Changes In Oxidative Stress Parameters Research Articles

Exploring the mechanisms of alcohol-related damage in oral mucosa – is oxidative stress associated with the increase in cell proliferation in rat tongue epithelium?

Context: Alcohol consumption has been related to a cell proliferation increase in oral epithelium but its mechanism remains unclear.Objective: The aim of this study was to investigate whether oxidative stress parameters are implicated in the induction of cell proliferation in rat tongue epithelium after different times of chronic alcohol consumption.Materials and methods: Cell proliferation was assessed in tongue epithelium using AgNOR (argyrophilic proteins related to active nucleolar organizer regions) quantification. Oxidative stress parameters [lipid peroxidation, protein carbonyls, superoxide dismutase activity and catalase (CAT) activity and immunocontent] and Nrf2 immunocontent were quantified in tongue homogenates.Results and discussion: Mean AgNOR numbers (mAgNOR) per nucleus was 2.22 ± 0.30 in ventral tongue epithelium after 120 days of alcohol consumption (vs. 1.87 ± 0.18 for control animals and 1.91 ± 0.23 for animals treated with alcohol for 60 days) indicating cell proliferation increase (p < 0.05, ANOVA followed by Tukey post hoc). Interestingly, 60 days of alcohol consumption induced changes in oxidative stress parameters, but no alteration in cell proliferation. Vitamin E co-treatment was conduced in order to evaluate its possible protective effects. The 120 day Tween + vitamin E + alcohol treatment induced an increase in mAgNORs when compared to the Tween + vitamin E treated group (respectively 2.10 ± 0.30 vs. 1.77 ± 0.11, p < 0.05, ANOVA followed by Tukey post hoc), showing that vitamin E co-treatment had no protective effects. In addition, an inverse association was observed between CAT activity and AgNORs quantity (R = −0.32; p < 0.05, Person’s correlation) as well as the possible involvement of Nrf2 in alcohol-related damage.Conclusions: Our findings suggest that the increase in cell proliferation associated with alcohol-related damage has no direct relation with an imbalance in oxidative parameters. In contrast, our results indicate that hydrogen peroxide may be implicated in cellular signaling during proliferation in the oral mucosa.

Curcumin encapsulated in chitosan nanoparticles: A novel strategy for the treatment of arsenic toxicity

Water-soluble nanoparticles of curcumin were synthesized, characterized and applied as a stable detoxifying agent for arsenic poisoning. Chitosan nanoparticles of less than 50nm in diameter containing curcumin were prepared. The particles were characterized by TEM, DLS and FT-IR. The therapeutic efficacy of the encapsulated curcumin nanoparticles (ECNPs) against arsenic-induced toxicity in rats was investigated. Sodium arsenite (2mg/kg) and ECNPs (1.5 or 15mg/kg) were orally administered to male Wistar rats for 4weeks to evaluate the therapeutic potential of ECNPs in blood and soft tissues. Arsenic significantly decreased blood δ-aminolevulinic acid dehydratase (δ-ALAD) activity, reduced glutathione (GSH) and increased blood reactive oxygen species (ROS). These changes were accompanied by increases in hepatic total ROS, oxidized glutathione, and thiobarbituric acid-reactive substance levels. By contrast, hepatic GSH, superoxide dismutase and catalase activities significantly decreased on arsenic exposure, indicative of oxidative stress. Brain biogenic amines (dopamine, norepinephrine and 5-hydroxytryptamine) levels also showed significant changes on arsenic exposure. Co-administration of ECNPs provided pronounced beneficial effects on the adverse changes in oxidative stress parameters induced by arsenic. The results indicate that ECNPs have better antioxidant and chelating potential (even at the lower dose of 1.5mg/kg) compared to free curcumin at 15mg/kg. The significant neurochemical and immunohistochemical protection afforded by ECNPs indicates their neuroprotective efficacy. The formulation provides a novel therapeutic regime for preventing arsenic toxicity.

Changes in oxidative stress parameters in relation to age, growth and reproduction in the short-lived catarina scallop Argopecten ventricosus reared in its natural environment

Increase in oxidative damage and decrease in cellular maintenance is often associated with aging, but, in marine ectotherms, both processes are also strongly influenced by somatic growth, maturation and reproduction. In this study, we used a single cohort of the short-lived catarina scallop Argopecten ventricosus, to investigate the effects of somatic growth, reproduction and aging on oxidative damage parameters (protein carbonyls, TBARS and lipofuscin) and cellular maintenance mechanisms (antioxidant activity and apoptosis) in scallops, caged in their natural environment. The concentrations of protein carbonyls and TBARS increased steeply during the early period of fast growth and during reproduction in one-year-old scallops. However, oxidative damage was transient, and apoptotic cell death played a pivotal role in eliminating damage in gill, mantle and muscle tissues of young scallops. Animals were able to reproduce again in the second year, but the reduced intensity of apoptosis impaired subsequent removal of damaged cells. In late survivors low antioxidant capacity and apoptotic activity together with a fast accumulation of the age pigment lipofuscin was observed. Rates of oxygen consumption and oxidative stress markers were strongly dependent on somatic growth and reproductive state but not on temperature. Compared to longer-lived bivalves, A. ventricosus seems more susceptible to oxidative stress with higher tissue-specific protein carbonyl levels and fast accumulation of lipofuscin in animals surviving the second spawning. Superoxide dismutase activity and apoptotic cell death intensity were however higher in this short-lived scallop than in longer-lived bivalves. The life strategy of this short-lived and intensely predated scallop supports rapid somatic growth and fitness as well as early maturation at young age at the cost of fast cellular degradation in second year scallops.

Status of Oxidative Stress in Patients With Renal Cell Carcinoma

Although oxidative stress is implicated in renal cell carcinoma pathogenesis, to our knowledge changes in oxidative stress parameters in patients who undergo surgery for renal cell carcinoma have not been studied previously. We investigated the status of oxidative stress in patients with renal cell carcinoma. Reactive oxygen species, nitric oxide and glutathione were measured in the blood of 68 patients with renal tumor and in 30 age matched normal controls. Levels were measured again 1 week, and 1 and 2 months postoperatively in patients who underwent surgery for renal cell carcinoma. Levels of superoxide dismutase, catalase and lipid peroxidation were measured in tumor tissue and in normal renal parenchyma in 51 patients with renal tumor. Significantly increased reactive oxygen species and nitric oxide, and decreased glutathione were observed in patients with renal cell carcinoma compared to normal subjects and in patients with benign tumors. Superoxide dismutase and lipid peroxidation were increased and catalase was decreased in tumor tissue compared to normal renal tissue. Oxidative stress correlated with renal cell carcinoma grade and stage but decreased after curative resection. Patients with metastatic disease had persistently increased oxidative stress parameters. Antioxidant enzyme levels in benign tumor tissue were significantly higher than in renal cell carcinoma. Patients with renal cell carcinoma have increased oxidative stress, which is effectively alleviated by curative resection. In patients with benign tumors antioxidant defense mechanisms maintain normal redox status.

Toluene effects on oxidative stress in brain regions of young-adult, middle-age, and senescent Brown Norway rats

The influence of aging on susceptibility to environmental contaminants is not well understood. To extend knowledge in this area, we examined effects in rat brain of the volatile organic compound, toluene. The objective was to test whether oxidative stress (OS) plays a role in the adverse effects caused by toluene exposure, and if so, if effects are age-dependent. OS parameters were selected to measure the production of reactive oxygen species (NADPH Quinone oxidoreductase 1 (NQO1), NADH Ubiquinone reductase (UBIQ-RD)), antioxidant homeostasis (total antioxidant substances (TAS), superoxide dismutase (SOD), γ-glutamylcysteine synthetase (γ-GCS), glutathione transferase (GST), glutathione peroxidase (GPX), glutathione reductase (GRD)), and oxidative damage (total aconitase and protein carbonyls). In this study, Brown Norway rats (4, 12, and 24 months) were dosed orally with toluene (0, 0.65 or 1 g/kg) in corn oil. Four hours later, frontal cortex, cerebellum, striatum, and hippocampus were dissected, quick frozen on dry ice, and stored at − 80 °C until analysis. Some parameters of OS were found to increase with age in select brain regions. Toluene exposure also resulted in increased OS in select brain regions. For example, an increase in NQO1 activity was seen in frontal cortex and cerebellum of 4 and 12 month old rats following toluene exposure, but only in the hippocampus of 24 month old rats. Similarly, age and toluene effects on glutathione enzymes were varied and brain-region specific. Markers of oxidative damage reflected changes in oxidative stress. Total aconitase activity was increased by toluene in frontal cortex and cerebellum at 12 and 24 months, respectively. Protein carbonyls in both brain regions and in all age groups were increased by toluene, but step-down analyses indicated toluene effects were statistically significant only in 12 month old rats. These results indicate changes in OS parameters with age and toluene exposure resulted in oxidative damage in frontal cortex and cerebellum of 12 month old rats. Although increases in oxidative damage are associated with increases in horizontal motor activity in older rats, further research is warranted to determine if these changes in OS parameters are related to neurobehavioral and neurophysiological effects of toluene in animal models of aging.

Taurine Is More Effective than Melatonin on Cytochrome P450 2E1 and Some Oxidative Stress Markers in Streptozotocin-Induced Diabetic Rats

Melatonin and taurine have alleviative effects in streptozotocin (STZ)-induced diabetic rats. Male Wistar rats were divided into nondiabetic, diabetic, diabetic melatonin supplemented and diabetic taurine supplemented groups. At the end of the study, both blood and liver were collected for determination of some oxidative stress parameters, and hepatic cytochrome P450 2E1 (CYP2E1) enzyme activity and gene expression. An increased CYP2E1 activity and expression level with a concomitant significant change in oxidative stress parameters were found in STZ-induced diabetic rats. Taurine or melatonin supplementation to the diabetic rats alleviated these experimental parameters with a more significant effect for taurine than that of melatonin. Suppression of β-hydroxybutyrate (β-HB) production by taurine can be one of the mechanisms of a reduction in CYP2E1. Taurine was effective more than melatonin in reducing CYP2E1 activity and expression; therefore antioxidants might prove beneficial in type 1 diabetes associated with manifestations of liver injury.

Assessment of oxidative stress in Rhamdia quelen exposed to agrichemicals

Due to the proximity of crop and fish culture areas, some agrichemicals that could be harmful for fish could enter into fishponds by different ways, such as by leaching through rain. Rhamdia quelen (Teleostei) were exposed to sublethal concentrations of methyl parathion (MP), a glyphosate based herbicide (Gly), and tebuconazole (Teb). The liver of R. quelen exposed to MP and Teb showed enhanced levels of thiobarbituric acid reactive substances (TBARS), higher than in the control fish (56% and 59%, respectively). In contrast, Gly did not alter the TBARS generation. The protein carbonyl content increased only in fish exposed to Teb. Fish exposed to the three agrichemicals showed a significant decrease of catalase activity (52%, 48%, and 67%, respectively) and increased glutathione-S-transferase (57%, 46%, and 160%, respectively) activity. Fish exposed to MP, Gly, and Teb showed higher reduced glutathione (151%, 472%, and 130%, respectively, when compared with the control levels) and ascorbic acid concentrations (121%, 102%, and 184%, respectively),while the non-protein thiol content increased only in R. quelen exposed to tebuconazole. Fish exposed to MP and Teb showed several pathological changes in the liver, including hepatocyte degeneration and bile stagnation. The present work reports for the first time the toxicity of the pesticide MP and the fungicide Teb in R. quelen, and as in other works, suggests the relatively lower liver toxicity of Gly for fish. The data presented herein demonstrate that sublethal concentrations of MP and Teb cause changes in oxidative stress parameters as well as hepatic cell injuries in R. quelen, and that these parameters have the potential to be developed as bioindicators of exposure to these agrichemicals.

Kinetic change of oxidative stress in cerebrospinal fluid of mice infected with Angiostrongylus cantonensis

The cerebrospinal fluid (CSF) of C57BL/6 mice infected with Angiostrongylus cantonensis was examined for kinetic changes in oxidative stress parameters, including reactive oxygen species (ROS), superoxide dismutase (SOD), catalase, malondialdehyde (MDA), 8-isoprostane, and 8-hydroxy-2′-deoxyguanosine (8-OHdG). The ROS increased gradually in the early stage of infection. During days 12–30 post-infection, the infected mice revealed ROS levels significantly higher than that in uninfected controls (P < 0.001). The ROS levels peaked at day 24 and then returned to that observed in uninfected controls at day 45 post-infection. The kinetics of MDA, 8-isoprostane, and 8-OHdG concentration changes observed in the CSF of the infected mice corresponded with kinetic changes in ROS levels. Thus, the excess ROS caused lipid peroxidation and DNA damage to cells in the central nervous system (CNS) of mice infected with A. cantonensis despite the increased antioxidant SOD and catalase enzyme activities during post-infection days 12–30. The oxidative stress in the CNS of C57BL/6 mice was apparently increased by diseases associated with A. cantonensis infection.

Are cefuroxime and vancomycin really safe on the corneal endothelial cells?

To investigate the biochemical changes of the oxidant/antioxidant balance in corneal tissue, and determine the relative corneal endothelial toxicities of the following intracameral antibiotic agents: cefuroxime and vancomycin. The experiment was conducted using New Zealand rabbits. The rabbits were randomly divided into three experimental groups as follows: cefuroxime group (n=10), vancomycin group (n=10), and control group (n=10). Only the right eyes of the rabbits were used in this study. Twenty eyes received injections of 0.1 ml of one of the two antibiotic preparations, and ten control eyes received injections of 0.1 ml of balanced salt solution. Corneal thickness and clarity were measured before, and 3 and 6 h after surgery. The corneal tissues of the rabbits were extracted and homogenized in 2 ml of physiological saline, and kept at -80 degrees C. In the corneal tissue, malondialdehyde (MDA) and total thiol (SH) levels were measured with spectrophotometric methods. Friedman and Kruskal-Wallis tests were used for statistical analysis. Neither cefuroxime nor vancomycin caused corneal thickening and edema at 3 and 6 h after injection, and no anterior chamber reaction was observed in both groups at both measurement times. The level of SH significantly decreased, while the level of MDA significantly increased in the corneal tissue in the cefuroxime group (p=0.001 and p<0.001 respectively). In contrast, no statistically significant change in oxidative-stress parameters was observed in the vancomycin group (p=0.165 and p=0.876 respectively). Corneal endothelial cells are very sensitive to any form of toxic exposure. Using intracameral cefuroxime during the anterior segment surgery may be more toxic on the endothelial tissue in patients with vulnerable corneal endothelium. Because of the definite risk of dosage errors, these agents should be prepared in the hospital pharmacy and not in the operating theatre.

DHEA effects on myocardial Akt signaling modulation and oxidative stress changes in aged rats

The secretion of DHEA-synthesized mainly in the adrenal cortex-increases in the postnatal aging, peaks in the twenties and decreases with age afterwards. Exogenous DHEA can exert a dual effect depending on dose and on tissue. Akt is a serine/threonine kinase whose activity has been seen as an interventional approach for cardiomyopathic damage resulting from aging changes. In order to evaluate DHEA effects over myocardial Akt protein expression associated to oxidative stress markers during aging, male Wistar rats (3 and 18 months) were assigned into two groups: control or DHEA (10 mg/kg, subcutaneously, for 5 weeks). In the aged group, we found increased lipid peroxidation and glutathione-S-transferase activity. DHEA produced an increase in p-Akt protein expression and a decrease in SOD activity in both ages. Akt pathway activation might be related to changes in oxidative stress parameters according to age.

The toxicity and pharmacokinetics of dihydrosanguinarine in rat: A pilot study

The quaternary benzo[ c]phenanthridine alkaloid sanguinarine (SG) is the main component of Sangrovit ®, a natural livestock feed additive. Dihydrosanguinarine (DHSG) has recently been identified as a SG metabolite in rat. The conversion of SG to DHSG is a likely elimination pathway of SG in mammals. This study was conducted to evaluate the toxicity of DHSG in male Wistar rats at concentrations of 100 and 500 ppm DHSG in feed for 90 days (average doses of 14 and 58 mg DHSG/kg body weight/day). No significant alterations in body or organ weights, macroscopic details of organs, histopathology of liver, ileum, kidneys, tongue, heart or gingiva, clinical chemistry or hematology markers in blood in the DHSG-treated animals were found compared to controls. No lymphocyte DNA damage by Comet assay, formation of DNA adducts in liver by 32P-postlabeling, modulation of cytochrome P450 1A1/2 or changes in oxidative stress parameters were found. Thus, repeated dosing of DHSG for 90 days at up to 500 ppm in the diet (i.e. approximately 58 mg/kg/day) showed no evidence of toxicity in contrast to results published in the literature. In parallel, DHSG pharmacokinetics was studied in rat after oral doses 9.1 or 91 mg/kg body weight. The results showed that DHSG undergoes enterohepatic cycling with maximum concentration in plasma at the first or second hour following application. DHSG is cleared from the body relatively quickly (its plasma levels drop to zero after 12 or 18 h, respectively).

Acute effect of oral flavonoid-rich dark chocolate intake on coronary circulation, as compared with non-flavonoid white chocolate, by transthoracic Doppler echocardiography in healthy adults

Purpose To assess the effects of the oral intake of flavonoid-rich dark chocolate on coronary circulation, we measured coronary flow velocity reserve (CFVR) by noninvasive transthoracic Doppler echocardiography (TTDE) in healthy adult subjects. Materials and methods The study was a randomized, single-blind design conducted for 2 weeks in 39 healthy men (mean age 29.7 ±3.9 years, range 23–40 years). Subjects were randomly assigned a daily intake of either flavonoid-rich dark chocolate (Meiji Black Chocolate 45 g, Meiji Seika kaisya Ltd, including cacao polyphenol 550 mg/day, 200 kcal) or non-flavonoid white chocolate (Meiji White Chocolate 35 g, Meiji Seika kaisya Ltd, including cacao polyphenol 0 mg/day, 140 kcal) as a control. CFVR was recorded by TTDE, and assessed before and after 2 weeks of intake. At the same time, we also assessed serum asymmetric dimethylarginine, 8-isoprostanes, and malondialdehyde-modified low-density lipoprotein (MDA-LDL) as markers of oxidative stress. Results Flavonoid-rich dark chocolate consumption significantly improved CFVR (3.38 ± 0.49 before intake, 4.28 ± 0.85 after intake; p < 0.01), whereas non-flavonoid white chocolate consumption did not (3.28 ± 0.49 before intake, 3.16 ± 0.49 after intake; p = 0.44). All predictor variables were used as dependent variables in a multiple regression model of the incremental change in CFVR after 2 weeks of chocolate intake. Intake of dark (but not white) chocolate, MDA-LDL, triglyceride (TG) and heart rate (HR) significantly influenced the change of CFVR after 2 weeks of intake ( p < 0.01) according to the multiple regression formula: Y = 1.01 X 1 − 0.005 X 2 − 0.003 X 3 − 0.017 X 4 ( Y = change in CFVR after 2 weeks of chocolate intake, X 1 = intake of dark (but not white) chocolate, X 2 = MDA-LDL, X 3 = TG, X 4 = HR). Conclusion Flavonoid-rich dark chocolate intake significantly improved coronary circulation in healthy adults, independent of changes in oxidative stress parameters, blood pressure and lipid profile, whereas non-flavonoid white chocolate had no such effects.

Health effects in children aged 3–6 years induced by environmental lead exposure

Objectives To investigate the involvement of oxidative damage in lead-induced toxicity in children aged 3–6 years and to enlighten whether oxidative stress indicators are correlated with the known indices of lead toxicity. Methods Blood samples were collected from 408 subjects (217 boys and 191 girls) in the urban kindergartens. The age range of the subjects was 3–6 years. Blood lead levels (BLLs) were analyzed by flameless atomic absorption spectrophotometry. Activities of δ-aminolevulinic acid dehydratase (ALAD), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and contents of glutathione (GSH) in erythrocyte and levels of plasma malondialdehyde (MDA) were analyzed spectrophotometrically in these children. Results Children with BLLs >or=100 μg/L had significantly decreased erythrocyte ALAD activities and increased plasma MDA levels compared to the children with BLLs <100 μg/L. No significant changes were observed in erythrocyte SOD and GSH-Px activities and GSH levels associated with elevated BLLs in these children. Conclusion Present data indicate that oxidative damage could be induced by lead in children with BLLs >or=100 μg/L, and this may partly be attributed to the inhibited ALAD activities. Statistically significant changes of oxidative stress parameters in preschool children while BLLs were more than 100 μg/L could be implicated that oxidative damage might contribute to lead-induced intellectual impairment.

Changes in oxidative stress parameters in fish as response to direct uranium exposure

The objectives of the present work were (1) to estimate the bioaccumulation of natural uranium (U) in a representative freshwater fish and (2) to assess the response of parameters involved in the defense against reactive oxygen species, in relation with the metal concentration and the exposure duration. Juvenile rainbow trout (Oncorhynchus mykiss) were exposed to a range of U concentrations in water (20, 100 and 500 μ g U l-1 ) during 10 days. The activity of antioxidant enzymes superoxide dismutases (SOD) and catalase were measured in trout liver. In parallel, U analysis were performed in water and in trout gills. A significant accumulation of U occurred in trout gills in relation with the concentrations of U in water. SOD and catalase activities were both decreased by the exposure to U. U seemed to partly inhibit the antioxidant system of trout, indicating a potential enlarged sensitivity of exposed fish to oxidative damages.

Changes of Oxidative Stress Parameters in Diabetic Pregnancy

The molecular aetiology of disturbed embryogenesis and other unfavourable outcomes in offspring of diabetic mothers is not fully understood. Experimental studies have suggested an involvement of radical oxygen species (ROS) in the teratological process. To investigate if maternal diabetes in humans is capable of inducing alterations in vascular oxidative stress parameters and whether such changes are associated with disturbances in foetal development. Seventy patients with pre-gestational diabetes (PGDM) were chosen for the study: 29 (41.4%) belonged to class B according to White, 15 (21.4%) to class C, 8 (11.4%) to class D, 3 (4.3%) to class F, 3 to class R and 12 (17.1%) to class F/R. In 20 (28.6%) patients from this group an unfavourable outcome was noted. All patients were subjected to intensive insulin therapy. Glycaemia was estimated by daily self-monitoring, and diurnal glucose profiles and glycated haemoglobin (HbA1c) concentrations were measured monthly. Oxidative stress was evaluated as changed superoxide dismutase, catalase and glutathione peroxidase activities as well as of malondialdehyde (MDA) and peroxides concentrations in maternal erythrocytes and blood serum. Prior to conception, the mean glycaemia in the group that had a planned pregnancy was 6.6mmol/l and HBA1c was 9.35%. Throughout the course of pregnancy, these parameters were maintained at a level of 6.7 mmol/l and 7.85%, respectively. The activity of all antioxidative enzymes was lower before than during pregnancy, and so was the concentration of MDA. The MDA concentrations were higher in patients with elevated glycaemia and with an unfavourable outcome. The investigated ROS, the glycaemia level, as well as the concentration of HBA1c did not show any significant differences between pregnancies with and without vascular complications. Patients with a favourable perinatal outcome presented a higher activity of antioxidant enzymes, than those with unfavourable outcome, throughout the whole course of pregnancy. The appearance of unfavourable perinatal outcomes in relation to parameters of oxidative stress was assessed by logistic regression. Both SOD and GPX activities, as well as peroxides' concentration, showed significant correlations (p < 0.005) with foetal complications. However, after mean glucose levels in the studied group were included into these analyses, this relationship was only evident with SOD and GPX activity (p < 0.0016). Oxidative stress is one of several important factors contributing to unfavourable outcome of human diabetic pregnancy.

Oxidative Stress Status in Kidney Tissue after Losartan and Atenolol Treatment in Experimental Renal Failure

Background/Aims: Rats with subtotal nephrectomy (5/6NPX) rapidly develop systemic hypertension and proteinuria. The aim of our study was to evaluate the changes in oxidative stress parameters after 2 and 4 weeks of treatment with renin-angiotensin system (RAS)-blocking agent losartan and beta-blocking agent atenolol in experimental chronic renal failure (CRF). Methods: After 5/6NPX, rats were immediately treated with losartan or atenolol. The lipid peroxidation (LPO) products malondialdehyde and 4-hydroxyalkenals and oxidized and reduced glutathione values were measured in the renal cortex tissue and in blood; isoprostanes in urine. Results: There were no differences in the blood pressure values, serum creatinine levels or in daily proteinuria using both antihypertensive treatments. Losartan treatment lowered significantly LPO in kidney tissue after 2 and 4 weeks of treatment compared with untreated and atenolol-treated animals and induced the decrease of excretion of isoprostanes in urine at the end of the study. There was no ameliorating impact of losartan or atenolol observed in the blood status of oxidative stress in this period of time. Conclusion: In the early period of experimental CRF, losartan treatment but not atenolol treatment induces significant decline in LPO grade in the kidney tissue of nephrectomized rats. RAS blockade in the kidney influences local tissue LPO in a much greater extent than in blood.

Antioxidant effect of acetylsalicylic and salicylic acid in rat brain slices subjected to hypoxia

Acetylsalicylic acid (ASA) reduces the incidence of ischemic stroke mainly through its antithrombotic action; however, it also has a direct neuroprotective effect. The present study was designed to evaluate the effect of ASA on oxidative stress and the activity of nitric oxide synthase (NOS) in an in vitro model of hypoxia in rat brain slices. Rat brain slices were perfused with nitrogen (hypoxia) for a maximum of 120 min, after which we measured lipid peroxidation, glutathione levels, glutathione-related enzyme activities, and constitutive nitric oxide synthase (cNOS) and inducible nitric oxide synthase (iNOS) activities. In brain tissue subjected to hypoxia, ASA reduced oxidative stress and iNOS activity (all increased by hypoxia), but only when used at higher concentrations. The effects of salicylic acid (SA) were similar but more intense than were those of ASA. After oral administration, the effect of SA was much greater than that of ASA, and the decrease in cell death with SA was seen much more clearly. In view of the greater effect of SA compared to ASA on changes in oxidative stress parameters in a model of hypoxia, and higher brain concentrations of SA when it is administered alone than when ASA is given (undetectable levels), we conclude that SA plays an important role in the cytoprotective effect in brain tissue after ASA administration.

Oxidative effects of lead in young and adult Fisher 344 rats.

Lead poisoning has been extensively studied over the years. Many adverse physiological and behavioral impacts on the human body have been reported due to the entry of this heavy metal. It especially affects the neural development of children. The current study investigates the effect of lead exposure in young (1.5 months) and adult (10 months) male Fisher 344 rats. Five weeks of lead administration resulted in a profound change in the lead levels in the red blood cells (RBCs) of the young lead-exposed group (37.0 +/- 4.47 microg/dl) compared to the control (<1 microg/dl) and adult (27.4 +/- 8.38 microg/dl) lead-exposed groups. Therefore, this study confirms the fact that gastrointestinal absorption of lead in young is greater than that of adults. Furthermore, glutathione and glutathione disulfide (GSSG) levels in RBCs, liver, and brain tissues were measured to determine thiol status; malondialdehyde (MDA) levels of lipid peroxidation and catalase activity were measured to assess changes in oxidative stress parameters. Liver GSSG and MDA levels were significantly higher in the young lead-exposed group than those in the adult lead-exposed group. In RBCs and brains, however, adult lead-exposed animals have shown more elevated MDA levels than young animals exposed to the same lead treatment.

TCDD-mediated oxidative stress in male rat pups following perinatal exposure.

2,3,7,8-tetrachlorododibenzo-p-dioxin (TCDD) is a highly persistent trace environmental contaminant and is one of the most potent toxicants known. Exposure to TCDD has been shown to cause oxidative stress in a variety of animal models. In this study, pregnant Long Evans rats were dosed with 1 microg TCDD/kg on gestational day (GD) 15 so as to investigate oxidative stress in the liver of male pups following gestational exposure to TCDD. Lipid peroxidation (TBARS), production of reactive oxygen species (ROS), and total glutathione (GSH) were assayed to identify changes in oxidative stress parameters in the pup liver at GD 21 and postnatal days (PND) 4, 25, 32, 49, and 63. Mean ROS levels in pups were elevated at all time points tested with a significant elevation at PND 4 and PND 25. However, pup hepatic lipid peroxidation was unchanged throughout the time course. In addition, hepatic total GSH levels were not significantly changed although the means for the TCDD-treated groups were less than those of the controls at all time points except PND 49. The results indicate that although the levels of ROS are increased following gestational/lactational exposure, this increase does not translate to direct oxidative damage or significant changes to endogenous antioxidant defense mechanisms. Further investigation into the effect of gestational/lactational exposure in pups should include additional endpoints for further characterization of the time course of the response, the effect upon extrahepatic tissues, and investigation of differences between male and female offspring.

Changes in oxidative stress parameters and acid phosphatase activity in the pre-regressing and regressing tail of Indian jumping frog Polypedates maculatus (Anura, Rhacophoridae)

Activities of acid phosphatase (normal and Co 2+-sensitive), superoxide dismutase and catalase and levels of lipid peroxidation, hydrogen peroxide were compared in the tails of tadpoles of stage III, XVIII, XXI and XXIII, respectively, of the Indian Jumping frog Polypedates maculatus. It is noticed that acid phosphatase activity (normal and Co 2+-sensitive), and levels of lipid peroxidation and hydrogen peroxide increased during tail regression. There is also an increase in the level of superoxide dismutase and catalase in the regressing tail. A positive correlation between activity of acid phosphatase and lipid peroxidation, hydrogen peroxide and lipid peroxidation, acid phosphatase and hydrogen peroxide was noticed in the tail of tadpoles during different developmental stages, suggesting a critical interaction between reactive oxygen species and lysosomal activity during metamorphosis.