vivo, MBSAE provided dose-dependent protection against ethanol-induced gastric and duodenal macroscopic and histological alterations. Also, it inhibited secretory profile disturbances and lipid peroxidation, and preserved normal antioxidant enzyme activities and nonenzymatic antioxidant levels. More importantly, we showed that acute alcohol intoxication increased gastric and duodenal calcium, hydrogen peroxide, and free iron levels, whereas MBSAE treatment protected against intracellular mediator deregulation. In conclusion, we suggest that MBSAE has potent protective effects against alcohol-induced peptic ulcer in rat. This protection might be related in part to its antioxidant properties as well as its opposite effects on some studied intracellular mediators.

Effects of repeated restraint stress and WiFi signal exposure on behavior and oxidative stress in rats.

Today, due to technology development and aversive events of daily life, Human exposure to both radiofrequency and stress is unavoidable. This study investigated the co-exposure to repeated restraint stress and WiFi signal on cognitive function and oxidative stress in brain of male rats. Animals were divided into four groups: Control, WiFi-exposed, restrained and both WiFi-exposed and restrained groups. Each of WiFi exposure and restraint stress occurred 2 h (h)/day during 20 days. Subsequently, various tests were carried out for each group, such as anxiety in elevated plus maze, spatial learning abilities in the water maze, cerebral oxidative stress response and cholinesterase activity in brain and serum. Results showed that WiFi exposure and restraint stress, alone and especially if combined, induced an anxiety-like behavior without impairing spatial learning and memory abilities in rats. At cerebral level, we found an oxidative stress response triggered by WiFi and restraint, per se and especially when combined as well as WiFi-induced increase in acetylcholinesterase activity. Our results reveal that there is an impact of WiFi signal and restraint stress on the brain and cognitive processes especially in elevated plus maze task. In contrast, there are no synergistic effects between WiFi signal and restraint stress on the brain.

Protective effect of chamomile (Matricaria recutita L.) decoction extract against alcohol-induced injury in rat gastric mucosa.

BACKGROUND: Matricaria recutita L. (Asteraceae), German chamomile, has been widely used in the traditional Tunisian medicine because of having the powerful health benefits. the current study was conducted to determine the protective effect of chamomile (Matricaria recutita L.) decoction extract (CDE) in ethanol-induced ulcer and oxidative stress on gastric mucosa in rat. METHODS: Adult male wistar rats were used and divided into seven groups: Control, EtOH, EtOH+various doses of CDE (25, 50 and 100mg/kg, b.w.), EtOH+famotidine (FAM) and EtOH+ascorbic acid (AA). Gastric ulceration was induced by EtOH (4g/kg, b.w. p.o.). RESULTS: Firsly, we found that acute alcohol administration leads to mark macroscopic and histologic changes in gastric mucosa. EtOH also induced lipoperoxidation (486.99%), thiol (-SH) groups decrease (40.98%) as well as antioxidant enzyme activity depletion such as superoxide dismutase (SOD) (49.05%), catalase (CAT) (46.80%) and glutathione peroxidase (GPx) (38.20%). Our results also demonstrated that alcohol intoxication increased tissue and plasmatic hydrogen peroxide, calcium and free iron levels. More importantly, CDE reversed all macroscopic, histologic and biochemical changes induced by EtOH administration. CONCLUSION: A potential gastropreotective effect of CDE against EtOH-induced ulcer and oxidative stress might be partially to its antioxidant properties as well as to various gastric mucosal defense mechanisms, including protection of gastric sulfhydryls and its opposite effect on some intracellular mediators such as free iron, hydrogen peroxide and calcium.

Involvement of oxidative stress in the mechanism of p,p'-DDT-induced nephrotoxicity in adult rats.

The 1,1,1-trichloro-2,2-bis(4-chlorophenyl) ethane (p,p'-DDT) is an organochlorine pesticide that persists in the environment and has a risk to human health. We investigated whether p,p'-DDT-induces nephrotoxicity in rats and whether oxidative stress and apoptosis are involved in the pathogenesis of this process. Male rats received the pesticide at doses of 50 and 100 mg/kg for 10 days. Renal damage was evaluated by histopathological examination and serum markers. The oxidative stress was evaluated by lipid peroxidation (LPO), metallothioneins (MTs) and protein carbonyl levels. Antioxidant enzymes were assessed by determination of superoxide dismutase (SOD) and catalase (CAT) activities. Glutathione-dependent enzymes and reducing power in kidney were evaluated by glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST) activities. Renal tubular cells apoptosis was assessed through the TUNEL assay. After 10 days of treatment, an increase of serum creatinine and urea levels occurred, LPO and protein carbonyl levels were increased, while MTs level, SOD and CAT activities were decreased. Besides, the GPx, GR, GST, and GSH activities were decreased. Histological alterations in kidney tissue and intense apoptosis in renal tubular cells were observed. These results suggest that DDT sub-acute treatment causes oxidative stress and apoptosis, which may be the chief mechanisms of DDT-induced nephrotoxicity.

Mechanisms of chromium hexavalent-induced apoptosis in rat testes.

Hexavalent chromium (CrVI)-containing compounds, present in industrial settings and in the environment, are known as carcinogens and mutagens. The present study is designed to test the hypothesis that oxidative stress mediates CrVI-induced apoptosis in testis. Male Wistar rats received an intraperitoneal injection of potassium dichromate at doses of 1 and 2 mg kg-1. Superoxide anion production was assessed by the determination of the reduction of cytochrome c and iodonitrotetrazolium, lipid peroxidation (LPO), metallothioneins (MTs), and catalase (CAT) activity. Apoptosis was evaluated by DNA fragmentation detected by agarose gel electrophoresis. Germinal cells apoptosis was detected by toluidine blue staining. The expression of Bax and Bcl-2 proteins (Pts) was also investigated. After 15 days of treatment, an increase of LPO and MT levels occurred, while CAT activity was decreased. Testicular tissues of treated rats showed pronounced degradation of the DNA into oligonucleotides as seen in the typical electrophoretic DNA ladder pattern. Intense apoptosis was observed in germinal cells of Cr-exposed rats. Bax Pt expression was induced in spermatogonia and spermatocytes cells of CrVI-treated rats. In contrast, Bcl-2 Pt was occasionally observed in germ cells of CrVI-exposed rats. These results clearly suggest that CrVI subacute treatment causes oxidative stress in rat testis leading to apoptosis.

Chamomile decoction extract inhibits human neutrophils ROS production and attenuates alcohol-induced haematological parameters changes and erythrocytes oxidative stress in rat.

BACKGROUND: The aim of this study was to evaluate the protective effects of subacute pre-treatment with chamomile (Matricaria recutita L.) decoction extract (CDE) against stimulated neutrophils ROS production as well as ethanol (EtOH)-induced haematological changes and erythrocytes oxidative stress in rat. METHODS: Neutrophils were isolated and ROS generation was measured by luminol-amplified chemiluminescence. Superoxide anion generation was detected by the cytochrome c reduction assay. Adult male wistar rats were used and divided into six groups of ten each: control, EtOH, EtOH + various doses of CDE (25, 50, and 100 mg/kg, b.w.), and EtOH+ ascorbic acid (AA). Animals were pre-treated with CDE extract during 10 days. RESULTS: We found that CDE inhibited (P ≤ 0.0003) luminol-amplified chemiluminescence of resting neutrophils and N-formyl methionylleucyl-phenylalanine (fMLF) or phorbolmyristate acetate (PMA) stimulated neutrophils, in a dose-dependent manner. CDE had no effect on superoxide anion, but it inhibited (P ≤ 0.0004) H2O2 production in cell free system. In vivo, CDE counteracted (P ≤ 0.0034) the effect of single EtOH administration which induced (P < 0.0001) an increase of white blood cells (WBC) and platelets (PLT) counts. Our results also demonstrated that alcohol administration significantly (P < 0.0001) induced erythrocytes lipoperoxidation increase and depletion of sulfhydryl groups (-SH) content as well as antioxidant enzyme activities as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). More importantly, we found that acute alcohol administration increased (P < 0.0001) erythrocytes and plasma hydrogen peroxide (H2O2), free iron, and calcium levels while the CDE pre-treatment reversed increased (P ≤ 0.0051) all these intracellular disturbances. CONCLUSIONS: These findings suggest that CDE inhibits neutrophil ROS production and protects against EtOH-induced haematologiacal parameters changes and erythrocytes oxidative stress. The haematoprotection offered by chamomile might involve in part its antioxidant properties as well as its opposite effect on some intracellular mediators such as H2O2, free iron, and calcium.

Ameliorative and antioxidant effects of myrtle berry seed (Myrtus communis) extract during reflux-induced esophagitis in rats.

Context Myrtle, Myrtus communis L. (Myrtaceae), is a medicinal plant well known for its richness in phenolic compounds and its beneficial effects for the treatment of gastrointestinal disorders.Objective In the present work, the protective effect of the myrtle berry seed aqueous extract (MBSAE) against esophageal reflux (ER)-induced damage in esophagus mucosa as well as the mechanisms implicated was determined.Materials and methods In this respect, adult male Wistar rats were used and divided into seven groups: Control, ER, ER + various doses of MBSAE, ER + famotidine or ER + gallic acid. The ER was induced and animals were per orally (p.o.) treated with MBSAE or reference molecules during 6 h. The phytochemical screening was determined using colourimetric analysis.Results MBSAE is rich in total polyphenols and anthocyanins and exhibited an important in vitro antioxidant activity. In vivo, we firstly found that ER led to marked macroscopic and histopathological changes in esophagus. The results showed, also, that the ER was accompanied by a state of oxidative stress as assessed by an increase of lipid peroxidation, a decrease of the sulphhydryl groups and glutathione levels, as well as antioxidant enzyme activities depletion. MBSAE abrogated all morphological, histopathological and biochemical alterations. We showed also that ER increased esophageal calcium, hydrogen peroxide (H2O2) and free iron levels while MBSAE treatment protected against intracellular mediators deregulation.Conclusion Our data suggest that MBSAE exerted a potential protective effect against ER-induced damage in rat esophagus, at least in part, due to its antioxidant properties.

Does static magnetic field-exposure induced oxidative stress and apoptosis in rat kidney and muscle? Effect of vitamin E and selenium supplementations.

Static magnetic fields (SMFs) effect observed with radical pair recombination is one of the well-known mechanisms by which SMFs interact with biological systems. Our aim was to study whether SMF induces oxidative stress and apoptosis in rat tissues and to evaluate the possible protector effect of selenium (Se) and vitamin E (vit E) supplementations. Rats were randomly divided into control, SMF-exposed, Se-treated, vit E-treated, SMF exposed rats and co-treated with Se, and SMF exposed rats and co-treated with vit E. After animal sacrifice, catalase (CAT) activity and malondialdehyde (MDA) concentration were measured and apoptosis inducing factor (AIF) immunohistochemical labeling was performed in kidney and muscle. Exposure of rats to SMF (128 mT, 1 h/day for 5 days) increased the MDA concentrations (+25%) and CAT activities (+34%) in kidney but not in muscle. By contrast, the same treatment failed to induce a caspase-independent pathway apoptosis in both tissues. Interestingly, Se pre-treatment inhibited the increase of MDA concentrations and CAT activities in kidney in SMF-exposed rats. However, vit E administration corrected only MDA levels in rat kidney. In conclusion, exposure to SMF induced oxidative stress in kidney that can be prevented by treatment with Se or vit E.

Chemical composition, antioxidant properties and hepatoprotective effects of chamomile (Matricaria recutita L.) decoction extract against alcohol-induced oxidative stress in rat.

The present study assessed the chemical composition, antioxidant properties, and hepatoprotective effects of subacute pre-treatment with chamomile (Matricaria recutita L.) decoction extract (CDE) against ethanol (EtOH)-induced oxidative stress in rats. The colorimetric analysis demonstrated that the CDE is rich in total polyphenols, total flavonoids and condensed tannins, and exhibited an important in vitro antioxidant activity. The use of LC/MS technique allowed us to identify 10 phenolic compounds in CDE. We found that CDE pretreatment, in vivo, protected against EtOH-induced liver injury evident by plasma transaminases activity and preservation of the hepatic tissue structure. The CDE counteracted EtOH-induced liver lipoperoxidation, preserved thiol -SH groups and prevented the depletion of antioxidant enzyme activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). We also showed that acute alcohol administration increased tissue and plasma hydrogen peroxide (H(2)O(2)), calcium and free iron levels. More importantly, CDE pre-treatment reversed all EtOH-induced disturbances in intracellular mediators. In conclusion, our data suggest that CDE exerted a potential hepatoprotective effect against EtOH-induced oxidative stress in rat, at least in part, by negatively regulating Fenton reaction components such as H(2)O(2) and free iron, which are known to lead to cytotoxicity mediated by intracellular calcium deregulation.

Hepatoprotective effect of carob against acute ethanol-induced oxidative stress in rat.

The present study was undertaken to determine whether subacute treatment with aqueous extract of carob (Ceratonia siliqua L.) pods (AECPs) protects against ethanol (EtOH)-induced oxidative stress in rat liver. Animals were divided into four groups: control, carob, EtOH and EtOH + carob. Wistar rats were intraperitoneally pretreated with AECP (600 mg/kg body weight (bw)) during 7 days and intoxicated for 6 h by acute oral administration of EtOH (6 g/kg bw) 24 h after the last injection. We found that acute administration of EtOH leads to hepatotoxicity as monitored by the increase in the levels of hepatic marker aspartate aminotransferase and alanine aminotransferase as well as hepatic tissue injury. EtOH also increased the formation of malondialdehyde in the liver, indicating an increase in lipid peroxidation and depletion of antioxidant enzyme activities as superoxide dismutase, catalase and glutathione peroxidase. Subacute carob pretreatment prevented all the alterations induced by EtOH and returned their levels to near normal. Importantly, we showed that acute alcohol increased hepatic and plasmatic hydrogen peroxide and free iron levels. The carob pretreatment reversed EtOH effects to near control levels. These data suggest that carob could have a beneficial effect in inhibiting the oxidative damage induced by acute EtOH administration and that its mode of action may involve an opposite effect on plasma and tissue-free iron accumulation. Indeed, carob can be offered as a food additive to protect against EtOH-induced oxidative damage.