White spot syndrome virus infection decreases the activity of antioxidant enzymes in Fenneropenaeus indicus

White spot syndrome virus (WSSV) is the causative agent of White Spot disease of shrimp, causing mass mortalities in aquaculture. WSSV infection causes oxidative stress by the release of reactive oxygen species (ROS) that are toxic to the cells. The antioxidant enzymes associated with oxidative stress during the process of pathogenesis of WSSV in the infected tissues (hemolymph, hepatopancreas, gills and muscle) of Fenneropenaeus indicus were quantitatively determined at different time intervals post infection (0, 24, 48, 72 and after 72 h (moribund)). The level of lipid peroxidation, the activities of superoxide dismutase, catalase, glutathione peroxidase, and also the activities of the non-enzymic antioxidants glutathione-S-transferase, reduced glutathione and glutathione reductase in healthy and WSSV-infected hemolymph, hepatopancreas, gills and muscle of F. indicus showed marked differences at different times during the course of infection. The level of lipid peroxidation was higher in WSSV-infected muscle, hemolymph, gills and hepatopancreas than in uninfected F. indicus. Significant reductions in the activities of superoxide dismutase, catalase, glutathione-S-transferase, reduced glutathione, glutathione peroxidase and glutathione reductase were observed in WSSV-infected compared with uninfected animals. The increased lipid peroxidation in WSSV-infected shrimp may be due to increased oxidative stress in the cells as a result of depletion of antioxidant scavenger systems. The reduced activity of antioxidant enzymes in WSSV-infected animals could be due to inactivation of antioxidant enzymes by oxidative stress thereby generating free radicals, which accumulate in the cells. Further understanding of the biochemical alterations induced by viral infections, including changes in the antioxidant status and oxidative stress, could help to advance the therapeutic armamentarium for control of WSSV in shrimp.     

Erythrocyte antioxidant activity, serum ceruloplasmin, and trace element levels in subjects with alcoholic liver disease.

Erythrocyte antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) and reduced glutathione, serum ceruloplasmin, and serum trace elements (copper, zinc, iron, and selenium) related to antioxidant enzymes were assayed in subjects with alcoholic liver disease of different degrees of severity. The erythrocytes of subjects with moderate and severe alcoholic liver cirrhosis had an unbalanced antioxidant system (normal superoxide dismutase, low catalase and glutathione peroxidase activities, and low glutathione content). Serum ceruloplasmin levels were in the normal range. Levels of the serum trace elements zinc and selenium were significantly low in subjects with moderate and severe cirrhosis, whose red cell half-life was also significantly short, as measured by radioactive chromium. These data suggest that the erythrocytes of subjects with moderate and severe alcoholic liver cirrhosis are less protected against oxidant stress. The particular erythrocyte antioxidant system and serum trace element pattern may play a role in the genesis of hemolytic disorders and of alcoholic hepatic damage.     

Ageing alters aortic antioxidant enzyme activities in Fischer-344 rats.

Oxidative stress imposed by reactive oxygen species is now believed to contribute to hypertension, atherosclerosis and ageing of the vasculature all involving a loss of relaxation. The antioxidant enzymes glutathione peroxidase, superoxide dismutase and catalase play a crucial role in defending against the ravages of oxidative stress. Our purpose was to characterize age-related changes in glutathione peroxidase, superoxide dismutase and catalase in the rat aorta. Aortas were extracted from seven young (4 months), seven middle aged (18 months) and seven old (24 months) animals. Analysis of variance was used with Fisher-LSD post hoc to determine mean differences among glutathione peroxidase, superoxide dismutase and catalase. Aortic glutathione peroxidase activities rose steadily with age expressed in micromol mg protein-1 min-1 +/- SEM (young: 141 +/- 22; middle aged: 198 +/- 18; old: 229 +/- 26) reaching significance between young and old. Superoxide dismutase activities significantly decreased in middle aged when compared with young (young: 22 +/- 2 vs. middle aged: 15 +/- 2 U mg protein-1) before trending upward again in old age (19 +/- 2). Catalase activities dropped significantly between young and old when expressed in mU mg protein-1 (young: 230 +/- 30; middle aged: 173 +/- 18; old: 144 +/- 23). Ratios for the various enzymes indicate a shrinking contribution of catalase with ageing, with an enhanced role for glutathione peroxidase in the antioxidant defence. These data in aortas of ageing rats show a complex alteration of the antioxidant profile.     

Oxidative stress and antioxidant defenses in goldfish liver in response to short-term exposure to arsenite

Arsenic is an environmental pollutant capable of causing oxidative stress, disturbance of metabolism, and cancer development. The present study was undertaken to investigate the effects of exposure to sodium arsenite on the glutathione pool, lipid peroxidation, protein carbonyl levels, global DNA methylation, and activities of six antioxidant enzymes in goldfish liver. In a preliminary experiment, 7-day exposure to 200 microM sodium arsenite, but not 10 or 100 microM, disturbed the glutathione status. A detailed investigation of oxidative stress development and antioxidant responses was further examined during different periods of exposure to 200 microM sodium arsenite. This treatment increased lipid peroxide levels after 1 and 4 days of exposure but did not affect thiobarbituric acid reactive substances and protein carbonyls. Oxidized glutathione and the oxidative stress index rose after 4 days, but de novo glutathione synthesis decreased both parameters after 7 days. Activities of the main antioxidant enzymes-superoxide dismutase, catalase, and glutathione peroxidase, were elevated after longer periods of exposure, indicating an enhanced antioxidant response. Arsenite exposure led to DNA hypomethylation, which is an early marker of disturbed epigenetic regulations. The findings suggest that goldfish livers cope with arsenic-induced oxidative stress mainly through adaptive changes in the glutathione pool and antioxidant enzymes.     

Effect of lemon verbena supplementation on muscular damage markers, proinflammatory cytokines release and neutrophils�� oxidative stress in chronic exercise

Intense exercise is directly related to muscular damage and oxidative stress due to excessive reactive oxygen species (ROS) in both, plasma and white blood cells. Nevertheless, exercise-derived ROS are essential to regulate cellular adaptation to exercise. Studies on antioxidant supplements have provided controversial results. The purpose of this study was to determine the effect of moderate antioxidant supplementation (lemon verbena extract) in healthy male volunteers that followed a 90-min running eccentric exercise protocol for 21 days. Antioxidant enzymes activities and oxidative stress markers were measured in neutrophils. Besides, inflammatory cytokines and muscular damage were determined in whole blood and serum samples, respectively. Intense running exercise for 21 days induced antioxidant response in neutrophils of trained male through the increase of the antioxidant enzymes catalase, glutathione peroxidase and glutathione reductase. Supplementation with moderate levels of an antioxidant lemon verbena extract did not block this cellular adaptive response and also reduced exercise-induced oxidative damage of proteins and lipids in neutrophils and decreased myeloperoxidase activity. Moreover, lemon verbena supplementation maintained or decreased the level of serum transaminases activity indicating a protection of muscular tissue. Exercise induced a decrease of interleukin-6 and interleukin-1β levels after 21 days measured in basal conditions, which was not inhibited by antioxidant supplementation. Therefore, moderate antioxidant supplementation with lemon verbena extract protects neutrophils against oxidative damage, decreases the signs of muscular damage in chronic running exercise without blocking the cellular adaptation to exercise.     

Borneol administration protects primary rat hepatocytes against exogenous oxidative DNA damage

Experimental evidences suggest that most essential oils possess a wide range of biological and pharmacological activities that may protect tissues against oxidative damage. In this study, we investigated DNA-protective effect of borneol, a component of many essential oils, against oxidative DNA damage induced in primary cultures of rat hepatocytes. Borneol was added to drinking water of Sprague-Dawley rats and DNA resistance against oxidative agents was compared in hepatocytes originated from control and borneol-treated rats. Oxidative stress induced by visible light-excited methylene blue (MB/VL) or 2,3-dimethoxy-1,4-naphthoquionone (DMNQ) resulted in increased levels of DNA lesions measured by the modified single cell gel electrophoresis. Borneol (17 or 34 mg/kg body weight) added to drinking water of rats for 7 days reduced the level of oxidative DNA lesions induced in their hepatocytes by MB/VL or DMNQ. To explain the increased resistance of DNA towards oxidative stress, we measured the base-excision repair (BER) capacity in liver cell extracts of control and borneol-supplemented rats on DNA substrate of HepG2 cells containing oxidative damage. Our results showed that administration of borneol in drinking water had no effect on incision activity of hepatocytes isolated from supplemented rats. The spectrophotometric assessment of enzymatic antioxidants superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and the flow cytometric assessment of total intracellular glutathione (iGSH) in primary hepatocytes of borneol-supplemented rats showed no changes in SOD and GPx activities but higher iGSH content particularly in hepatocytes of higher borneol dose (34 mg/kg) supplemented rats in comparison to control animals. Despite the fact that borneol had no effect either on BER of oxidative DNA damage or on the levels of antioxidant enzymes and manifested no reducing power and radicals scavenging activity, it increased significantly the level of non-enzymatic antioxidant iGSH which could reduce the oxidative DNA lesions induced by MB/VL or DMNQ.     

Ageing alters aortic antioxidant enzyme activities in Fischer-344 rats

Oxidative stress imposed by reactive oxygen species is now believed to contribute to hypertension, atherosclerosis and ageing of the vasculature all involving a loss of relaxation. The antioxidant enzymes glutathione peroxidase, superoxide dismutase and catalase play a crucial role in defending against the ravages of oxidative stress. Our purpose was to characterize age-related changes in glutathione peroxidase, superoxide dismutase and catalase in the rat aorta. Aortas were extracted from seven young (4 months), seven middle aged (18 months) and seven old (24 months) animals. Analysis of variance was used with Fisher-LSD post hoc to determine mean differences among glutathione peroxidase, superoxide dismutase and catalase. Aortic glutathione peroxidase activities rose steadily with age expressed in μmol mg protein^?1 min^?1± SEM (young: 141 ± 22; middle aged: 198 ± 18; old: 229 ± 26) reaching significance between young and old. Superoxide dismutase activities significantly decreased in middle aged when compared with young (young: 22 ± 2 vs. middle aged: 15 ± 2 U mg protein^?1) before trending upward again in old age (19 ± 2). Catalase activities dropped significantly between young and old when expressed in mU mg protein^?1 (young: 230 ± 30; middle aged: 173 ± 18; old: 144 ± 23). Ratios for the various enzymes indicate a shrinking contribution of catalase with ageing, with an enhanced role for glutathione peroxidase in the antioxidant defence. These data in aortas of ageing rats show a complex alteration of the antioxidant profile.     

Genetic damage in wood dust-exposed workers

Exposure to wood dust is common in carpentry workshops. Wood dust is known to be a human carcinogen, with a very high relative risk of adenocarcinoma of the nasal cavities and paranasal sinuses. The goal of this investigation was to conduct genotoxicity monitoring of carpenters involved in wooden furniture industry in order to test possible wood dust-induced genotoxic effects due to occupational exposure. The level of genetic damage was determined by comet, micronucleus and chromosomal aberration (CA) assays in peripheral blood lymphocytes (PBL) of 60 carpentry workers. In addition, the micronucleus test in buccal epithelial cells was carried out in the same subjects. Total antioxidant enzyme activities were measured by the indices: superoxide dismutase, glutathione peroxidase and catalase. A group of 60 non-exposed subjects matched by age, smoking and alcohol consumption habits were chosen as controls. The effect of age, smoking, alcohol consumption and duration of exposure was also analysed in the subjects of the present study. The results showed a statistically significant increase in mean DNA damage by comet assay, micronuclei frequency in buccal cells as well as PBL and frequency of CA in the exposed workers when compared to controls (P < 0.05). Analysis of the data showed that all the confounding factors had a significant effect on DNA damage and micronucleus frequency in buccal epithelial cells and PBL. Smoking and alcohol consumption did not have any significant effect by chromosomal aberration test. Antioxidant enzyme levels significantly decreased in the exposed subjects. Our findings indicate enhanced levels of genotoxicity in carpenters. Hence, these workers may have an increased cancer risk.     

In vitro mitigation of arsenic toxicity by tea polyphenols in human lymphocytes.

The groundwater arsenicals have brought dreadful misery for the people residing in the endemic regions of West Bengal, India. Arsenic-related anomalies include arsenicosis, hyperkera-tosis, gastric complications, liver fibrosis, peripheral neuropathy, and cancer. Some of these diseases have been frequently associated with overproduction of reactive oxygen species that cause DNA damage and improper functioning of body's antioxidant defense mechanism. Natural polyphenols present in tea serve as excellent antioxidants. In the present study, an attempt has been made to elucidate the role of representative polyphenols and extracts of green and black tea in modulating sodium arsenite (As III)-induced DNA damage in normal human lymphocytes. Comet assay was used to detect the DNA damage. Arsenic-induced oxidative stress was measured with generation of reactive oxygen species, lipid peroxidation, and activity of some antioxidant enzymes. Expression of some repair enzymes such as poly(ADP-ribose) polymerase and DNA polymerase beta was measured to assess the effect of tea on DNA repair. Tea afforded efficient reduction of As III-induced DNA damage in human lymphocytes. Tea also quenched the excessive production of reactive oxygen species by arsenic, reduced the elevated levels of lipid peroxidation, and increased the activity of antioxidant enzymes such as catalase, superoxide dismutase, and glutathione peroxidase. Furthermore, tea enhanced recovery of DNA damage, which was indicative of repair as confirmed by unscheduled DNA synthesis and pronounced expression of DNA repair enzyme poly(ADP-ribose) polymerase. It is speculated that the antioxidant potential and repair-inducing capacity of tea might help in combating the severe genotoxic effects induced by arsenic in the human population.     

Effects of Nigella sativa on oxidative stress and beta-cell damage in streptozotocin-induced diabetic rats

The aim of the present study was to evaluate the possible protective effects of Nigella sativa L. (NS) against beta-cell damage from streptozotocin (STZ)-induced diabetes in rats. STZ was injected intraperitoneally at a single dose of 50 mg/kg to induce diabetes. NS (0.2 ml/kg/day, i.p.) was injected for 3 days prior to STZ administration, and these injections were continued throughout the 4-week study. Oxidative stress is believed to play a role in the pathogenesis of diabetes mellitus (DM). To assess changes in the cellular antioxidant defense system, we measured the activities of antioxidant enzymes (such as glutathione peroxidase (GSHPx), superoxide dismutase (SOD), and catalase (CAT)) in pancreatic homogenates. We also measured serum nitric oxide (NO) and erythrocyte and pancreatic tissue malondialdehyde (MDA) levels, a marker of lipid peroxidation, to determine whether there is an imbalance between oxidant and antioxidant status. Pancreatic beta-cells were examined by immunohistochemical methods. STZ induced a significant increase in lipid peroxidation and serum NO concentrations, and decreased antioxidant enzyme activity. NS treatment has been shown to provide a protective effect by decreasing lipid peroxidation and serum NO, and increasing antioxidant enzyme activity. Islet cell degeneration and weak insulin immunohistochemical staining was observed in rats with STZ-induced diabetes. Increased intensity of staining for insulin, and preservation of beta-cell numbers were apparent in the NS-treated diabetic rats. These findings suggest that NS treatment exerts a therapeutic protective effect in diabetes by decreasing oxidative stress and preserving pancreatic beta-cell integrity. Consequently, NS may be clinically useful for protecting beta-cells against oxidative stress.     

Age-related changes in Cu,Zn superoxide dismutase, Se-dependent and -independent glutathione peroxidase and catalase activities in specific areas of rat brain.

Oxidative injury of tissues involves both accumulation of damage due to persistent oxidative stress and loss of the proper balance of antioxidative enzymes. These events may produce a faster rate of tissue senescence. In this regard, we have assayed the antioxidative enzyme activities (Cu,Zn superoxide dismutase, glutathione peroxidase and catalase), in various areas of rat brain (prefrontal cortex, parietal cortex, hippocampus, hypothalamus, caudate nucleus, mesencephalon and lower brain stem) for the age groups of 3, 6, 12, 24 months. The results obtained show that the levels of antioxidant enzyme activities differed considerably in the various brain parts studied. Furthermore, changes in the specific activities of superoxide dismutase, catalase, and glutathione peroxidase did not follow the same pattern as a function of aging. In particular, in prefrontal cortex and caudate nucleus, superoxide dismutase and glutathione peroxidase activities did not change, while catalase activity decreased. In parietal cortex and mesencephalon, superoxide dismutase and glutathione peroxidase activities increased, but the catalase activity decreased in parietal cortex and did not change in mesencephalon. In lower brain stem, the activities of glutathione peroxidase and catalase decreased in 3-12-month-old rats. The activity of glutathione peroxidase was increased in the hippocampus and was decreased in hypothalamus during aging. In this area the catalase activity was also significantly diminished.     

Importance of a threshold for error accumulation in cell degenerative processes. I. Modulation of the threshold in a model of free radical-induced cell degeneration

Antioxidant enzymes (catalase, superoxide dismutase and glutathione peroxidase) have been injected into human fibroblasts exposed to 2 atm O2 in order to test if the threshold of oxidative damage versus antioxidant defenses could be modulated and if the damage remains reversible beyond the threshold. Cell damage was estimated by thymidine incorporation and cell survival curves. The proportion of dividing cells, measured by thymidine incorporation, rapidly decreased after O2 incubation: no cells could divide after 15 h of hyperoxia. However, cells incubated for a short time and injected with a high concentration of any of the three enzymes divided like non-oxygen-incubated cells: the enzymes could protect the cells against their loss of division potential. However, when cells were incubated for a longer period and/or when the injected enzyme concentration was lower, cells were either less or not protected and could no longer divide. These results suggest the presence of a threshold for the oxidative damage which cannot be totally repaired and which impairs the cell division; this threshold can, however, be modulated by supplementation of antioxidant enzymes, glutathione peroxidase being the most efficient.     

Decrease in Antioxidant Status of Plasma and Erythrocytes from Geriatric Population

Background: Ageing is associated with an accumulation of free radical damage, which leads to physiological and clinical modifications. The study aims to find out the status of lipid profile, antioxidant enzymes, malondialdehyde in geriatric population. Patients/methods: The study was conducted on 150 subjects (75 healthy control between the ages of 20–30 years and 75 elderly subjects between ages of 50–70 years as cases). The following parameters were analyzed using the standard reference methods: lipid profile, reduced glutathione, glutathione peroxidase, glutathione reductase, catalase, superoxide dismutase and malondialdehyde. Results: The present study was conducted to estimate the oxidative stress parameters in geriatric population. Highly significant increase in total cholesterol (TC), triglyceride (TG), LDL-cholesterol (LDL-C), VLDL-cholesterol (VLDL-C), malondialdehyde, catalase and decrease in high density lipoprotein cholesterol (HDL-C), reduced glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase was observed in geriatrics when compared with their younger counterparts. Conclusion: This study concluded that there is enhanced oxidative stress and decreased antioxidant defence in geriatrics as compared to younger subjects which could play an important role in ageing. Dyslipidemia has become one of the important risk factors for the increasing prevalence of cardiovascular diseases. There is lack of awareness on the relationship between blood lipids and the risk of cardiovascular diseases in geriatric population. The strategy of early prevention should be adopted against dyslipidemia.     

Lisinopril as an antioxidant in hypertension?

Lisinopril is an inhibitor of the renin-angiotensin system. Does lisinopril minimize oxidative damage in spontaneously hypertensive rats (SHR) in comparison with the normotensive genetic controls Wistar Kyoto (WKY)? The authors note that lisinopril contained lipid peroxidation, elevated tissue glutathione levels, and influenced the activity of antioxidant enzymes such as catalase and glutathione peroxidase. Studies in humans testing the hypothesis that lisinopril has antioxidant function in vivo are warranted.     

Protective effect of the cruciferous vegetable mustard leaf (Brassica campestris) against in vivo chromosomal damage and oxidative stress induced by gamma-radiation and genotoxic chemicals

We evaluated the possible protective effect of the popular Indian cruciferous vegetable mustard leaf (Brassica campestris) against chromosomal damage and oxidative stress induced by gamma-radiation, cyclophosphamide (CPH) and urethane (URE), in mice. In vivo bone marrow micronucleus test was performed to assess chromosomal damage, and oxidative stress was monitored by estimating the changes in lipid peroxidation and the status of glutathione (GSH) as well as redox cycle antioxidants. Pretreatment with 50-250 mg/kg body wt of mustard leaf extract (MLE) for seven days significantly reduced the frequencies of micronuclei induced by gamma-radiation, CPH and URE. The protective effect against chromosomal damage was associated with modulation of lipid peroxidation as well as an increase in GSH and the GSH-dependent enzyme glutathione S-transferase (GST). Mass spectral analysis showed the presence of glucosinolates in MLE used for the pretreatment of mice. These findings indicate that intake of the green leafy cruciferous vegetable mustard leaf can lead to protection against in vivo genotoxicity and oxidative stress.     

Prevention of cisplatin-induced nephrotoxicity by glucosides of ascorbic acid and alpha-tocopherol

BACKGROUND: Cisplatin is one of the most widely used cytotoxic therapeutic agents for the treatment of cancer. This drug, at effective higher doses, causes many physiological adverse effects such as nephrotoxicity and genotoxicity. The toxicity of the drug has been attributed to the induction of oxidative free radicals. METHODS: Following intraperitoneal administration of cisplatin and ascorbic acid monoglucoside (AsAG) or alpha-tocopherol monoglucoside (TMG), investigations were conducted on levels of serum urea and creatinine, peroxidation of lipids in renal tissues, renal antioxidants and histopathology of renal tissue. RESULTS: Administration of cisplatin to mice induced a marked renal failure, characterized by significant increase in serum urea and creatinine levels in addition to severe alterations in renal tissue architecture. Cisplatin also induced oxidative stress as indicated by increased lipid peroxidation and decreased levels of reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase in renal tissues. Administration of AsAG or TMG markedly reduced the cisplatin-induced higher plasma creatinine and urea levels and counteracted the deleterious effects of cisplatin on oxidative stress markers and protected the tissues from the cisplatin-induced lipid peroxidation. CONCLUSION: These results indicated that AsAG or TMG has a protective effect against cisplatin-induced renal damage in mice. The protection is mediated by preventing the decline of antioxidant status. The results have implications in use of AsAG or TMG in human application for protecting against drug-induced nephrotoxicity.     

Lycopene attenuates oxidative stress and heart lysosomal damage in isoproterenol induced cardiotoxicity in rats: A biochemical study

The present study was designed to investigate the cardioprotective potential of lycopene (LYC) on isoproterenol (ISO)-induced oxidative stress and heart lysosomal damage in rats. Male Sprague Dawley rats were pretreated with LYC (4mg/kg, p.o.) once daily for 21 days. After the treatment period, ISO (85mg/kg) was injected subcutaneously, once daily, to rats for 2 days. Hemodynamic parameters, cardiac marker enzymes, antioxidant, and oxidative stress parameters in serum and heart tissues were measured. ISO treated rats showed significant changes in heart rates, heart weights and serum lipid profiles. The activity of aspartate aminotranferase (AST), lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB) and cardiac troponin T (cTnT) were increased significantly (p<0.01) in the serum of ISO rats. The levels of lipid peroxides (thiobarbituric acid reactive substances, TBARS), protein carbonyl content (PCC) and neutrophil infiltration marker; myeloperoxidase (MPO) were significantly (p<0.01) increased. In addition, the activities of lysosomal enzymes (beta-glucuronidase, beta-N-acetylglucosaminidase, and cathepsin-d) in the serum and heart of ISO rats were increased significantly. Furthermore, a marked decrease in the levels of serum and cardiac reduced glutathione (GSH), vitamin C and cardiac enzymatic antioxidants; superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were observed. In vitro study confirmed the strong antioxidant effect of LYC on total antioxidant activity. In conclusion, the present study demonstrated that LYC supplementation to ISO rats significantly ameliorated lysosomal membrane damage as well as the alterations in cardiac enzymes, lipid profile and oxidative stress markers. These findings revealed the cardioprotective effects of LYC against ISO-induced oxidative stress and cardiotoxicity in rats. These observed effects are mediated via antioxidant power and free radical scavenging activity of LYC.     

Hepatoprotection with a chloroform extract of Launaea procumbens against CCl4-induced injuries in rats

ABSTRACT: BACKGROUND: Launaea procumbens (Asteraceae) is used as a folk medicine to treat hepatic disorders in Pakistan. The effect of a chloroform extract of Launaea procumbens (LPCE) was evaluated against carbon-tetrachloride (CCl4)-induced liver damage in rats. METHODS: To evaluate the hepatoprotective effects of LPCE, 36 male Sprague-Dawley rats were equally divided into six groups. Animals of group 1 (control) had free access to food and water. Group II received 3 ml/kg of CCl4 (30% in olive oil v/v) via the intraperitoneal route twice a week for 4 weeks. Group III received 1 ml of silymarin via gavage (100 mg/kg b.w.) after 48 h of CCl4 treatment whereas groups IV and V were given 1 ml of LPCE (100 and 200 mg/kg b.w., respectively) after 48 h of CCl4 treatment. Group VI received 1 ml of LPCE (200 mg/kg b.w.) twice a week for 4 weeks. The activities of the antioxidant enzymes catalase, peroxidase (POD), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), glutathione reductase (GSR), glutathione (GSH) and lipid peroxidation (thiobarbituric acid reactive substances (TBARS)) were measured in liver homogenates. DNA damage, argyrophilic nucleolar organizer regions (AgNORs) counts and histopathology were studied in liver samples. Serum was analyzed for various biochemical parameters. Phytochemical composition in LPCE was determined through high-performance liquid chromatography (HPLC). RESULTS: LPCE inhibited lipid peroxidation, and reduced the activities of aspartate transaminase, alanine transaminase, alkaline phosphatase, and lactate dehydrogenase in serum induced by CCl4. GSH contents were increased as were the activities of antioxidant enzymes (catalase, SOD, GST, GSR, GSH-Px) when altered due to CCl4 hepatotoxicity. Similarly, absolute liver weight, relative liver weight and the number of hepatic lesions were reduced with co-administration of LPCE. Phyochemical analyses of LPCE indicated that it contained catechin, kaempferol, rutin, hyperoside and myricetin. CONCLUSION: These results indicated that Launaea procumbens efficiently protected against the hepatotoxicity induced by CCl4 in rats, possibly through the antioxidant effects of flavonoids present in LPCE. KEYWORDS: Launaea procumbens, hepatic injuries, flavonoids, antioxidant enzymes, carbon tetrachloride.     

Blood antioxidant parameters in sickle cell anemia patients in steady state

Sickle cell anemia (SCA) is a hereditary disorder with higher potential for oxidative damage due to chronic redox imbalance in red cells. We measured antioxidant enzymes including catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD). We also determined oxidative damage of proteins in hemolysate of red blood cells (RBCs) and plasma (carbonyl assay). We characterized the membrane damage in terms of lipid peroxidation by accumulation of malonaldehyde (MDA) by HPLC in 30 healthy controls and 20 SCA patients in steady-state condition. Twenty (9 males/11 females) adult SCA patients and 30 healthy controls were studied. All patients and control subjects had antioxidant (CAT, GPx, SOD, carbonyl and MDA) and hematological parameters done. Our data show that SCA patients had significant higher GPx and SOD activities than healthy controls. Carbonyl assay was noted in plasma but not in hemolysate. An enhanced production of MDA was observed in the serum of SCA patients. Our data support the growing evidence that patients with SCA are subjected to chronic oxidative stress and are able to oxidative damage in biological macromolecules such as proteins and lipids.     

Effect of dequalinium on the oxidative stress in Plasmodium berghei-infected erythrocytes

The bisquinoline drug dequalinium (DQ) has demonstrated remarkable activity against some infection diseases, including malaria. Oxidative stress represents a biochemical target for potential antimalarials. In this work, we have tested the ability of this compound to modify the oxidative status in Plasmodium berghei-infected erythrocytes. After hemolysis, activities of superoxide dismutase (SOD), catalase (CAT), glutathione cycle, and dehydrogenase enzymes were investigated. The activity of glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGLD) in infected cells were diminished by this drug compared to controls (300% and 80% approximately, respectively), while glutathione peroxidase (GPx), glutathione transferase (GST), and glutathione levels were also lowered. As a compensatory response, we could appreciate an increase of SOD activity (20% approximately) in infected cells treated with DQ; however, catalase was not affected by the compound. Lipid peroxidation was also decreased by this drug, protecting the cells from the hemolysis caused by the infection. In conclusion, oxidative stress represents a biochemical event which is modulated by DQ, interfering with the antioxidant regular activities in P. berghei infection.