TBARS Levels Research Articles

Spondias tuberosa inner bark extract exert antidiabetic effects in streptozotocin-induced diabetic rats

Ethnopharmacological relevanceDiabetes mellitus (DM) is one of the most important medical emergencies of the 21st century. However, commercially available oral drugs with antidiabetic properties have been limited because of potential side effects, such as: hypoglycemia, weight gain, hepatic dysfunction and abdominal discomfort. As well as antidiabetic drugs, many types of medicinal herbal supplements are utilized as alternative treatments for DM and related comorbidities. Spondias tuberosa Arruda (Anacardiaceae), popularly known as “umbu”, has been used in traditional medicine to treat a vast range of diseases, including DM, infections, digestive disorders, diarrhea and menstrual abnormalities. Aim of the studyThis study evaluated the effect of the hydroethanolic extract of the inner stem bark of Spondias tuberosa (EEStb) in streptozotocin-induced diabetic rats. Materials and methodsDiabetes was induced in rats by a single injection of STZ (40 mg/kg i.p.). Diabetic rats were treated with 250 mg/kg or 500 mg/kg of the EEStb for 21 days. Water intake, urinary volume, body weight, as well as biochemical parameters, such as cholesterol total (TC), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), hepatic and muscle glycogen urea, alanine and aspartate aminotransferase, total protein, albumin, and glucose blood levels, were analyzed. We also determined the hepatic antioxidant state, as well as both of insulin and glucose tolerance. ResultsThe extract was evaluated by HPLC, and the major components of EESTb were identified (i.e. gallic acid and quercetin). The 500 mg/kg dosage of EEStb significantly decreased fasting blood glucose and post-prandial glucose. The EEStb also reduced urinary volume, food and water intake, as well as decreased body weight gain. Diabetic rats that received EEStb had a lower loss of muscle mass and white adipose tissue. Additionally, EEStb improved the urinary excretion of urea and glucose. The extract significantly decreased triglycerides, total cholesterol and VLDL in diabetic rats. However, no significant effect was observed on the levels of total and HDL cholesterol. EEStb treatment prevented hepatotoxic diabetic-induced, improved GSH:GSSG ratio, SOD and CAT activity as well as reduced nitrite and TBARs levels. ConclusionsOur results demonstrate that EEStb has antioxidant and hepatoprotective effects as well as improves insulin sensibility in diabetic rats. This indicates that S. tuberosa could be a potential resource for alternative therapies in the treatment of hyperglycemic conditions. These results also support the use of EEStb in ethnomedicine for the management of diabetes.

Short-term 2.1 GHz radiofrequency radiation treatment induces significant changes on the auditory evoked potentials in adult rats

Purpose: There is a growing interest in the usage of radiofrequency radiation (RF) as a noninvasive brain stimulation method. Previously reported data demonstrated that RF exposure caused a change in brain oscillations. Therefore, we aimed to investigate effects of RF on brain oscillation by measuring the auditory response of different brain regions in rats.Materials and methods: Rats were randomly divided into three groups (n = 12 per each group): Cage control (C), sham rats (Sh), and rats exposed to 2.1 GHz RF for 2 h/day for 7 days. At the end of the exposure, auditory evoked potentials (AEPs) were recorded at different locations in rats. Latencies and amplitudes of AEPs, evoked power, inter-trial phase synchronization, and auditory evoked gamma responses were obtained in response to an auditory stimulus. Furthermore, TBARS levels and 4-HNE, GFAP, iNOS, and nNOS expressions were evaluated in all groups.Results: Peak-to-peak amplitudes of AEPs were significantly higher in the RF group compared with the Sh group. There is no significant difference in peak latencies of AEPs between groups. Beside, evoked power, inter-trial phase synchronization, and auditory evoked gamma responses were significantly higher in the RF group compared with the Sh group. In addition, the RF group had significantly lower TBARS and 4-HNE levels than the Sh group. There were no significant differences between groups for GFAP, nNOS, and iNOS levels, and between the C and RF groups for all parameters.Conclusions: Our present findings suggest that short-term RF treatment under chosen experimental conditions have statistically significant effect on neuronal networks of rats by probably reducing oxidative damage. However, this effect must be further studied for possible noninvasive brain stimulation.

Selenothymidine protects against biochemical and behavioral alterations induced by ICV-STZ model of dementia in mice

The present study evaluated the neuroprotective effects of one selenium-containing AZT derivative compound (S1073) in memory and learning impairment caused by Intracerebroventricular-streptozotocin (ICV-STZ). ICV-STZ in mice causes impairment of energy metabolism with oxidative damage and cholinergic dysfunction, and provides a relevant model for sporadic dementia of Alzheimer's type (AD). Acetylcolinesterase (AChE), Catalase (CAT), dichlorofluorescein oxidation (DCFH), TBARS and thiol content were measured. Swiss adult mice were pre-treated with S1073 [1 mmol/kg] (i.p.) and after 30 min of the injection received a bilateral dose of STZ [11.3 μmol/l]. After 8 days' STZ injection, we performed the behavioral experiments (Beaker test, Open field and Morris water maze task). ICV-STZ caused significant learning and memory impairments, which were significantly improved by S1073 pre-treatment. A significant increase in cerebral DFCH, TBARS levels and AChE activity and a disturbance in the memory and learning were observed in ICV-STZ injected animals. S1073 significantly ameliorated all alterations induced by ICV-STZ in mice. All these findings support the neuroprotective role of S1073 in mice model of Alzheimer's dementia-type induced by ICV-STZ, which may be associated with its antioxidant activity and/or with its inhibitory effect in brain AChE. In fact, in silico analysis indicated that S1073 may be an inhibitor of AChE.

Effect of daily intake of a low-alcohol orange beverage on cardiovascular risk factors in hypercholesterolemic humans

Oxidative stress, inflammation status, endothelial dysfunction, and imbalanced lipid metabolism play a major role in cardiovascular disease. Bioactive compounds and moderate alcohol consumption have been associated with decreased cardiovascular risk. This study aimed to evaluate the effect on cardiovascular risk factors of a low-alcohol beverage derived from the alcoholic fermentation of orange juice. Eighteen individuals with moderately high cholesterol levels were randomly assigned to an experimental group (n = 9) who drank 500 mL/day of the orange beverage for 2 weeks or a control group (n = 9) who drank no orange beverage. Blood samples were drawn at the beginning and end of the study period. Consumption of the beverage significantly decreased plasma levels of total cholesterol (−15.6%), LDL-cholesterol (−17.8%), LDL-cholesterol/HDL-cholesterol ratio (−21.4%), catalase (−25.5%), TBARS (−42.6%), and sVCAM-1 (−5.8%). This orange beverage would have a potential capacity to improve cardiovascular risk in hypercholesterolemic humans, supporting its future consideration as a functional beverage.

Antioxidative response and photosynthetic performance of common fig (Ficus carica L.) leaves after short-term chilling stress

Common fig (Ficus carica L.) is widely cultivated Mediterranean species. Such warm-climate species are adapted to elevated temperatures and are susceptible to chilling stress (0-12°C) [1]. However, occasional short chilling periods are common during growing season in temperature areas what can affect functionality of the plant [2]. The aim of this work was to investigate influence of short-term low temperature (chilling) on PSII photochemistry and antioxidative response in young, still developing leaves of common fig. Leaves were detached from the tree, acclimated at room temperature in dark for 12h and then exposed to low temperature (10°C) and low irradiation (50 µmolm-2s-1) for 4h. Dark adapted leaves were considered as the control. Photosynthetic performance was analyzed by measuring in vivo chlorophyll fluorescence increase (JIP test). The production of H2O2, lipid peroxidation (TBARS) and activity of antioxidative enzymes: superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione reductase (GR) and guaiacol peroxidase (GPOD) were measured as well. Maximum quantum yield of PSII (Fv/Fm) and overall photosynthetic performance (PItotal) decreased in leaves exposed to the chilling stress. Exposure to low temperature decreased absorption of light energy (ABS), trapping (TR0) of absorbed light energy and electron transport (ET0) further than primary acceptor (QA-) while energy dissipation (DI0) remained the same compared to the control. Moreover, reduction of the end electron acceptor (RE0) at photosystem I (PSI) also decreased after exposure to low temperature. The obstruction of photosynthetic electron transport flow is well documented reason for increased H2O2 production in leaves exposed to short-term chilling stress [1, 3]. In spite of increased H2O2 accumulation, the increase in TBARS level was not observed in the investigated leaves. Low temperatures inhibited activities of SOD and GPOD, while the CAT, APX and GR activities increased compared to the control. Our results suggest that antioxidative system was enough efficient to prevent the oxidative damage in biomembranes of fig leaves exposed to the chilling stress at 10°C.

Effects of melatonin on thymic and oxidative stress dysfunctions during Trypanosoma cruzi infection.

Although the exact etiology of Chagas disease is not completely elucidated, thymic atrophy and oxidative stress are believed to be important contributors to the pathogenesis during acute Trypanosoma cruzi (T.cruzi) infection. We hypothesized that exogenous melatonin, administered by gavage (5mg/kg, p.o., gavage) to young (5weeks old) and middle-aged (18months old) male Wistar rats, would modulate thymic oxidative damage and reverse the age-related thymus regression during T.cruzi acute infection. Increased levels of superoxide anion (O2- ) were detected in the thymus of infected animals, and treatment with melatonin reverted this response. We found reduced TBARS levels as well as a significant increase in superoxide dismutase (SOD) activity in the thymus of all middle-aged melatonin-treated animals, infected or not with T.cruzi. Furthermore, melatonin increased the thymic expression of SOD1 and SOD2 in middle-aged control animals. Nox2 expression was not affected by melatonin treatment in young or middle-aged animals. Melatonin reverted the age-related thymic regression as revealed by the increase in thymus weight, total number of thymocytes, and reduction in age-related accumulation of double-negative thymocytes. This is the first report to directly examine the effects of melatonin treatment on the thymic antioxidant/oxidant status and thymic changes during T.cruzi infection. Our results revealed new antioxidant features that turn melatonin a potentially useful compound for the treatment of Chagas disease, a condition in which an excessive oxidative damage occurs.

Copper Increases Brain Oxidative Stress and Enhances the Ability of 6-Hydroxydopamine to Cause Dopaminergic Degeneration in a Rat Model of Parkinson's Disease.

Redox properties enable copper to perform its essential role in many biological processes, but they can also convert it into a potentially hazardous element. Its dyshomeostasis may have serious neurological consequences, and its possible involvement in Parkinson's disease and other neurodegenerative disorders has been suggested. The in vitro and ex vivo ability of copper to increase oxidative stress has already been demonstrated, and the aim of the present study was to assess in vivo the capacity of copper to cause brain oxidative damage and its ability to increase the dopaminergic degeneration induced by 6-hydroxydopamine. We found that chronic copper administration (10mgCu2+/kg/day, IP) causes its accumulation in different brain areas (cortex, striatum, nigra) and was accompanied by an increase in TBARS levels and a decrease in protein free-thiol content in the cortex. A decrease in catalase activity and an increase in glutathione peroxidase activity were also observed in the cortex. The intrastriatal administration of Cu2+ caused an increase in some indices of oxidative stress (TBARS and protein free-thiol content) in striatum and nigra, but was unable to induce dopaminergic degeneration. However, when copper was intrastriatally coadministered with 6-hydroxydopamine, it increased dopaminergic degeneration, a fact that was also accompanied by an increase in the assayed indices of oxidative stress, a decrease in catalase activity, and an augmentation in glutathione activity. Evidently, copper cannot cause neurodegeneration per se, but may potentiate the action of other factors involved in the pathogenesis of Parkinson's disease through oxidative stress.

Protective role of eugenol on arsenic induced oxidative DNA damage and modulatory effect of GSTO2 polymorphism

Arsenic exposure is one of the major health problem worldwide. It is related with various cancers and numerous other pathological effects. The present work was aimed to study the ameliorative effects of eugenol against arsenic mediated oxidative DNA damage using Sister chromatid exchanges (SCE), comet, and lipid peroxidation assays as biomarkers. For the genotyping of GSTO2, PCR RFLP method was used. The treatment with sodium arsenite showed dose dependent increase in frequency of SCE, comet tail moment (Tm), and lipid peroxidation (TBARS levels). On administration of eugenol (10 and 20 µM) significant dose dependent decrease in the number of SCE, Tm value, and TBARS levels observed in arsenic treated cultured peripheral blood lymphocytes. Nonsignificant effects of GSTO2 polymorphism perceived on arsenic genotoxicity and eugenol antigenotoxicity. The results of the present work suggest a protective role of eugenol against arsenic induced genotoxic and oxidative damage in cultured human peripheral blood lymphocytes. Practical application Arsenic contamination of groundwater is one of the leading environmental issues worldwide. Chronic exposure of arsenic cause several health problems including tumor manifestation. The results of the present study suggest the use of indigenous dietary elements, herbs, shrubs as a safer and effective preventative medicine against heavy metal induced genotoxicity and oxidative stress.

Fungicide tolerant Bradyrhizobium japonicum mitigate toxicity and enhance greengram production under hexaconazole stress

Bacterial strain RV9 recovered from greengram nodules tolerated 2400μg/mL of hexaconazole and was identified by 16S rDNA sequence analysis as Bradyrhizobium japonicum (KY940048). Strain RV9 produced IAA (61.6μg/mL), ACC deaminase (51.7mg/(protein·hr)), solubilized TCP (105μg/mL), secreted 337.6μg/mL EPS, and produced SA (52.2μg/mL) and 2,3-DHBA (28.3μg/mL). Exopolysaccharides produced by strain RV9 was quantified and characterized by SEM, AFM, EDX and FTIR. Beyond tolerance limit, hexaconazole caused cellular impairment and reduced the viability of strain RV9 revealed by SEM and CLSM. Hexaconazole distorted the root tips and altered nodule structure leading thereby to reduction in the performance of greengram. Also, the level of antioxidant enzymes, proline, TBARS, ROS and cell death was increased in hexaconazole treated plants. CLSM images revealed a concentration dependent increase in the characteristic green and blue fluorescence of hexaconazole treated roots. The application of B. japonicum strain RV9 alleviated the fungicide toxicity and improved the measured plant characteristics. Also, rhizobial cells were localized inside tissues as revealed by CLSM. Colonization of B. japonicum strain RV9 decreased the levels of CAT, POD, APX, GPX and TBARS by 80%, 5%, 13%, 13% and 19%, respectively over plants grown at 80μg/(hexaconazole·kg) soil. The ability to detoxify hexaconazole, colonize plant tissues, secrete PGP bioactive molecules even under fungicide pressure and its unique ability to diminish oxidative stress make B. japonicum an attractive choice for remediation of fungicide polluted soils and to concurrently enhance greengram production under stressed environment.

The beneficial effects of 18β-glycyrrhetinic acid on the experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mouse model

Aim: The aim of this study was to investigate the beneficial effects of 18β-glycyrrhetinic acid (GA) on the experimental allergic encephalomyelitis (EAE) in C57BL/6 mice. GA is a natural substance found in the root of licorice and is used in traditional Chinese medicine. It has many pharmacological activities such as antioxidant, anti-inflammatory, and anti-cancer effects.Materials and methods: A total of 40 C57BL/6 mice were divided equally into four groups: (1) Control, (2) EAE, (3) GA and (4) GA + EAE. 14 days after induction of EAE with MOG35-55 and pertussis toxin, mice were treated with GA at doses of 100 mg/kg/day for 7 days intraperitoneally.Results: To our results, oxidative stress and lipid peroxidations (elevated TBARS levels, decreased GPx, SOD, CAT, and GSH levels) were significantly (p < .01) increased, causing EAE in brain tissue. Also, histopathological damage (Caspase-3 and IL-17 activity, p ≤ .01) and cytokine levels (TNF-α and IL-1β, p < .01) were induced with EAE in mice brain tissue. On the other hand, GA treatment significantly (p < .01) reversed oxidative histological and immunological alterations caused by EAE.Conclusions: In conclusion, the GA treatment can protect the brain tissue against EAE in mice with its antioxidant and anti-inflammatory properties.

Roles of selenoprotein K and selenium status in the etiopathogenesis of preeclampsia: Their relationships with maternal lipid peroxidation, oxidative DNA damage, and glutathione peroxidase

Abstract. Objective: Preeclampsia (PE) is a complex disease and the underlying mechanisms are not known yet. It is well known that selenium and oxidative stress play a role in the pathogenesis of various diseases as well as PE. The aim of the study was to investigate the changes in selenium status, as an essential trace element, and selenoprotein K (SelK), a newly described selenoprotein which has been suggested to have an antioxidant function in some tissues in patients with preeclampsia. We also aimed at investigating their relationships with maternal lipid peroxidation, oxidative DNA damage, and glutathione peroxidase (GPx) activities. Materials and methods: 38 healthy pregnant and 48 pregnant women with PE were included in the study. Serum selenium levels were measured by graphite-furnace atomic absorption spectrophotometry. Plasma TBARS levels were analyzed by spectrophotometric method; GPx activities, 8OHdG, and SelK levels were determined by ELISA. Results: Plasma TBARS and 8OHdG levels were found to be increased in the PE group compared to the healthy pregnant group. Plasma SelK levels and GPx activities were found to be lower in the PE group than in the healthy control group. However, there was no significant difference in serum selenium levels between two groups. Furthermore, a significant correlation was determined between plasma SelK levels and GPx activities in PE patients group (r = 0.743; p < 0.01). Likewise, a significant positive correlation was found between plasma 8OHdG and TBARS levels (r = 0.457; p < 0.01), serum selenium levels and plasma GPx activities (r = 0.663; p < 0.01), serum selenium and plasma SelK levels (r = 0.851; p < 0.01) in PE. Conclusion: Our findings indicated that a selenoprotein SelK and a selenoenzyme GPx play a role in the etiopathogenesis of PE. Decreases in these antioxidant systems were associated with increase in lipid and DNA oxidation in PE patients. Underlying mechanisms of SelK and its interactions with selenium status and GPx in PE should be clarified in details with further studies.

Energy drink and alcohol combination leads to kidney and liver alterations in rats

The aim of this study was to evaluate the acute toxicity of the association of energy drink and alcohol in male Wistar rats. Animals were treated by oral gavage with 10 ml/kg distilled water (control); 10 ml/kg energy drink (ED10); 3.2 mg/kg caffeine + 40 mg/kg taurine; 2 g/kg alcohol 20%; 2 g/kg alcohol 20% + ED10; and 2 g/kg alcohol 20% + 3.2 mg/kg caffeine + 40 mg/kg taurine. Behavioral alterations were observed for 6 h after treatment. Animals presented significant differences in the frequency of rearing, ambulation, grooming, wakefulness and tachypnea along time. Caffeine + taurine increased the levels of TBARS and total thiols in kidneys. ED10 increased lipoperoxidation in liver. The association of ED10 + alcohol induced nephrotoxicity observed by the increase of urinary N-acetyl-β-d-glucosaminidase (NAG) activity. Histopathological analysis showed the presence of congestion and hydropic and hyaline degenerations in the livers of ED10 + alcohol treated rats, and hemorrhage in the liver of alcohol + caffeine + taurine group. In kidneys, hyaline degeneration was observed in ED10; ED10 + alcohol; caffeine + taurine; and alcohol + caffeine + taurine. Hemorrhage was present in the kidneys of all groups. The combination of energy drinks and alcohol is not safe for the consumers. Therefore, precautionary measures should be disseminated among risk populations, especially the teenagers.

Induction chemotherapy reduces extracellular heat shock protein 72 levels, inflammation, lipoperoxidation and changes insulin sensitivity in children and adolescents newly diagnosed with acute lymphoblastic leukemia.

BackgroundAcute lymphoblastic leukemia (ALL) is associated with higher levels of pro-inflammatory cytokines and oxidative stress. Recently, the levels of extracellular heat shock protein 72 (eHSP72) were found to be elevated in ALL, and its elevation associated with poor prognosis. Therefore, considering the possible role of eHSP72 as a modulator of the immunological system and metabolism, the aim of this study was to describe the response of eHSP72 to the induction phase of chemotherapy, along with metabolic, inflammatory and oxidative stress markers, in children and adolescents newly diagnosed with ALL.MethodsNineteen patients were recruited and analysed before and after the induction phase of chemotherapy (with 28 days of duration). Blood samples were taken for the analysis of C-reactive protein (CRP), levels of lipoperoxidation, insulin (and HOMA-IR), cortisol, glucose, lipid profile and eHSP72.ResultsWe found that induction phase of chemotherapy leads to a drop in glucose levels (from 101.79±19 to 75.8±9.7 mg/dL), improvements on inflammation (CRP levels, p<0.01) and oxidative stress (TBARS levels, p<0.01), reduction on eHSP72 (p=0.03) and improved insulin sensitivity (HOMA-IR, p=0.02).ConclusionOur results indicate that eHSP72 may have an immune and metabolic role and could be used as a marker of the treatment success and metabolic changes in children with ALL.

L-Amino acid oxidase from Cerastes vipera snake venom: Isolation, characterization and biological effects on bacteria and tumor cell lines

A homodimeric l-amino acid oxidase enzyme (Cv-LAAOI) was isolated from the venom of Cerastes vipera (Egyptian Sand viper) using gel filtration followed by anion exchange chromatography. The molecular mass of Cv-LAAO is 120 kDa in its native form and 60 kDa in its monomeric form. The optimum enzyme activity was achieved on l-Leucine as a substrate in 50 mM buffer pH 7.5 at 50 °C. The Cv-LAAOI activity was significantly reduced by increasing the temperature over 40 °C, lost 75% of its activity at 60 °C and inhibited completely at 80 °C. The Cv-LAAOI attains the highest substrate specificity towards L-Met. The results have also indicated that Mn2+ enhances the enzyme activity by 10%, while Cu2+, Hg2+, Ni2+, Co2+ have suppressive effects on the Cv-LAAOI activity. On the other hand, EDTA has no significant effect on the enzyme activity. The kinetic parameters of Cv-LAAOI activity (Km, Kcat and Vmax) estimated on l-Leucine at pH 8 and 37 °C were found to be 2 mM, 12 S−1 and 16.7 μmol/min/ml, respectively. In addition, the results have shown that Cv-LAAOI exhibits a significant bactericidal activity against gram-positive and gram-negative bacteria, particularly Staphylococcus aureus and Escherichia coli with MIC values of 20 μg/ml. Moreover, Cv-LAAOI has exhibited a considerable cytotoxic activity against breast cancer cell line (MCF-7) with IC50 value 2.75 ± 0.38 μg/ml compared with different tumor cell lines (liver HepG2, lung A549, colon HCT116 and prostate PC3). Furthermore, Cv-LAAOI has triggered antiproliferative activity via extensive H2O2 generation as indicated by the increase in H2O2 and TBARS levels accompanied by the depletion in the catalase activity (CAT) in MCF-7 treated cells compared to the untreated ones. Thus, these findings clearly indicate that Cv-LAAOI has a selective cytotoxic effect on breast cancer cell line, demonstrating a great prospective for future use in cancer therapy.

POSSIBLE EFFECT OF DATE PALM FRUIT EXTRACT ON SOMEBIOCHEMICAL AND HEMATOLOGICAL PARAMETERS IN RATS INTOXICATED WITH METHOMYLINSECTICIDE

The present work was designed to evaluate the protective role of date palm extract (DPE) as an antioxidant against toxicity induced with different doses; 1/5 LD50 and 1/10 LD50 of the methomyl. The changes in antioxidant parameters (SOD and CAT activities and GSH concentration) in addition to level of TBARS as an index of lipid peroxidation and NO concentration were investigated. In addition, the alteration in liver functions (ALAT, ASAT, ALP, TBIL,GGT, albumin, globulin and total proteins) was assessed. Also, some hematological parameters such as RBCs, WBCs count, lymphocyte, monocytes, neutrophils, platelets count, Hb concentration and HCT were measured. A patch of 42 male Wistar albino rats of average weight (125±5g) at the beginning of the experiment was divided into 7 main groups; I: control group, II:DPE group, rats were treated orally with DPE at a dose (1 g/k/day)for 2 weeks, III: DPE group, rats were treated orally with DPE at a dose (1 g/k/day) for 4 weeks. Methomyl groups; IV: rats were intoxicated with a 1/5LD50 for 2 weeks V: rats were intoxicated with a 1/10LD50for two weeks, VI: groups treated with DPE for two weeks as a protection before given DPE and methomyl1/5LD50for two weeks, VII: groups treated with DPE for two weeks as a protection before given DPE and methomyl 1/10LD50for two weeks. Each group contains 6 rats. The results showed a significant rise in TBARS, NO, ALAT, ASAT, ALP, GGT, and TBIL, while a significant reduction in some other parameters (CAT, SOD, GSH, Total protein, albumin).Significant decreases in some hematological parameters (RBCs, Hb, HCT and PLT, WBCs and lymphocytes) were reported. Also, the results showed a significant increase in neutrophils and eosinophils atin rats intoxicated with methomyl when compared to the control groups. The administration of the DPE ameliorated the deteriorative effects of the methomyl. In conclusion, the results obtained revealed that the administration of DPE had hepatoprotective effects against methomyl insulet in male Wistar albino rats by inhibiting oxidative stress through ROS scavenging activity and improvement of the biochemical markers.

Hypochlorite modified albumins promote cell death in the tubule interstitium in rats via mitochondrial damage in obstructive nephropathy and the protective effects of antioxidant peptides

A major feature of the injury sustained by the kidney during obstructive nephropathy is a profound induction of apoptosis in the tubular epithelium. In this study, we explored the central roles of mitochondria and the mechanism of the protective effect of the mitochondrial targeted peptides in tubular cell apoptosis and interstitial fibrosis during obstructive nephropathy. Unilateral ureter obstruction (UUO) was performed on rats, and the animals were randomly assigned to intravenous treatment with normal saline, rat serum albumin (RSA), or HOCl-rat serum albumin (HOCl-RSA) in the presence or absence of SS-31. A sham-operation control group was set up by left ureteral dissociation but not ligation. Compared with the control group, UUO animals displayed fibrotic abnormalities, accompanied by increased expression of collagen-I, fibronectin, α-SMA protein and mRNA in the renal interstitium. They also displayed oxidative stress, as evidenced by increased levels of HOCl-alb, TBARS, and mitochondrial reactive oxygen species (ROS) and a decrease in MnSOD activity in the renal homogenate. Damage to mitochondrial structure and functions was observed, as evidenced by a decrease in the mitochondrial membrane potential (MMP), ATP production, mtDNA copy number alterations and release of cytochrome C (cyto C) from the mitochondria to the cytoplasm. These changes were accompanied by activation of caspase-3, caspase-7, caspase-9, and PARP-1 and increased apoptotic cells in the proximal tubules. HOCl-RSA challenge further exacerbated the above biological effects in UUO animals, but these effects were prevented by administration of SS-31. These data suggested that accumulation of HOCl-alb may promote tubular cell apoptosis and interstitial fibrosis, probably related to mitochondrial oxidative stress and damage, and that SS-31 might contribute to apoptotic pathway suppression via scavenging of ROS in the mitochondria.

Bioactive Compounds of Kimchi Inhibit Apoptosis by Attenuating Endoplasmic Reticulum Stress in the Brain of Amyloid β-Injected Mice

This study investigated the inhibitory effects of kimchi bioactive compounds against endoplasmic reticulum (ER) stress-induced apoptosis in amyloid beta (Aβ)-injected mice. Mice received a single intracerebroventricular injection of Aβ25-35, except for the normal group. Mice were subjected to oral administration of 10 mg of capsaicin, 50 mg of 3-(4'-hydroxyl-3',5'-dimethoxyphenyl)propionic acid (HDMPPA), 50 mg of quercetin, 50 mg of ascorbic acid, or 200 mg of kimchi methanol extract (KME) per kilogram of body weight for 2 weeks ( n = 7 per group). In the in vitro blood-brain barrier (BBB) permeability test, all bioactive compounds penetrated the BBB except ascorbic acid. The protein expression level of APP, BACE, and p-Tau elevated by Aβ injection was decreased by kimchi bioactive compounds ( P < 0.05). Quercetin, HDMPPA, and KME decreased oxidative stress, as indicated by ROS and TBARS levels ( P < 0.05). The protein expression level of ER stress markers GRP78, p-PERK, p-eIF2α, XBP1, and CHOP and the proapoptotic molecules Bax, p-JNK, and cleaved caspases-3 and -9 decreased ( P < 0.05). In contrast, the protein expression level of antiapoptotic molecules Bcl2 and cIAP increased ( P < 0.05). These results were supported by histological analysis.

Oxidative stress markers and thrombomodulin plasma levels in women with early and late severe preeclampsia

BackgroundPreeclampsia (PE) is a pregnancy disease associated with oxidative stress and endothelial dysfunction. It can be classified according to the severity and onset-time of clinical symptoms (early PE:<34 weeks, late PE:≥34 weeks). MethodsWe evaluated markers of oxidative stress (thiobarbituric acid reactive substances-TBARs and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide)-MTT) and endothelial lesion (thrombomodulin-TM) in early (N = 24) and late severe PE(N = 22) and normotensive pregnant women(N = 26). ResultsMTT levels were higher in early sPE than in normotensive pregnancy (P = 0.03). No difference was found comparing late sPE versus normotensive pregnancy, and early sPE versus late sPE. TM levels were higher in early sPE comparing to late sPE women (P = 0.05), but no difference was found between early or late sPE versus normotensive groups. TBARs levels did not differ significantly among the three groups. These data suggest that endothelial lesion and the antioxidant status are more pronounced in early sPE. Moreover, lipid peroxidation might be an early event in PE, stimulating a compensatory antioxidant defense later in pregnancy. ConclusionsLongitudinal studies involving pregnant women with risk factors for PE development and including other methods for oxidative stress and endothelial lesion determination should be conducted in order to better evaluate the role of these processes in PE pathogenesis.

The ameliorative effect of Homalium nepalense on carbon tetrachloride-induced hepatocellular injury in rats

The purpose of this study was to evaluate ameliorative effects of Homalium nepalense Benth. (Flacourtiaceae) on CCl4-induced hepatocellular injury in rats. Oxygen-radical absorbance-capacity (ORAC) and cell-based-antioxidant-protection-in-erythrocytes (CAP-e) were performed and found that the ethyl acetate fractions of bark (HNEB) and leaf (HNEL) showed a remarkable degree of antioxidant activities in a dose dependent manner. Antioxidant potential HNEB was higher than HNEL and was comparable with trolox. HNEB and HNEL at 300 and 400 mg/kg showed significant hepatoprotective activities against CCl4-induced hepatotoxicity as evidenced by restoration of SGOT, SGPT, ALP, TB and TP level. The level of TBARS, SOD, CAT and GSH were significantly improved and restored towards normal value. Both fractions at 400 mg/kg showed remarkable improvements in marker levels as comparable to silymarin. Histopathological observations of liver tissues revealed the reduction of necrosis with appearance of sinusoidal space, central vein, and bile duct both in case of HNEB and HNEL. GC–MS and LC–MS confirmed occurrence of a total 53 no. of phytocompounds in HNEB and HNEL. Based on their retention times-(RT) and mass-to-charge-ratios-(m/z), some of the major bioactive compounds were catechol (5.89%), 5-hydroxymethylfurfural (5.87%), salicylic acid (4.89%), eugenol (1.60%), doconexent (0.31%), β-sitosterol (1.59%), 2,3-dihydro-3,5-dihydroxy-6-methyl-4H-pyran-4-one (1.15%), coniferyl alcohol (2.99%), hexadecanoic acid methyl ester (1.05%), and betulin (1.20%). H. nepalense possesses significant hepatoprotection effect because of its antioxidant constituents.

Effect of lutein on lipid profile in hypercholesterolemic rats

Background: Hyperlipidemia or Dyslipidemia is the major cause of atherosclerosis1 and associated conditions. Low levels of high-density-lipoprotein cholesterol (HDL-C) are the major causes of increased atherogenic risk 1. Aggressive cholesterol reduction in patients with atherosclerotic disease is now the standard of care2. In addition to life style modification, patients with risk factors need lipid lowering drug therapy. The drugs available now do not reduce LDL oxidation, and oxidative stress associated with hyperlipidemia. In recent years, antioxidants have been subjected to epidemiological studies4 that have related their consumption to a reduction in the incidence of oxidative damage related diseases.Methods: Hypercholesterolemia was induced in rats by administration of high cholesterol diet for 30 days in standard rat chow diet. Rats were divided into four groups of six each. Group-I and II with intake of normal diet and High cholesterol diet respectively. Group III and IV are given high cholesterol diet along with Lutein 50mg/kg and Atorvastatin 5mg/kg orally once daily respectively. At the end of 30 days animals were subjected to overnight fasting. Blood samples were drawn by retro-orbital puncture for biochemical analysis. The animals were sacrificed after thiopentone injection and liver and aorta were dissected out and processed for histopathological study and biochemical analysis.Results: Lutein treated group showed even more significant reduction in TBARS levels than the normal control group and Atorvastatin treated group. The efficacy of Lutein in slowing down the atherosclerosis and fatty infiltration of liver is proved in this study.Conclusions: Hence the present study had shown significant hypolipidemic, antiatherogenic and antioxidant effect of Luetin in Hyperlipidemic rats.