Increase In TBARS Levels Research Articles

Anti-inflammatory and antioxidative effects of essential oil of Hyptis crenata on the intestinal injuries induced by methotrexate

Methotrexate (MTX) is an important drug for the treatment of cancer and other diseases. However, it induces many gastrointestinal inflammation-related side effects. The essential oil of Hyptis crenata (EOHc) has gastrointestinal protective and anti-inflammatory properties. Therefore, we aimed to investigate the effect of EOHc on MTX-induced intestinal inflammation in rats. Male Wistar rats were administered MTX or Saline for 3 days and EOHc (300 mg/kg) or vehicle for an additional 3 or 7 days. Half of the animal was euthanized 3 days after the end of MTX treatment (inflammation phase) and the remaining half euthanized 4 days later (post-inflammation phase). The MPO levels in the mucositis inflammation-related phase of the MTX-treated group were 284 % of the control in the duodenum (cont: 50,9 ± 9,97 U/mg of protein) and 231 % of the control in the ileum (cont: 30,4 ± 6,60 U/mg of protein). In the EOHc group, the levels were 50 % of control in the duodenum and 113 % in the ileum. During this phase, EOHc prevented the increase in TBARs levels and the decrease in thiol levels in the duodenum and jejunum. In the post-inflammation phase of mucositis, EOHc prevented the gastrointestinal transit alteration and, in general, increased food and water consumption. In conclusion, the observed effects, particularly the anti-inflammatory and antioxidant effects of EOHc, as well as its previously reported low toxicity, position EOHc as a promising candidate for reducing gastrointestinal side effects associated with the use of MTX.

Ameliorative Role of Vitamin C against Cypermethrin Induced Oxidative Stress and DNA Damage in Labeo rohita (Hamilton, 1822) Using Single Cell Gel Electrophoresis.

The present study was undertaken to evaluate cypermethrin (CYP)-induced oxidative stress [reactive oxygen species (ROS) and lipid peroxidation (LPO) in gills, muscles, brain, and liver tissues] and DNA damage/genotoxicity (peripheral blood erythrocytes) in a freshwater teleost rohu (Labeo rohita) and the protective role of vitamin C. The LC50 of CYP against rohu was found to be 4.5 µg/L in a semi-static culture system through probit analysis. Fingerlings of rohu were distributed into four groups (Group 1st served as a control, fed 35% protein basal diet and was not exposed to CYP; Group 2nd was fed a basal diet and exposed to CYP; Group 3rd and Group 4th were fed diets supplemented with vitamin C at the rate of 100 and 200 mg/kg diet, respectively, and exposed to CYP). Fingerlings were reared on a basal and vitamin C-supplemented diet for 28 days prior to exposure to CYP. The results indicate a time-dependent significant increase in ROS and LPO (indicated by time course increase in TBARS level) as well as DNA damage in terms of number of comets, % DNA in tail, tail moment, tail length, and olive tail moment after exposure to LC50 of CYP. However, statistically comparable results in both Groups 1st and 4th indicate the protective role of vitamin C. The results reveal the effectiveness of vitamin C as a feed additive for countering pesticides toxicity in Labeo rohita. The current study indicates CYP as a potential genotoxicant for fish and classifies SCGE as a reliable and sensitive tool for assessing DNA damage.

Acute effect of gold nanoparticles on neuropathic pain in a model of regional complex pain syndrome

We evaluated the effects of gold nanoparticles (AuNPs) administered in the acute phase of an animal model of Complex Regional Pain Syndrome Type I (CRPS-I). Oxidative stress parameters [substances reactive to thiobarbituric acid (TBA-RS), total sulfhydryl content (SH), protein carbonyl content and the activities of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px)] and pain, through mechanical and thermal allodynia, were evaluated in the blood and sciatic nerves of mice. Animals were anesthetized and an elastic tourniquet was used around the left hind paw for 120 minutes, followed by measurements of the mechanical threshold and thermal. Animals received intraperitoneal administrations of AuNPs at concentrations of 2.5 mg/L, 7.0 mg/L and 22.0 mg/L, Ankyrin Transient Potential Receptor 1 (TRPA1) antagonist (HC030031) or saline vehicle after induction of CRPS-I. AuNPs showed significant results in thermal and mechanical anti-allodynic effects on day 1 (2.5 mg/L), days 2 and 3 (7.0 and 22.0 mg/L). The TRPA1 reduced mechanical allodynia (days 1 and 2) and thermal allodynia (days 1, 2 and 3), in addition to reversing the changes caused by CRPS-I in oxidative stress. The CRPS-I model increased TBA-RS, reduced the total sulfhydryl content and increased CAT activity. The results showed that, at all concentrations, AuNPs reversed the increase in CAT. At 7.0 mg/L partially reversed and at 22.0 mg/L completely reversed the increase in TBA-RS levels and at 22.0 mg/L reversed the reduction in sulfhydryl content.

BIOMARKERS OF LIPID AND PROTEIN OXIDATION IN THE MUSCLE TISSUE OF RAINBOW TROUT (ONCORHYNCHUS MYKISS WALBAUM) TREATED IN VITRO WITH ROOT AND STEM EXTRACTS OF GREATER CELANDINE (CHELIDONIUM MAJUS L.)

The main aim of the present study was to evaluate the oxidative stress biomarkers [TBARS, carbonyl derivatives of oxidative modification of proteins (OMP), total antioxidant capacity (TAC)] in the muscle tissue of rainbow trout (Oncorhynchus mykiss Walbaum) after in vitro incubation with the root and stem extracts derived from greater celandine (Chelidonium majus L., CM) (at final concentrations of 5 and 2.5 mg/mL) collected in South Park in Słupsk in the Pomeranian Province (northern part of Poland). The current study demonstrated the increase in TBARS levels after in vitro incubation of rainbow trout muscle tissue with stem and root extracts of CM at a final concentration of 5 mg∙mL-1 compared to untreated control samples. There was a statistically significant increase in TBARS levels compared to controls. We obtained similar results after in vitro incubation with root and stem extracts of CM at a final concentration of 2.5 mg∙mL-1 with rainbow trout muscle tissue, where we also observed a statistically non-significant increase in TBARS levels. There was a decrease in the levels of aldehydic derivatives and ketonic derivatives of OMP in muscle tissue after incubation with extracts from roots and stems of CM at final concentrations of 5 mg∙mL-1 compared to untreated controls. There was a decrease in the levels of aldehydic and ketonic derivatives of OMP in muscle tissue after incubation with extracts from roots and stems of CM at final concentrations of 2.5 mg∙mL-1 compared to untreated controls. TAC levels in rainbow trout muscle tissue after in vitro incubation with extracts of CM roots and stems at final concentrations of 5 and 2.5 mg∙mL-1 were not statistically significantly increased. The present study investigated the antioxidant potential of CM. Extracts from CM roots and stems exert their activity by inhibiting protein damage.

Glucocorticoid-Induced Dose-Dependent Reproductive Impairments in Male Albino Rat

The present study is aimed at elucidating the effect of different doses of Dexamethasone (DEX) on testis and epididymis of male Wistar rats. Thirty-six rats were divided into six groups, each containing six rats: one control (CON), and five groups of rats treated with five (30 μg, 40 μg, 50 μg, 60 μg, 70 μg/100 g body weight) doses of dexamethasone intraperitoneally (i.p.) for twenty-one days. The results revealed a dose-dependent decrease in testes and epididymis weight. DEX-treated rats evidenced significant increase in TBARS levels, this being the highest in 70 μg/100 g body weight (bw) which could be a consequence of the highest level of free radical generation. The activity level of antioxidative enzymes Superoxide Dismutase (SOD), Catalase (CAT), Glutathione (GSH), and protein content significantly declined in dexamethasone-treated rats in a dose-dependent manner. Histological observation revealed different degrees of germ cell degeneration/alterations in testis and epididymis The present finding suggests that exposure to dexamethasone (70 μg/100 g bw) can potentially lead to severe impairments in male reproductive tissues (testis and epididymis) structure and function, which may consequently lead to male infertility.

Effects of Dietary Copper and Escherichia coli Challenge on the Immune Response and Gill Oxidative Balance in the Freshwater Mussel Diplodon chilensis.

Copper is a water and sediment pollutant that can be biomagnified by phytoplankton, and it often co-occurs with fecal bacteria. We addressed the combined effects of copper and Escherichia coli on the immune response and gill oxidative balance of the freshwater mussel Diplodon chilensis. Bivalves were sorted into four groups fed with 1) control algae, 2) bacteria (E. coli), 3) copper-enriched algae (Cu2+ ) algae, and 4) copper-enriched algae followed by bacteria (Cu2+ + E. coli). Cellular and humoral immune and cytotoxic variables were analyzed in hemolymph, and detoxifying/antioxidant enzyme activities (glutathione S-transferase [GST] and catalase [CAT]) and lipid peroxidation (thiobarbituric acid reactive substances [TBARS]) were studied in gill tissue. The total hemocyte number increased after Cu2+ exposure, independently of the E. coli challenge. The proportion of hyalinocytes significantly diminished in the E. coli and Cu2+ groups but not in Cu2+ + E. coli groups; granulocytes significantly increased with E. coli but not with Cu2+ + E. coli treatments. Phagocytic activity was higher in all treatments than in control mussels. Acid phosphatase activity was increased by E. coli and inhibited by Cu2+ and Cu2+ + E. coli. Both E. coli and Cu2+ but not Cu2+ + E. coli augmented alkaline phosphatase activity. The Cu2+ and Cu2+ + E. coli treatments reduced the lysosomal membrane stability and cell viability. Humoral bacteriolytic and phenol oxidase activities were not affected by any treatment. The Cu2+ treatment induced gill CAT and GST activities and increased TBARS levels. The Cu2+ + E. coli treatment reversed this CAT and GST stimulation and increased the Cu2+ effect on TBARS. Dietary Cu2+ affects bivalves' immunological and oxidative status and impairs defensive responses against bacteria. In turn, E. coli potentiates the gill oxidative effects of Cu2+ . Environ Toxicol Chem 2023;42:154-165. © 2022 SETAC.

Chlorpyrifos stimulates ABCC-mediated transport in the intestine of the rainbow trout Oncorhynchus mykiss

The organophosphorus pesticide chlorpyrifos, detected in water and food worldwide, has also been found in the Río Negro and Neuquén Valley, North Patagonia, Argentina, where the rainbow trout, Oncorhynchus mykiss, is one of the most abundant fish species. We analyzed whether chlorpyrifos affects the transport activity of the ATP-binding cassette protein transporters from the subfamily C (ABCC), which are critical components of multixenobiotic resistance.We exposed ex vivo O. mykiss middle intestine strips (non-polarized) and segments (polarized) for one hour to 0 (solvent control), 3, 10, and 20 μg L−1 and to 0, 10, and 20 μg L−1 chlorpyrifos, respectively. We estimated the Abcc-mediated transport rate by measuring the transport rate of the specific Abcc substrate 2,4-dinitrophenyl-S-glutathione (DNP-SG). In addition, we measured the enzymatic activity of cholinesterase, carboxylesterase, glutathione-S-transferase, and 7-ethoxyresorufin-O-deethylase (EROD, indicative of the activity of cytochrome P450 monooxygenase 1A, CYP1A). We also measured lipid peroxidation using the thiobarbituric acid reactive substances method and the gene expression of Abcc2 and genes of the AhR pathway, AhR, ARNT, and cyp1a, by qRT-PCR. Chlorpyrifos induced the DNP-SG transport rate in middle intestine strips in a concentration-dependent manner (49–71%). In polarized preparations, the induction of the DNP-SG transport rate was observed only in everted segments exposed to 20 μg L−1 chlorpyrifos (40%), indicating that CPF only stimulated the apical (luminal) transport flux. Exposure to chlorpyrifos increased GST activity by 42% in intestine strips and inhibited EROD activity (47.5%). In addition, chlorpyrifos exposure inhibited cholinesterase (34–55%) and carboxylesterase (33–42.5%) activities at all the concentrations assayed and increased TBARS levels in a concentration-dependent manner (71–123%). Exposure to 20 μgL−1 chlorpyrifos did not affect the mRNA expression of the studied genes. The lack of inhibition of DNP-SG transport suggests that chlorpyrifos is not an Abcc substrate. Instead, CPF induces the activity of Abcc proteins in the apical membrane of enterocytes, likely through a post-translational pathway.

Development, optimization, and validation of Inflammatory Bowel Disease rat model using isotretinoin

Backgroundand Purpose: Inflammatory Bowel Disease (IBD) is a persistent bio-psychological disorder with the absence of actual pathological reason. Association between IBD and isotretinoin has been reported by many human and in vitro studies. However, in this study, our focus is on finding the causal relationship between IBD and isotretinoin for the development of a new animal model. MethodsTwenty-eight Sprague Dawley rats were taken for this study and divided into five groups (i.e. Group 1: Normal control, Group 2: Standard IBD Model Group (Indomethacin treated), Group 3: Isotretinoin low dose (7 mg/kg), Group 4: Isotretinoin medium dose (35 mg/kg), Group 5: Isotretinoin high dose (70 mg/kg). The rats were treated according to assigned treatment and observed on different days to evaluate the severity of IBD with the help of symptomatical (nausea, diarrhea, stool consistency, etc.) activity, biochemical parameters, macroscopy, and histological analyses. Key resultsDuring the entire study period, body weight, stool consistency and frequency of the animals had been observed daily. No significant reduction in body weight was observed between the disease induced and normal control animals; however, it was observed that the stool consistency of the animals became less (mucus in stool) day by day and stool frequency increased (frequent defecation) in the different isotretinoin groups compared to the control group. There was statistically significant increase in TBARS levels of isotretinoin low (p < 0.05), medium (p < 0.001) and high dose (p < 0.01) treated group was observed, as compared to control group. Similarly, statistically significant effects of isotretinoin on GSH level (p < 0.01), CAT activity (p < 0.01), and SOD (p < 0.01) were also observed. Increase in TNF-α levels found significantly higher in isotretinoin medium dose (35 mg/kg) treated group (p < 0.001) as compared with control group as well as standard IBD model group. All the three-isotretinoin treated groups (Isotretinoin low dose: p < 0.001; Isotretinoin medium dose: p < 0.001; Isotretinoin high dose: p < 0.001) depicted significant difference in macroscopic scores as compared with control group; these results are comparable with standard IBD model group. Histological analyses revealed that, among three-dose groups of isotretinoin, there was excessive amount of crypt abscesses, infiltration of inflammatory cells, and formation of ulceration observed in isotretinoin medium dose treated group. ConclusionAs standard indomethacin treated group, isotretinoin also caused significant damage to intestinal mucosa, and form ulceration in gastrointestinal tract. Compared to control group, isotretinoin significantly worsens the disease condition, which were comparable to the indomethacin-treated group; however, isotretinoin at the dose of 35 mg/kg caused maximum severe damage to the intestinal mucosa.

Oxidative Stress Biomarkers in the Blood of Rainbow Trout (Oncorhynchus mykiss Walbaum) and Equine Plasma after Incubation with Hemp Oil "Annabis Bio"

Industrial hemp is a multi-use crop that has been widely cultivated to produce fibers and nutrients, such as protein, dietary fiber, minerals, and unsaturated fatty acids, which make them a good fortifying component in food production. The antioxidant capability of hemp oils has been reported. In the current study, for evaluating the antioxidant activity of commercial hemp oil "Annabis BIO" derived from certified industrial hemp seeds without the psychoactive substance THC (Olomouc, Czech Republic), biomarkers of oxidative stress [2-thiobarbituric acid reactive substances (TBARS), oxidatively modified proteins (OMP), total antioxidant capacity (TAC)] were used in models of the blood collected from adult healthy rainbow trout (Oncorhynchus mykiss Walbaum), the blood of rainbow trout with clinical symptoms of ulcerative dermal necrosis (UDN), and equine plasma. A volume of 0.1 mL of the hemp oil was added to 1.9 mL of fish blood or equine plasma. After incubation of the mixture for 60 min with continuous stirring, biomarkers of oxidative stress were studied in samples. After in vitro incubation of hemp oil with the blood of clinically healthy rainbow trout, we noted a statistically significant decrease in biomarkers of lipid peroxidation by 55.6% (p &lt;0.05). The highest increase in TBARS level was observed after in vitro incubation of hemp oil with the blood of UDN-affected rainbow trout. In vitro incubation of hemp oil with equine plasma resulted in a statistically significant increase in the level of ketonic derivatives (by 29%, p &lt;0.05) and aldehydic derivatives of OMP (by 33.1%, p &lt;0.05). Incubation of hemp oil with the blood of UDN-affected trout resulted in a decrease of the ketonic derivative of OMP (by 43.3%, p &lt;0.05). Incubation of hemp oil with equine plasma, we observed a statistically significant decrease in TAC level by 56.6% (p &lt;0.05). Similarly, after incubation hemp oil with blood samples of UDN-affected trout, a statistically significant decrease in total antioxidant capacity (by 59.3%, p &lt;0.05) was observed. The results suggest that the investigated hemp oil have shown varied antioxidant capacities. Accordingly, this study proposes that the therapeutic benefit of this hemp oil can be, at least in part, attributed to using different biological materials (blood, plasma) used in vitro in the current study.

EFFECT OF BONE MARROW ASPIRATE IN DENERVATION-INDUCED SKELETAL MUSCLE ATROPHY

The aim: To evaluate muscle changes after sciatic nerve damage with the injection of bone marrow aspirate cells. Materials and methods: 36 rabbits underwent sciatic nerve cross-section and neuroraphy, bone marrow aspirate cells were injected directly or 7 weeks after neuroraphy. Changes in skeletal muscle morphology (photomicrographs of histological sections were analyzed for morphometric analysis of collagen region, quantitative analysis of conducted collagen density and measurement of muscle fibers diameter) and biochemical parameters (catalase activity, superoxide dismutase and glutathione peroxidase measurements and level of TBARS was determined) at 8, 12, and 16 weeks were examined. Results: There is atrophy of muscle fibers in denervated muscles, and it has a negative tendency between 8 and 12 weeks. Delayed bone marrow aspirate cells injection into the muscles at 7 week – delayed atrophy and formation of TBA reactive substances. But bone marrow aspirate cells injection into the muscles directly after neuroraphy increased collagen formation, and development of fibrosis in areas of atrophy. Conclusions: Sciatic nerve injury results in atrophy of muscle tissue, which is partially delayed after delayed bone marrow aspirate cells injection at week 7. Muscle atrophy was characterized by a sharp increase in TBARS levels at 12 and 16 weeks and catalase activity at 12 weeks, and changes in biochemical parameters were partially normalized after the use of cell aspirates, to a greater extent with delayed injection.

Hepatic susceptibility to oxidative damage after repeated concomitant exposure to aspartame and aflatoxin B1 in rats

The potential interactions among food additives/contaminants and the consequences to biological systems is a topic that is rarely addressed in scientific literature. Thus, the current study investigated if the combined administration of ASP and AFB1 would impair hepatic and renal oxidative status. Male Wistar rats received during 14 days once a day ASP (75 mg/Kg) and/or AFB1 (250 µg/Kg) through intragastric route. At the end of experimental protocol, samples of liver and kidneys were collected for assessing biochemical markers of oxidative status. In the hepatic tissue, the treatment with a single substance (ASP or AFB1) caused an increase in TBARS levels, and a reduction in non-enzymatic antioxidant defenses (Vit C and NPSH levels and FRAP test). In the kidneys, TBARS levels were increased only in the group that received ASP + AFB1. The association reduced NPSH content, while the treatment with AFB1 reduced the FRAP levels. GST and CAT activities were increased in all treatments. Overall, ASP and AFB1 association presented higher toxic effects to the tissues. To the best of our knowledge, this is the first study demonstrating that the associated use of both ASP and AFB1 induces more extensive injuries in comparison to the effects caused by each one alone. Therefore, these data demonstrated that concomitant exposure to ASP and AFB1 potentiated their oxidative damage in hepatic tissue, suggesting that this organ is particularly sensitive to the toxic action induced by these substances.

MiADMSA abrogates sodium tungstate-induced oxidative stress in rats

Tungsten (W) and its compounds have emerged as a relatively new area of environmental health concern in the last decade. Tungsten is environmentally benign due to its increasing use in armour-piercing munitions and as a replacement for lead in other ammunition. It has also been identified in various hazardous waste sites and therefore been proposed for inclusion in the Environmental Protection Agency National Priorities List. The major objective of this study was to evaluate the therapeutic efficacy of orally administered monoisoamyl 2, 3-dimercaptosuccinic acid (MiADMSA) against tungstate induced oxidative injury in blood, liver and kidneys of male Wistar rats. MiADMSA, a thiol chelator has gained wide recognition recently as a future chelating drug of choice specifically for arsenic and was chosen for this study as tungstate ions too have an affinity toward the –SH group thus, being less bioavailable in the body. We determined the effects of MiADMSA (50 mg/kg, p.o.) against sodium tungstate (500 ppm in drinking water, daily for 28 days) induced biochemical changes indicative of oxidative stress in blood, and other soft tissues of of male Wistar rats. Tungsten exposure led to an increased levels of Reactive Oxygen Species (ROS) in liver, kidney, spleen and blood accompanied also by an increase in TBARS levels. The GSH: GSSG ratio also showed a decrease on sodium tungstate intoxication. Treatment with MiADMSA restored most of the sodium tungstate-induced alterations in the biomarkers suggestive of oxidative stress. These preliminary results led us to conclude that sub-acute exposure to tungstate-induced oxidative stress could be effectively reduced by the administration of MiADMSA and thus might be a promising antidote for studying in detail its efficacy in reducing body tungstate burden and its excretion post tungstate exposure.

A toxicological comparison between two uranium compounds in Artemia salina: Artificial seawater containing CaCO3

Uranium (U) mining is an aquatic environmental concern because most of these harmful compounds are discharged into freshwater, reaching the saline environment as the final destination of this contaminated water. Carbonates are present in ocean waters and are essential for benthic organisms, however they may influence the U-induced toxicity. Thus, the aim of this study was to compare the toxicity of uranium nitrate (UN) and uranium acetate (UA) in Artemia salina (AS), which is one of the leading representatives of the marine biota. The cultures of AS (instar II) maintained in artificial seawater containing CaCO3 were exposed for 24 h to different concentrations of U compounds. The results showed that AS were more sensitive to UN (LC50 ≈ 15 μM) when compared with UA (LC50 ≈ 245 μM) indicating higher toxicity of this U compound. Calculated U speciation indicated that Ca2UO2(CO3)3 and (UO2)2CO3(OH)3- complexes predominated under our experimental conditions. The immobilization/lethality was observed after 9 h of exposure for both U compounds. However, only UN caused a significant decrease (≈40%) in the acetylcholinesterase (AChE) activity when compared with control. In order to observe preliminary toxicity effects, we evaluated oxidative stress parameters, such as catalase (CAT) activity, TBARS formation, radical species (RS) generation and cell membrane injury and/or apoptosis (CMI). In this study, we demonstrate that U compounds caused a significant decrease in CAT activity. Similarly, we also observed that UN increased TBARS levels in AS at concentrations 5 times lower than AU (10 μM and 50 μM, respectively). Furthermore, RS generation and CMI were enhanced only on AS treated with UN. Overall, the effects observed here were remarkably significant in AS exposed to UN when compared with AU. In this study, we showed different profiles of toxicity for both U compounds, contributing significantly to the current and scarce understanding of the aquatic ecotoxicity of this heavy metal.

Integrated analysis of the quality of water bodies from the lower Paraná River basin with different productive uses by physicochemical and biological indicators

The Paraná River basin is one of the most important in South America and is affected by human activities that take place on its margins. In particular, the De la Cruz stream flows through an industrial pole and the Arrecifes River goes mainly through agricultural fields. The aim of this study was to evaluate the water quality of the De la Cruz stream (S1) and the Arrecifes River (S2) by means of physicochemical parameters, including metals and pesticides concentrations. Since amphibians are good indicators of environmental quality, bioassays with Rhinella arenarum were carried on. For lethal and sublethal parameters, embryos and larvae were exposed to a dilution gradient of water samples and AMPHITOX Solution (AS) as negative control for 504 h. For the determination of oxidative stress biomarkers (Catalase -CAT-, Glutathione S-Transferase -GST-, Reduced Glutathione -GSH-, and lipid peroxidation -TBARS-), embryos and larvae were exposed to undiluted water samples and AS. For the determination of micronuclei, larvae at hind limb bud stage (S.28) were exposed to undiluted water samples, simultaneously with negative and positive controls (AS and cyclophosphamide 40 mg/L, respectively). Dissolved oxygen was low in both sites and the copper levels exceeded the Argentine limit for the protection of aquatic life. In embryos exposure, water sample from S1 caused lethal effects (504h-LC50 = 49 (28–71.6)%), increased TBARS levels, and GST and CAT activities. In larvae exposure, water sample from this site decreased CAT activity, while the water sample from S2 caused important lethal effects (504h-LC50 = 98.72 (60.60–302.52)%), low GSH levels and increased GST activity. Water samples from both sites induced higher micronuclei frequency than the negative control. This study alerts about the degradation of water quality of the studied sites including lethal and sublethal effects in R. arenarum that can jeopardize the native populations of this species.

Effect of Solanum torvum Swartz on diabetic neuropathy in alloxan-induced diabetic rats

Solanum torvum Swartz is a well-known traditional herbal medicinal plant used in diabetes and diabetes-related complications. The objective of the study was to evaluate the effect of S. torvum on diabetic neuropathy in alloxan-induced diabetic rats. Diabetes was induced in Wistar rats by using a single intraperitoneal injection of alloxan monohydrate (150 mg/kg; i.p.). After confirmation of diabetes, rats received metformin (120 mg/kg, p.o.) and STME (30 and 100 mg/kg, p.o) for 5 weeks. Diabetic rats showed significant (P <0.05) behavioural changes, increase in blood glucose levels, decrease in relative organ weight of pancreas, significant (P <0.05) decrease in reduced glutathione (RGSH) and significant (P <0.05) increase in TBARS levels. While STME (100 mg/kg) treated diabetic rats significantly (P <0.05) reversed the above parameters as compared to diabetic rats. Treatment with STME (100 mg/kg) has also reversed histopathological changes as observed in diabetic control rats. The study suggests that methanolic extract of S. torvum ameliorates diabetic neuropathy in alloxan-induced diabetic rats.

REDOX ALTERATIONS IN PREGNANT WOMEN: ANTIOXIDANT EFFECT OF LEMONGRASS (CYMBOPOGON CITRATUS (DC.) STAPF) ALTERAÇÕES REDOX EM GESTANTES: EFEITO ANTIOXIDANTE DO CAPIM-LIMÃO (CYMBOPOGON CITRATUS (DC.) STAPF)

Purpose: This study aimed to verify the redox profile of different gestational phases of pregnant women, in addition to the antioxidant potential of the Cymbopogon citratus leaves infusion. Methods: The infusion characterization was performed by measuring total phenolics, flavonoids and condensed tannins levels. The oxidative damage markers to lipids and proteins in plasma and erythrocytes were evaluated by measuring the TBARS and carbonylated proteins (CP) levels and antioxidant activity by GSH levels. The antioxidant effects of the infusion (20 g/L) were evaluated by measuring the same markers after the pregnant women erythrocytes incubation with the same infusion. The phytochemicals with the highest concentration founded in infusion were flavonoids, followed by tannins and phenolics. Results: It was observed an increase in TBARS levels in the 2 nd gestational phase in plasma, concomitant with a decrease in GSH levels in the 2 nd and 3 rd phases, and CP in the 1 st and 4 th gestational phases in relation to control. It was observed a decrease in all markers levels in erythrocytes in the 1 st and 2 nd phases. Analyzing the antioxidant potential of the infusion on erythrocytes, it was observed a decrease in TBARS concomitant with an increase in GSH levels, being little effective in reversing protein damage. Conclusion: Thus, it is suggested that the infusion could be used as adjuvant to vitamin supplements recommended during pregnancy.

The effect of cilostazol on hippocampal memory and oxidative stress biomarkers in rat model of diabetes mellitus

Diabetes is a global public health crisis worldwide, particularly in developing countries. Diabetes is characterized by a consistent elevation in blood glucose level which leads to several complications including cognitive impairment. Hippocampus, a brain structure responsible for memory, is vulnerable to damage caused by hyperglycemia-induced oxidative stress. In this study, we evaluated the effect of cilostazol, a selective phosphodiesterase 3 inhibitor, on hippocampal memory and oxidative stress biomarkers in streptozotocin-induced diabetes model. Cilostazol was administered to rats intraperitoneally at dose 3 mg/kg. Spatial learning and memory were tested using radial arm water maze (RAWM). BDNF protein, TBARS levels and different antioxidant biomarkers were assessed after dissection of the hippocampus. The diabetic rats showed an increase in the number of the errors during RAWM performance. However, treatment with cilostazol could not showed an improvement in animal’s learning and memory performance. The results revealed that diabetic rats showed an increase in TBARS levels and a decrease in an antioxidant enzyme activities (superoxide dismutase (SOD) and glutathione peroxidase (GPx)). Moreover, cilostazol was able to normalize diabetes-induced reduction in the hippocampus activity of SOD and GPx. Moreover, administration of cilostazol normalized diabetes-induced increase in TBARS level, without any significant effect on BDNF level or catalase activity. In conclusion, cilostazol showed no improvement in the learning and memory functions which could be due to the lack of significant cognitive impairment induced by streptozotocin administration. However, cilostazol had shown antioxidant activity through normalization of hippocampal oxidative stress biomarkers.

Effect of dietary oxidized oil and vitamin E on growth performance, lipid peroxidation and fatty acid profile ofLabeo rohitafingerlings

A 3 × 3 factorial experiment was conducted on Labeo rohita fingerlings to evaluate the effect of dietary oxidized oil and vitamin E. Nine experimental diets were made, based on three degrees of oil oxidation (fresh oil, low oil oxidation and high oil oxidation), and each level of oxidation was further supplemented with three levels of vitamin E (0, 100 and 1,000 mg/kg). Weight gain% and specific growth rate (SGR) of fish fed fresh fish oil and low oil oxidation level were significantly higher than highly oxidized oil. Moreover, vitamin E supplemented fish also showed better growth performance. Oil oxidation caused a significant reduction in the concentrations of α‐tocopherol and increase in TBARS level and antioxidant enzyme activities in fish liver and muscles. However, increasing the dietary vitamin E abrogated these effects. Dietary vitamin E supplementation improved the fatty acid, more specifically polyunsaturated fatty acids profile of oxidized oil fed fish. In conclusion, dietary oxidized fish oil increased the oxidative stress condition of fish but supplementation of high dose of vitamin E prevented lipid oxidation, improved growth performance and fatty acid profile of L. rohita.

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.

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.