Protective Effect of Hyperbaric Oxygen on Cognitive Impairment Induced by <Emphasis Type="SmallCaps">d</Emphasis>-Galactose in Mice

Memory decline is characteristic of aging and age-related neurodegenerative disorders. This study was designed to investigate the protective effect of hyperbaric oxygen (HBO) against cognitive impairment induced by d-galactose (d-gal) in mice. d-gal was intraperitoneally injected into mice daily for 8 weeks to establish the aging model. HBO was simultaneously administered once daily. The results indicate that HBO significantly reversed D-gal-induced learning and memory impairments. Studies on the potential mechanisms of this action showed that HBO significantly reduced oxidative stress by increasing superoxide dismutase, glutathione peroxidase, and catalase levels, as well as the total anti-oxidation capability, while decreasing the content of malondialdehyde, nitric oxide, and nitric oxide synthase in the hippocampal CA1 region. HBO also inhibited advanced glycation end-product formation and decreased levels of tumor necrosis factor-α and interleukin-6. Moreover, HBO significantly attenuated d-gal-induced pathological injury in the hippocampus, as well as β-amyloid protein_1?42 expression and retained BDNF expression. Furthermore, HBO decreased p16, p21 and p53 gene and protein expression in the hippocampus of d-gal-treated mice. In conclusion, the protective effect of HBO against d-gal-induced cognitive impairment was mainly due to its ability to reduce oxidative damage, suppress inflammatory responses, and regulate aging-related gene expression.     

Brain Mitochondrial Dysfunction in Ovariectomized Mice Injected with <Emphasis Type="SmallCaps">d</Emphasis>-Galactose

Our previous studies reveal that long-term exposure of ovariectomized rodents to d-galactose results in pathophysiologic alterations associated with Alzheimer’s disease. The current study was to address whether mitochondrial dysfunction was involved in the pathogenesis of this model. Ovariectomized mice were administered intraperitoneally with d-galctose (100 mg/kg body weight) once a day for 8 weeks. Brain tissues from model mice showed decreases in reduced glutathione level, total antioxidative capabilities, total superoxide dismutase activity and glutathione peroxidase activity but an increase in malondialdehyde level, compared with those from sham-operated plus saline-injected mice. Activities of brain mitochondrial respiratory chain (complex I, II, III and IV) were reduced in model group. In contrast, ATP synthase (F₁F₀-ATPase) activity was not significantly different between the two groups. Moreover, electron microscopy identified ultrastructural impairments of hippocampal mitochondria in model mice. These results demonstrated that brain mitochondrial degeneration caused by oxidative stress participated in the etiology of ovarian hormone deprivation and d-galactose-induced neurodegeneration.     

<Superscript>1</Superscript>H-NMR-Based Metabonomics Study on the Restorative Effect of Soybean Polypeptide in Rats of Oxidative Damaged Induced by <Emphasis Type="SmallCaps">d</Emphasis>-Galactose

Soybean polypeptide TTYY has substantial antioxidant activity. The present study aimed to investigate the mechanisms of the potential ability of TTYY to allow rats to recover from oxidative damage using ¹H-NMR-based metabonomics. Male Wistar rats received injections of d-galactose to establish the oxidative damage model, then gavaged with TTYY. After treatment, principal component analysis and partial least squares-discriminant analysis were performed to identify different metabolic profiles based on the ¹H-NMR spectra of urine from rats and liver antioxidant capacity analysis were also performed. The oxidation-induced changed in biological endpoints were reversed to a certain extent in the rats treated with TTYY compared with the control group. The potential biomarkers in the urine were identified as follows: pyruvate, 2-ketoglutarate, alanine, glycine, citrate, creatine, lactate, and acetate. The results show that TTYY may counterbalance the oxidative damage induced by d-galactose, and most likely plays a role in the changes observed in certain metabolic pathways including those involved in energy, amino acid, and glycolysis metabolisms.     

Inhibition of <Emphasis Type="SmallCaps">d</Emphasis>-Amino-Acid Oxidase Activity Induces Pain Relief in Mice

(1). We investigated the effects of inhibiting d-amino-acid oxidase (DAO) activity on nociceptive responses through the use of mutant ddY/DAO⁻ mice, which lack DAO activity, and through the application of a selective inhibitor of DAO, sodium benzoate, in the tail flick test, hot-plate test, formalin test, and acetic acid-induced writhing test. (2). Compared with normal ddY/DAO⁺ mice, ddY/DAO⁻ mice showed significantly prolonged tail withdrawal latency in the tail flick test and licking/jumping latency in the hot-plate test, as well as significantly reduced duration of licking/biting in the late phase of the formalin test and the number of abdominal writhing in the acetic acid-induced writhing test. (3). In addition, we investigated the effects of sodium benzoate in Kunming mice having normal DAO activity. (4). Intravenous administration of sodium benzoate (400 mg/kg) significantly inhibited pain responses of the late phase of the formalin test and abdominal writhing responses in the acetic acid-induced writhing test, with no effects on the early phase flinch responses in the formalin test, nociceptive responses in the tail flick test, or hot-plate test. (5). These results suggest that DAO acts as a pro-nociceptive factor in pain, particularly chronic pain, transmission and modulation, and may be a target for pain treatment.     

Temporal Gene Expression Profile in Hippocampus of Mice Treated with <Emphasis Type="SmallCaps">d</Emphasis>-galactose

(1) Rodent chronically treated with D-galactose (D-gal) is increasingly used in pharmacological studies on aging; however, its mechanism remains unclear. The present study investigated the alterations of gene expression in the hippocampus of D-gal-treated mice. (2) C57 mice were subcutaneously injected with D-gal for 2, 4, and 8 weeks or vehicle, and then were subjected to behavioral tests. Gene expression profiles in hippocampus of each group were finally examined with cDNA microarray. (3) Both 4- and 8-week D-gal treatment led to a decrease of discrimination index in object recognition test, and 8-week D-gal-treated mice showed significant spatial learning & memory impairment in Morris water maze test. In comparison with the vehicle control group, the 2-, 4-, and 8-week D-gal treatment repressed the expression of 10, 13, and 30 genes by 2-fold or more, respectively. The early pattern was mainly characterized by down regulation of genes involved in ion transport. The delayed pattern included genes involved in protein biosynthesis, transport and signal transduction, which were highly related to synaptic functions. (4) These findings will contribute to the understanding of the mechanism of learning and memory impairment in mice treated with D-galactose.     

Structure of the K82 Capsular Polysaccharide from <Emphasis Type="Italic">Acinetobacter baumannii</Emphasis> LUH5534 Containing a <Emphasis Type="SmallCaps">d</Emphasis>-Galactose 4,6-Pyruvic Acid Acetal

Type K82 capsular polysaccharide (CPS) was isolated from Acinetobacter baumannii LUH5534. The structure of a linear tetrasaccharide repeating unit of the CPS was established by sugar analysis along with one- and two-dimensional ¹H and ¹³C NMR spectroscopy. Proteins encoded by the KL82 capsule gene cluster in the genome of LUH5534 were assigned to roles in the synthesis of the K82 CPS. In particular, functions were assigned to two new glycosyltransferases (Gtr152 and Gtr153) and a novel pyruvyltransferase, Ptr5, responsible for the synthesis of D-galactose 4,6-(R)-pyruvic acid acetal.     

Acetyl-<Emphasis Type="SmallCaps">l</Emphasis>-Carnitine Attenuates Arsenic-Induced Oxidative Stress and Hippocampal Mitochondrial Dysfunction

Augmentation of mitochondrial oxidative stress through activating a series of deadly events has implicated as the main culprit of arsenic toxicity and therapeutic approaches based on improving mitochondrial function hold a great promise for attenuating the arsenic-induced toxicity. Acetyl-l-carnitine (ALC) through balancing the coenzyme A (CoA)/acyl-CoA ratio plays an important role in mitochondrial metabolism and thereby can help protect hippocampal neurons from oxidative damage. In the present study, we aimed to explore the effect of arsenic interactions on the mitochondrial function in the hippocampus of rats. Rats were randomly divided into five groups of control (distilled water), sodium arsenite (NaAsO₂, 20 mg/kg), and co-treatment of NaAsO₂ with various doses of ALC in three groups (100, 200, 300 mg/kg) and were treated orally for 21 consecutive days. Our results point out that arsenic exposure caused oxidative stress in rats’ hippocampus, which led to the reactive oxygen species (ROS) generation, mitochondrial swelling, the collapse of the mitochondrial membrane potential, and release of cytochrome c. It also altered Bcl-2/Bax expression ratio and increased caspase-3 and caspase-9 activities. Furthermore, arsenic exposure via activation of NF-κB and microglia increased inflammation. ALC could concentration-dependently counteract the arsenic-induced oxidative stress, modulate the antioxidant defense capacity, and improve mitochondrial functions. In addition, ALC decreased the expression of both death-associated proteins and of inflammatory markers. These findings indicate that ALC improved the arsenic-induced hippocampal mitochondrial dysfunction which underlines the importance of ALC in providing a possible therapeutic strategy for the prevention of arsenic-induced neurodegeneration.     

<Emphasis Type="SmallCaps">l</Emphasis>-Carnitine Blood Levels and Oxidative Stress in Treated Phenylketonuric Patients

Aims l-Carnitine exerts an important role by facilitating the mitochondrial transport of fatty acids, but is also a scavenger of free radicals, protecting cells from oxidative damage. Phenylketonuria (PKU), an inborn error of phenylalanine (Phe) metabolism, is currently treated with a special diet consisting of severe restriction of protein-enriched foods, therefore potentially leading to l-carnitine depletion. The aim of this study was to determine l-carnitine levels and oxidative stress parameters in blood of two groups of PKU patients, with good and poor adherence to treatment. Methods Treatment of patients consisted of a low protein diet supplemented with a synthetic amino acids formula not containing Phe, l-carnitine, and selenium. l-Carnitine concentrations and the oxidative stress parameters thiobarbituric acid reactive species (TBARS) and total antioxidant reactivity (TAR) were measured in blood of the two groups of treated PKU patients and controls. Results We verified a significant decrease of serum l-carnitine levels in patients who strictly adhered to the diet, as compared to controls and patients who did not comply with the diet. Furthermore, TBARS measurement was significantly increased and TAR was significantly reduced in both groups of phenylketonuric patients relatively to controls. We also found a significant negative correlation between TBARS and l-carnitine levels and a significant positive correlation between TAR and l-carnitine levels in well-treated PKU patients. Conclusions Our results suggest that l-carnitine should be measured in plasma of treated PKU patients, and when a decrease of this endogenous component is detected in plasma, supplementation should be considered as an adjuvant therapy.     

Selenium and <Emphasis Type="SmallCaps">l</Emphasis>-Carnitine Reduce Oxidative Stress in the Heart of Rat Induced by 2.45-GHz Radiation from Wireless Devices

The aim of this study was to investigate the possible protective role of selenium and l-carnitine on oxidative stress induced by 2.45-GHz radiation in heart of rat. For this purpose, 30 male Wistar Albino rats were equally divided into five groups namely controls, sham controls, radiation-exposed rats, radiation-exposed rats treated with intraperitoneal injections of sodium selenite at a dose of 1.5 mg/kg/day, and radiation-exposed rats treated with intraperitoneal injections of l-carnitine at a dose of 1.5 mg/kg/day. Except for the controls and sham controls, the animals were exposed to 2.45-GHz radiation during 60 min/day for 28 days. The lipid peroxidation (LP) levels were higher in the radiation-exposed groups than in the control and sham control groups. The lipid peroxidation level in the irradiated animals treated with selenium and l-carnitine was lower than in those that were only exposed to 2.45-GHz radiation. The concentrations of vitamins A, C, and E were lower in the irradiated-only group relative to control and sham control groups, but their concentrations were increased in the groups treated with selenium- and l-carnitine. The activity of glutathione peroxidase was higher in the selenium-treated group than in the animals that were irradiated but received no treatment. The erythrocyte-reduced glutathione and β-carotene concentrations did not change in any of the groups. In conclusion, 2.45-GHz electromagnetic radiation caused oxidative stress in the heart of rats. There is an apparent protective effect of selenium and l-carnitine by inhibition of free radical formation and support of the antioxidant redox system.     

Topiramate Improves Neuroblast Differentiation of Hippocampal Dentate Gyrus in the <Emphasis Type="SmallCaps">d</Emphasis>-Galactose-Induced Aging Mice via Its Antioxidant Effects

Some anticonvulsant drugs are associated with cognitive ability in patients; Topiramate (TPM) is well known as an effective anticonvulsant agent applied in clinical settings. However, the effect of TPM on the cognitive function is rarely studied. In this study, we aimed to observe the effects of TPM on cell proliferation and neuronal differentiation in the dentate gyrus (DG) of the d-galactose-induced aging mice by Ki-67 and doublecortin (DCX) immunohistochemistry. The study is divided into four groups including control, d-galactose-treated group, 25 and 50 mg/kg TPM-treated plus d-galactose-treated groups. We found, 50 mg/kg (not 25 mg/kg) TPM treatment significantly increased the numbers of Ki-67⁺ cells and DCX immunoreactivity, and improved neuroblast injury induced by d-galactose treatment. In addition, we also found that decreased immunoreactivities and protein levels of antioxidants including superoxide dismutase and catalase induced by d-galactose treatment were significantly recovered by 50 mg/kg TPM treatment in the mice hippocampal DG (P < 0.05). In conclusion, our present results indicate that TPM can ameliorate neuroblast damage and promote cell proliferation and neuroblast differentiation in the hippocampal DG via increasing SODs and catalase levels in the d-galactose mice.     

Effects of the Methanolic Extract of <Emphasis Type="Italic">Vitellaria paradoxa</Emphasis> Stem Bark Against Scopolamine-Induced Cognitive Dysfunction and Oxidative Stress in the Rat Hippocampus

Vitellaria paradoxa C.F. Gaertn (Sapotaceae) is a perennial three which naturally grows in the northern part of Cameroon. It has been traditionally used in the Cameroonian folk medicine for treating inflammation and pain. In the present study, we evaluate the possible anti-amnesic and antioxidative effects of the methanolic extract of V. paradoxa stem bark in an Alzheimer’s disease (AD) rat model of scopolamine. Rats received a single injection of scopolamine (1.5 mg/kg) before behavioral testing and were treated with the methanolic extract (25 and 50 mg/kg), daily, for eight continuous days. Also, the antioxidant activity in the hippocampus was assessed using the total content of reduced glutathione and malondialdehyde levels. The scopolamine-treated rats exhibited the following: decrease of exploratory time and discrimination index within the novel object recognition test, decrease of spontaneous alternations percentage within Y-maze task, and increase of working memory errors, reference memory errors, and time taken to consume all five baits within radial arm-maze task. Administration of the methanolic extract significantly improved these parameters, suggesting positive effects on memory formation processes and antioxidant potential. Our results suggest that the methanolic extract ameliorates scopolamine-induced memory impairment by attenuation of the oxidative stress in the rat hippocampus.     

Exogenous Salicylic Acid Alleviates Growth Inhibition and Oxidative Stress Induced by Hypoxia Stress in <Emphasis Type="Italic">Malus robusta</Emphasis> Rehd

Salicylic acid (SA) as a signal molecule mediates many biotic and environmental stress-induced physiologic responses in plants. In this study we investigated the role of SA in regulating growth and oxidative stress in Malus robusta Rehd under both normoxic and hypoxic conditions. Hypoxia stress inhibited plant growth and dramatically reduced biomass. Addition of SA significantly alleviated the plant growth inhibition. The amounts of superoxide radicals (O₂ ⁻) and hydrogen peroxide (H₂O₂) significantly increased in leaves of the plants exposed to hypoxia stress and resulted in oxidative stress, which was indicated by accumulated concentration of malondialdehyde (MDA) and electrolyte leakage. Addition of SA significantly decreased the level of O₂ ⁻, electrolyte leakage, and lipid peroxidation and enhanced the activities of superoxide dismutase (SOD), peroxidase (POD), and ascorbate peroxidase (APX) under hypoxia stress. As important antioxidants, ascorbate (AsA) and glutathione (GSH) contents in the plant leaves were slightly increased by SA treatment compared to hypoxia stress treatment alone. It was concluded that SA could alleviate the detrimental effects of hypoxia stress on plant growth and of oxidative stress by enhancing the antioxidant defense system in leaves of M. robusta Rehd.     

The Protective Role of <Emphasis Type="SmallCaps">d</Emphasis>-Glucose Against 1-Methyl-4-Phenylpyridinium Ion (MPP<Superscript>+</Superscript>): Induced Mitochondrial Dysfunction in C6 Astroglial Cells

Impaired mitochondrial function in glial and neuronal cells in the substantia nigra is one of the most likely causes of Parkinson’s disease. In this study, we investigated the protective role of glucose on early key events associated with MPP⁺-induced changes in rat C6 astroglial cells. Studies were carried out to examine alterations in mitochondrial respiratory status, membrane potential, glutathione levels, and cell cycle phase inhibition at 48 h in 2 and 10 mM glucose in media. The results obtained suggest that MPP⁺ caused significant cell death in 2 mM glucose with LC₅₀ 0.14 ± 0.005 mM, while 10 mM glucose showed highly significant protection against MPP⁺ toxicity with LC₅₀ 0.835 ± 0.03 mM. This protection was not observed with cocaine, demonstrating its compound specificity. MPP⁺ in 2 mM glucose decreased significantly mitochondrial respiration, membrane potential and glutathione levels in a dose dependent manner, while 10 mM glucose significantly restored them. MPP⁺ in 2 mM glucose arrested the cells at G0/G1 and G2/M phases, demonstrating its dual inhibitory effects. However, in 10 mM glucose, MPP⁺ caused G0/G1 arrest only. In summary, the results suggest that loss of cell viability in 2 mM glucose group with MPP⁺ treatments was due to mitochondrial dysfunction caused by multilevel mechanism, involving significant decrease in mitochondrial respiration, membrane potential, glutathione levels, and dual arrest of cell phases, while 10 mM glucose rescued astroglial cells from MPP⁺ toxicity by significant maintenance of these factors.     

Involvement of <Emphasis Type="Italic">soxRS</Emphasis> Regulon in Response of <Emphasis Type="Italic">Escherichia coli</Emphasis> to Oxidative Stress Induced by Hydrogen Peroxide

The effect of hydrogen peroxide on the activity of soxRS and oxyR regulon enzymes in different strains of Escherichia coli has been studied. Treatment of bacteria with 20 μM H₂O₂ caused an increase in catalase and peroxidase activities (oxyR regulon) in all strains investigated. It is shown for the first time that oxidative stress induced by hydrogen peroxide causes in some E. coli strains a small increase in activity of superoxide dismutase and glucose-6-phosphate dehydrogenase (soxRS regulon). This effect is cancelled by chloramphenicol, an inhibitor of protein synthesis in prokaryotes. The increase in soxRS regulon enzyme activities was not found in the strain lacking the soxR gene. These results provide evidence for the involvement of the soxRS regulon in the adaptive response of E. coli to oxidative stress induced by hydrogen peroxide. __________ Translated from Biokhimiya, Vol. 70, No. 11, 2005, pp. 1506–1513. Original Russian Text Copyright ? 2005 by Semchyshyn, Bagnyukova, Lushchak.     

Oxidative Imbalance,Nitrative Stress,and Inflammation in C6 Glial Cells Exposed to Hexacosanoic Acid: Protective Effect of <Emphasis Type="Italic">N</Emphasis>-acetyl-<Emphasis Type="SmallCaps">l</Emphasis>-cysteine,Trolox, and Rosuvastatin

X-linked adrenoleukodystrophy (X-ALD) is an inherited neurometabolic disorder caused by disfunction of the ABCD1 gene, which encodes a peroxisomal protein responsible for the transport of the very long-chain fatty acids from the cytosol into the peroxisome, to undergo β-oxidation. The mainly accumulated saturated fatty acids are hexacosanoic acid (C26:0) and tetracosanoic acid (C24:0) in tissues and body fluids. This peroxisomal disorder occurs in at least 1 out of 20,000 births. Considering that pathophysiology of this disease is not well characterized yet, and glial cells are widely used in studies of protective mechanisms against neuronal oxidative stress, we investigated oxidative damages and inflammatory effects of vesicles containing lecithin and C26:0, as well as the protection conferred by N-acetyl-l-cysteine (NAC), trolox (TRO), and rosuvastatin (RSV) was assessed. It was verified that glial cells exposed to C26:0 presented oxidative DNA damage (measured by comet assay and endonuclease III repair enzyme), enzymatic oxidative imbalance (high catalase activity), nitrative stress [increased nitric oxide (NO) levels], inflammation [high Interleukin-1beta (IL-1β) levels], and induced lipid peroxidation (increased isoprostane levels) compared to native glial cells without C26:0 exposure. Furthermore, NAC, TRO, and RSV were capable to mitigate some damages caused by the C26:0 in glial cells. The present work yields experimental evidence that inflammation, oxidative, and nitrative stress may be induced by hexacosanoic acid, the main accumulated metabolite in X-ALD, and that antioxidants might be considered as an adjuvant therapy for this severe neurometabolic disease.     

<Emphasis Type="Italic">Bacopa monnieri</Emphasis> Extract Offsets Rotenone-Induced Cytotoxicity in Dopaminergic Cells and Oxidative Impairments in Mice Brain

Bacopa monnieri (BM), an ayurvedic medicinal herb is widely known for its memory enhancing ability and improvement of brain function. In this study, we tested the hypothesis that BM extract (BME) could offset neurotoxicant-induced oxidative dysfunctions in developing brain in a rotenone (ROT) mouse model. Pretreatment of dopaminergic (N27 cell lines) cells with BME exhibited significant cytoprotective effect as evidenced by the attenuation of ROT-induced oxidative stress and cell death. Further, the neuroprotective efficacy of BME was assessed in prepubertal mice administered ROT (i.p. 1.0 mg/kg b.w./day) for 7 days. BME treatment significantly offset ROT-induced oxidative damage in striatum (St) and other brain regions as evident by the normalized levels of oxidative markers (malondialdehyde, ROS levels, and hydroperoxides) and restoration of depleted GSH levels. Further, BME effectively normalized the protein carbonyl content in all brain regions suggesting its ability to prevent protein oxidation. Furthermore, BME treatment restored the activity levels of cytosolic antioxidant enzymes, neurotransmitter function, and dopamine levels in St. Based on our findings, we hypothesize that the neuroprotective effects of BM extract may be at least in part related to its ability to enhance reduced glutathione and antioxidant defenses in brain regions. It is suggested that BM may be effectively exploited as a prophylactic/therapeutic adjuvant for neurodegenerative disorders involving oxidative stress.     

Cognition Enhancing Activity of Sulforaphane Against Scopolamine Induced Cognitive Impairment in Zebra Fish (<Emphasis Type="Italic">Danio rerio</Emphasis>)

Several epidemiological studies have shown that consumption of large quantities of vegetables especially cruciferous vegetables (Broccoli and Brussels sprouts) can protect against chronic diseases. Sulforaphane, an isothiocynate found in cruciferous vegetables has been demonstrated to have neuroprotective effects in several experimental paradigms. This study was undertaken to examine the effect of sulforaphane on cognitive impairment in zebra fish model using a novel method of fear conditioning. Initially, the normal behaviour of zebra fishes was studied in light-dark tank for 10 min daily for 10 days. Fishes were then divided into seven groups of twelve in each. Group I served as normal, group II served as fear conditioned control, group III and group IV were sulforaphane (25 µM/L) and piracetam (200 mg/L) treated respectively. Group V served as scopolamine (400 µM/L) induced memory impairment fishes. Group VI and VII were sulforaphane (25 µM/L) and piracetam (200 mg/L) treated scopolamine induced memory impairment groups respectively. In normal behavioural analysis, fishes preferred to stay in dark compartment. The average number of entries into the dark and time spent in dark were significantly more. Fishes in group II to VII were individually subjected to fear conditioning passive avoidance task and evaluated for learned task memory. It was observed that the average number of entries into dark and time spent in dark were significantly decreased. After exposure to respective treatment fishes in group III to VII were subjected to cognitive evaluation. There was no significant difference in cognition of group III and IV fishes exposed to sulforaphane and piracetam alone respectively. Fishes exposed to scopolamine showed a significant cognitive impairment. Sulforaphane exposure prior to scopolamine significantly retained the memory of learned task. These findings suggest that sulforaphane might be a promising therapeutic agent for cognitive enhancement in Alzheimer’s disease.     

Oxidative Processes Induced by <Emphasis Type="Italic">tert</Emphasis>-Butyl Hydroperoxide in Human Red Blood Cells: Chemiluminescence Studies

The erythrocyte is a good model for investigation of the mechanisms of cell damage induced by oxidizing agents. Oxidative damage to cell components and cellular metabolism results in impaired rheological properties of circulating red blood cells and is involved in the development of some pathologies. The aim of the present study was to elucidate further the oxidative processes induced by tert-butyl hydroperoxide (tBOOH) in erythrocytes, identify cellular targets damaged by the oxidant, as well as estimate the energy and stoichiometry of the reactions that occur. The generation of free radicals in the cell was registered using the chemiluminescence technique. The products of oxyhemoglobin (oxyHb) oxidation, changes in intracellular glutathione (GSH) pool, and accumulation of the stable products of membrane lipid peroxidation were concurrently measured. The oxidative processes induced by tBOOH in red blood cells can be described as follows: 1) rapid GSH oxidation (30-60 sec) by glutathione peroxidase; 2) formation of radicals in the reaction between tBOOH and cellular Hb, which are then immediately consumed in lipid peroxidation reactions; 3) generation of chemiluminescence by the radicals formed. Several stages of the oxidative processes can be revealed. The order of the chemiluminescence reaction (n) with respect to oxidant was estimated to be equal to 2.5 at oxidant concentrations less than 0.5 mM and equal to 1.0 at higher oxidant concentrations. The order of the reaction of membrane lipid peroxidation was found to be n = 2.2 at 0.25-0.6 mM tBOOH and n = 0.5 at higher oxidant concentrations. The apparent activation energy of membrane lipid peroxidation was 55.8 +/- 6.4 kJ/mol, and that of oxyHb oxidation was 108 +/- 16 kJ/mol. It is shown that the interaction of tBOOH and HOCl in erythrocytes is accompanied by changes in both the total number of radicals generated in the cell and the time corresponding to the maximal rate of radical generation.     

Anionic Surfactant,Linear Alkyl Benzene Sulphonate Induced Oxidative Stress and Hepatic Impairments in Fish <Emphasis Type="Italic">Channa punctatus</Emphasis>

Linear alkyl benzene sulphonate (LAS), one of the main ingredients used in synthetic detergents to enhance their cleansing properties. Indiscriminate and untreated discharge of detergents and their residues in both lantic and lotic habitats pose a variety of ecological threats and also adversely affect aquatic fauna. In vivo, LAS metabolism and biotransformation occurs via monooxygenases in liver, leading to Reactive Oxygen Species, ROS, production and consequently oxidative stress by disturbing cellular antioxidant enzymatic equilibrium. Present study aims to evaluate the activities of two widely distributed antioxidant enzymes viz., catalase (CAT) and superoxide dismutase (SOD) and ROS induced histological impairments in liver of freshwater fish, Channa punctatus. For the estimation of oxidative stress and hepatic impairments, well acclimatized fishes were divided in three groups. Fish of group G1 serves as control whereas fish of the other two groups, G2 and G3 were exposed to two fractions, 1/20th and 1/10th of 96 h LC₅₀ of LAS for 24, 48, 72 and 96 h of exposure periods. Our results showed a significant induction in CAT and SOD activities in liver tissue of C. punctatus in a dose and time dependent manner. ROS induced histopathological impairments in hepatic tissues are characterized by loosely arranged, irregularly distributed and degenerated hepatocytes with increased vacuolization and pyknotic nuclei. The results are quite suggestive that LAS intoxication generates oxidative stress by ROS production which brings about histopathological impairments in exposed fish.     

<Emphasis Type="Italic">Lactobacillus plantarum</Emphasis> CCFM639 Alleviate Trace Element Imbalance-Related Oxidative Stress in Liver and Kidney of Chronic Aluminum Exposure Mice

Aluminum (Al) has various adverse effects on health of humans and animals. The aim of present study was to demonstrate that Lactobacillus plantarum CCFM639 can alleviate the adverse effects on liver and kidney of mice caused by chronic Al exposure. Animals were assigned into control, CCFM639 only, Al only, Al plus CCFM639, and Al plus deferiprone groups. The strain was given by oral gavage for 14 weeks, and Al was introduced via drinking water for the first 8 weeks. Analyses of Al and trace elements levels in feces, blood, and tissues were performed. The biochemical markers (GSH, GPx, SOD, CAT, and MDA) of oxidative stress in livers and kidneys, as well as the levels of ALT, AST, BUN, and CRE in blood, were determined. Our results showed that L. plantarum CCFM639 can significantly reduce Al accumulation in tissues, regulate imbalance of trace elements, and thereby alleviate oxidative stress and pathological changes in hepatic and renal tissues. Therefore, L. plantarum CCFM639 could alleviate Al-induced hepatic and renal injuries, and the possible mechanisms may involve in regulating the imbalance of trace elements.