Antioxidant defenses and oxidative stress parameters in tissues of mud crab (Scylla serrata) with reference to changing salinity

The effects of salinity (10, 17 and 35 ppt) on O₂ consumption, CO₂ release and NH₃ excretion by crabs and oxidative stress parameters and antioxidant defenses of its tissues were reported. An increase in salinity caused a decrease in O₂ consumption and CO₂ release and an increase in ammonia excretion by crabs. Lipid peroxidation, protein carbonyl, H₂O₂ levels and total antioxidant capacity of the tissues elevated significantly at 35 ppt salinity except in abdominal muscle where H₂O₂ content was low. Ascorbic acid content of tissues was higher at 17 ppt salinity than at 10 and 35 ppt salinities. With increasing salinity, a gradual decrease in SOD, an increase in catalase, no change in GPx and a decrease followed by an increase in GR activities were recorded for abdominal muscle. While for hepatopancreas, an increase followed by a decrease in SOD and catalase, decrease in GPx and GR activities were noticed with increasing salinity. In the case of gills, a decrease followed by an increase in SOD, a decrease in catalase and GPx and an increase in GR activities were noted when the salinity increased from 10 ppt to 35 ppt. These results suggest that salinity modulation of oxidative stress and antioxidant defenses in Scylla serrata is tissue specific.     

Antioxidant effect of diphenyl diselenide against sodium nitroprusside (SNP) induced lipid peroxidation in human platelets and erythrocyte membranes: an in vitro evaluation

An in vitro evaluation on the antioxidant effect of diphenyl diselenide (PhSe)(2), an organochalcogenide, against sodium nitroprusside (SNP)-induced lipid peroxidation (LPO) was conduced. Human platelets and erythrocyte membranes (ghosts), as well as rat brain homogenates (S(1)), were pre-incubated with different concentrations of SNP (0-10 microM). All SNP concentrations tested significantly increased LPO in human platelets and S(1). Platelets were more sensitive to SNP-induced peroxidative damage when compared to S(1). SNP 10 microM decreased glutathione peroxidase (GPx) activity and did not affect glutathione reductase (GR) and catalase (CAT) activities in human platelets. However, ghosts were insensitive to SNP-induced LPO and no changes on GPx, GR and CAT activities were observed. Diphenyl diselenide significantly protected human platelets against SNP-induced LPO and recovered GPx inactivation. This effect was more evident at (PhSe)(2) concentrations above 2 microM. The presented results indicate that (PhSe)(2) exerts protective effects on SNP-induced oxidative damage in human blood components and in rat brain. These phenomena seem to be related to its thiol peroxidase-like activity and to a possible direct interaction with SNP and derivatives. Based on our results and on literature, diphenyl diselenide can be pointed as a promising antioxidant molecule.     

Selenium and mercury levels in rat liver slices co-treated with diphenyl diselenide and methylmercury

Organoseleno-compounds have been investigated for its beneficial effects against methylmercury toxicity. In this way, diphenyl diselenide (PhSe)₂ was demonstrated to decrease Hg accumulation in mice, protect against MeHg-induced mitochondrial dysfunction, and protect against the overall toxicity of this metal. In the present study we aimed to investigate if co-treatment with (PhSe)₂ and MeHg could decrease accumulation of Hg in liver slices of rats. Rat liver slices were co-treated with (PhSe)₂ (0.5; 5 µM) and/or MeHg (25 µM) for 30 min at 37 °C and Se and Hg levels were measured by inductively coupled plasma mass spectrometry (ICP-MS) in the slices homogenate, P1 fraction, mitochondria and incubation medium. Co-treatment with (PhSe)₂ and MeHg did not significantly alter Se levels in any of the samples when compared with compounds alone. In addition, co-treatment with (PhSe)₂ and MeHg did not decrease Hg levels in any of the samples tested, although, co-incubation significantly increased Hg levels in homogenate. We suggest here that (PhSe)₂ could exert its previously demonstrated protective effects not by reducing MeHg levels, but forming a complex with MeHg avoiding it to bind to critical molecules in cell.     

Selenium supplementation shows protective effects against patulin-induced brain damage in mice via increases in GSH-related enzyme activity and expression

Aims

This study was designed to investigate the protective effects of selenium supplementation on patulin-induced neurotoxicity.

Main methods

Mice were subjected to patulin for 8 weeks. Sodium selenite (Na₂SeO₃) and selenium–methionine (Se–Met) were supplemented with the diet, and we investigated the effects of selenium on patulin-induced neurotoxicity. The animals were randomly divided into 4 groups containing 6–8 mice each. The first group was used as a control, and only physiological saline (0.9%) was injected. The second group was treated with patulin (1 mg/kg) intraperitoneally. The third group was treated with patulin (1 mg/kg) along with a dietary supplementation of Na₂SeO₃ (0.2 mg Se/kg of diet). The fourth group was treated with patulin (1 mg/kg) plus Se–Met (0.2 mg Se/kg of diet).

Key findings

Patulin treatment increased oxidative damage in the brain, as evidenced by a decrease in non-protein thiol and total thiol groups, along with significant increases in GSSG, reactive oxygen species, thiobarbituric acid reactive substances and protein carbonyl levels. Moreover, the activities of glutathione peroxidase (GPx) and glutathione reductase were inhibited with patulin treatment. Selenium supplementation significantly ameliorated these biological parameter changes. In addition, selenium treatments significantly increased the mRNA levels of GPx-1, GPx-4 and thioredoxin reductase.

Significance

Our data show that selenium supplementation increases the activity and expression of glutathione-related enzymes and offers significant protection against brain damage induced by patulin.     

The role of the glutathione system in seizures induced by diphenyl diselenide in rat pups

The present study investigated the role of the glutathione system in seizures induced by diphenyl diselenide (PhSe)₂ (50 mg/kg) in rat pups (post natal day, 12–14). Reduced glutathione (GSH) (300 nmol/site; i.c.v.), administered 20 min before (PhSe)₂, abolished the appearance of seizures, protected against the inhibition of catalase and δ-aminolevulinic dehydratase (δ-ALA-D) activities and increased glutathione peroxidase (GPx) activity induced by (PhSe)₂. Administration of l-buthionine sulfoximine (BSO, a GSH-depleting compound) (3.2 μmol/site; i.c.v.) 24 h before (PhSe)₂ increased the percentage (42–100%) of rat pups which had seizure episodes, reduced the onset for the first convulsive episode. In addition, BSO increased thiobarbituric acid reactive species (TBARS) levels and decreased GSH content, catalase, δ-ALA-D and Na⁺, K⁺-ATPase activities. Treatment with sub effective doses of GSH (10 nmol/site) and d-2-amino-7-phosphonoheptanoic acid (AP-7, an antagonist of the glutamate site at the NMDA receptor; 5 mg/kg, i.p.) abolished the appearance of seizures induced by (PhSe)₂ in rat pups. Sub effective doses of GSH and kynurenic acid (an antagonist of strychnine-insensitive glycine site at the NMDA receptor; 40 mg/kg, i.p.) were also able in abolishing the appearance of seizures induced by (PhSe)₂. In conclusion, administration of GSH protected against seizure episodes induced by (PhSe)₂ in rat pups by reducing oxidative stress and, at least in part, by acting as an antagonist of glutamate and glycine modulatory sites in the NMDA receptor.     

Fluoride-Induced Oxidative Stress in Rat’s Brain and Its Amelioration by Buffalo (<Emphasis Type="Italic">Bubalus bubalis</Emphasis>) Pineal Proteins and Melatonin

Fluoride (F) becomes toxic at higher doses and induces some adverse effects on various organs, including brain. The mechanisms underlying the neurotoxicity caused by excess fluoride still remain unknown. The aims of this study were to examine F-induced oxidative stress (OS) and role of melatonin (MEL) and buffalo pineal proteins (PP) against possible F-induced OS in brain of rats. The 24 rats were taken in present study and were divided into four groups: control, F, F + PP, and F + MEL. The F group was given 150 mg/L orally for 28 days. Combined 150 ppm F and 100 μg/kg BW (i.p.) PP and F (150 ppm) + MEL (10 mg/kg BW, i.p.) were also administered. The activities of enzymatic, viz., superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione reductase (GR), and non-enzymatic, viz., reduced glutathione (GSH) concentration, and the levels of malondialdehyde (MDA) in the brain tissue were measured to assess the OS. Fluoride administration significantly increased brain MDA compared with control group, while GSH levels were decreased in fluoride-treated groups, accompanied by the markedly reduced SOD, GPx, GR, and SOD activity. Buffalo PP and MEL administration caused brain MDA to decrease but caused SOD, GPx, GR, GSH, and CAT activities to increase to significant levels in F-treated animals. Together, our data provide direct evidence that buffalo PP and MEL may protect fluoride-induced OS in brain of rats through mechanisms involving enhancement of enzymatic and non-enzymatic antioxidant defense system. Therefore, this study suggested that PP and MEL can be useful in control of neurotoxicity induced by fluoride.     

Diphenyl ditelluride targets brain selenoproteins in vivo: inhibition of cerebral thioredoxin reductase and glutathione peroxidase in mice after acute exposure

In this study, we investigated the effect of diphenyl ditelluride (PhTe)₂ administration (10 and 50?μmol/kg) on adult mouse behavioral performance as well as several parameters of oxidative stress in the brain and liver. Adult mice were injected with (PhTe)₂ or canola oil subcutaneously (s.c.) daily for 7?days. Results demonstrated that (PhTe)₂ induced prominent signs of toxicity (body weight loss), behavioral alterations and increased in lipid peroxidation in brain. 50?μmol/kg (PhTe)₂ inhibited blood δ-aminolevulinic acid dehydratase (δ-ALA-D), a redox sensitive enzyme. (PhTe)₂ caused an increase in cerebral non-protein thiol (NPSH) and protein thiol (PSH) groups. In the liver, 50?μmol/kg (PhTe)₂ decreased NPSH, but did not alter the content of protein thiol groups. (PhTe)₂ decreased cerebral antioxidant enzymes (catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), and thioredoxin reductase (TrxR). In liver, (PhTe)₂ increase SOD and GR and decreased GPx activity. Results obtained herein suggest that the brain was more susceptible to oxidative stress induced by (PhTe)₂ than the liver. Furthermore, we have demonstrated for the first time that TrxR is an in vivo target for (PhTe)_2. Combined, these results highlight a novel molecular mechanism involved in the toxicity of (PhTe)₂. In particular the inhibition of important selenoenzymes (TrxR and GPx) seems to be involved in the neurotoxicity associated with (PhTe)₂ exposure in adult mice.     

Modulation of antioxidant defence system in brain of rainbow trout (Oncorhynchus mykiss) after chronic carbamazepine treatment

We investigated the effect of long-term exposure to CBZ on the antioxidant system in brain tissue of rainbow trout. Fish were exposed to sublethal concentrations of CBZ (1.0 μg/L, 0.2 mg/L or 2.0 mg/L) for 7, 21, and 42 days. Oxidative stress indices (LPO and CP) and activities of antioxidant enzymes (SOD, CAT, GPx and GR) in fish brain were measured. In addition, non-enzymatic antioxidant (GSH) was determined after 42 days exposure. Carbamazepine exposure at 0.2 mg/L led to significant increases (p < 0.05) of LPO and CP after 42 days and, at 2.0 mg/L, after 21 days. Activities of the antioxidant enzymes SOD, CAT, and GPx in CBZ-treated groups slightly increased during the first period (7 days). However, activities of all measured antioxidant enzymes were significantly inhibited (p < 0.05) at 0.2 mg/L exposure after 42 days and after 21 days at 2.0 mg/L. After 42 days, the content of GSH in fish brain was significantly lower (p < 0.05) in groups exposed to CBZ at 0.2 mg/L and 2.0 mg/L than in other groups. Prolonged exposure to CBZ resulted in excess reactive oxygen species formation, finally resulting in oxidative damage to lipids and proteins and inhibited antioxidant capacities in fish brain. In short, a low level of oxidative stress could induce the adaptive responses of antioxidant enzymes, but long-term exposure to CBZ could lead to serious oxidative damage in fish brain.     

Induction of Oxidative Stress by Chronic and Acute Glutaric Acid Administration to Rats

1. Glutaric acidemia type I (GA I) is a neurometabolic disorder caused by deficiency of glutaryl-CoA dehydrogenase, which leads to tissue accumulation of predominantly glutaric acid (GA) and also 3-hydroxyglutaric acid to a lesser amount. Affected patients usually present progressive cortical atrophy and acute striatal degeneration attributed to the toxic accumulating metabolites. 2. In the present study, we determined a number of oxidative stress parameters, namely chemiluminescence, thiobarbituric acid-reactive substances (TBA-RS), total antioxidant reactivity (TAR), glutathione (GSH) levels, and the activities of catalase and glutathione peroxidase (GPx), in various tissues from rats chronically exposed to GA or to saline (controls). High GA concentrations, similar to those found in glutaric aciduria type I, were induced in the brain by three daily subcutaneous injections of saline-buffered GA (5 μmol/g body weight) to Wistar rats of 5–22 days of life. The parameters were assessed 12 h after the last GA administration in different brain structures, skeletal muscle, heart, liver, erythrocytes, and plasma. The lipid peroxidation parameters chemiluminescence and/or TBA-RS measurements were found significantly increased in midbrain, liver, and erythrocytes of GA-injected rats. The activity of GPx was significantly reduced in midbrain and markedly increased in liver. TAR measurement was significantly reduced in midbrain and liver. Furthermore, GSH levels were reduced in liver and heart. We also investigated the acute in vivo effect of GA administration on the same oxidative stress parameters in cerebral structures and erythrocytes from 22-day-old rats. We found that TBA-RS values were significantly increased in erythrocytes, TAR levels were markedly decreased in midbrain and cerebellum, and GPx activity mildly reduced in the midbrain. 3. These data showing an imbalance between antioxidant defences and oxidative damage, particularly in midbrain, liver, and erythrocytes from GA-injected rats, indicate that oxidative stress might be involved in GA toxicity and that the midbrain, where the striatum is located, is the brain structure more susceptible to GA chronic and acute exposition.     

Oxidized LDL and its correlation with lipid profile and oxidative stress biomarkers in young healthy Spanish subjects

The biological effects of oxidized LDL (oxLDL) may contribute to initiation and progression of the atherosclerotic process, and the association between cardiovascular disease and oxidation of LDL has been largely demonstrated. The objectives of this study were to establish the reference values of oxidative stress biomarkers in a young healthy Spanish population to determine the concentration of oxLDL and its relationship with lipid profile and with these biomarkers. oxLDL, F₂-isoprostanes, protein carbonyls (PC), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) were determinate by ELISA in 72 healthy subjects. Antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR) were carried out on a Hitachi 912 analyzer; lipid profile were assayed using automated systems (Cobas 711, Roche Diagnostics). All statistics were analyzed by using SPSS for Windows 15.0. SPSS Inc, Chicago, IL, USA. (Normal mean reference values): oxLDL (63.23 ± 16.23 U/L), (Male/Female 68.06 ± 17.69/58.39 ± 13.6 U/L), F₂-isoprostanes (2.26 ± 0.9 μg/g creatinine), PC (0.34 ± 0.15 nmol/mg), 8-OHdG (23.27 ± 10.58 ng/ml), SOD (931.97 ± 271.09 U/g Hb), GR (46.56 ± 11.68 U/L), GPx (27.58 ± 6.89 U/gHb (Male/Female 25.91 ± 5.03/29.2 ± 8.07 U/L)). OxLDL (63.23 U/L) was significantly (p < 0.05) positively correlated with BMI (22.53 Kg/m²), total cholesterol (175.79 mg/dl), triglycerides (87.58 mg/dl), LDL cholesterol (96.25 mg/dl), and uric acid (4.78 mg/dl), while negatively correlated with HDL-cholesterol (62.25 mg/dl). We have found different correlation between oxLDL and isoprostanes by gender with the rest of parameters. Normal reference values have been found significantly different for oxLDL and GPx by gender. Oxidized LDL is correlated with lipid profile but not with the oxidative stress biomarkers. Urinary isoprostanes are positively correlated with triglycerides and negatively with GR and GPx.     

Dealing with 1,3-bis(4-nitrophenyl)triazene as intermediary ligand in the synthesis of polymeric (μ-Se)Hg-clusters: One-pot synthetic procedures and X-ray structural characterization of [(PhSe)7Hg4BrPy]n

(PhSe)₂Hg reacts initially with HgBr₂ and further with 1,3-bis(4-nitrophenyl)triazene to give [(PhSe)₇Hg₄BrPy]_n (Py = pyridine) the first polymeric assembling of (μ-Se)Hg clusters obtained with a triazene as coordinating intermediary ligand. Each single molecule of adamantane alike [(PhSe)₇Hg₄BrPy] presents the Hg^II ions with a distorted tetrahedral configuration linked through asymmetric [μ-(Ph)Se]⁻ bridges. [(PhSe)₇Hg₄BrPy]_n represents an example of extended one-dimensional chains of closed anisotropic ME (E = S, Se, Te) systems. In these reactions the features of the intermediary ligands should determine the template which leads to single adamantane moieties or to fused ones.     

Anticancer effect of selenium/chitosan/polyethylene glycol/allyl isothiocyanate nanocomposites against diethylnitrosamine-induced liver cancer in rats

BackgroundNano-based drug delivery systems have shown several advantages in cancer treatment like specific targeting of cancer cells, good pharmacokinetics, and lesser adverse effects. Liver cancer is a fifth most common cancer and third leading cause of cancer-related mortalities worldwide.ObjectiveThe present study focusses to formulate the selenium (S)/chitosan (C)/polyethylene glycol (Pg)/allyl isothiocyanate (AI) nanocomposites (SCPg-AI-NCs) and assess its therapeutic properties against the diethylnitrosamine (DEN)-induced liver cancer in rats via inhibition of oxidative stress and tumor markers.MethodologyThe SCPg-AI-NCs were synthesized by ionic gelation technique and characterized by various characterization techniques. The liver cancer was induced to the rats by injecting a DEN (200 mg/kg) on the 8th day of experiment. Then DEN-induced rats treated with 10 mg/kg of formulated SCPg-AI-NCs an hour before DEN administration for 16 weeks. The 8-hydroxy-2′ -deoxyguanosine (8-OHdG) content, albumin, globulin, and total protein were examined by standard methods. The level of glutathione (GSH), vitamin-C & -E, and superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR) activities were examined using assay kits. The liver marker enzymes i.e., alanine transaminase (ALT), aspartate tansaminase (AST), γ-glutamyl transaminase (GGT), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP) activities, alpha fetoprotein (AFP) and carcinoembryonic antigen (CEA), Bax, and Bcl-2 levels, and caspase-3&9 activities was examined using assay kits and the liver histopathology was assessed microscopically by hematoxylin and eosin staining method. The effect of formulated SCPg-AI-NCs on the viability and apoptotic cell death on the HepG2 cells were examined using MTT and dual staining assays, respectively.ResultsThe results of different characterization studies demonstrated the formation of SCPg-AI-NCs with tetragonal shape, narrowed distribution, and size ranging from 390 to 450 nm. The formulated SCPg-AI-NCs treated liver cancer rats indicated the reduced levels of 8-OHdG, albumin, globulin, and total protein. The SCPg-AI-NCs treatment appreciably improved the GSH, vitamin-C & -E contents, and SOD, CAT, GPx, and GR activities in the serum of liver cancer rats. The SCPg-AI-NCs treatment remarkably reduced the liver marker enzyme activities in the DEN-induced rats. The SCPg-AI-NCs treatment decreased the AFP and CEA contents and enhanced the Bax and caspase 3&9 activities in the DEN-induced rats. The SCPg-AI-NCs effectively decreased the cell viability and induced apoptosis in the HepG2 cells.ConclusionThe present findings suggested that the formulated SCPg-AI-NCs remarkably inhibited the DEN-induced liver carcinogenesis in rats. These findings provide an evidence that SCPg-AI-NCs can be a promising anticancer nano-drug in the future to treat the liver carcinogenesis.     

Green tea catechins potentiate the neuritogenic action of brain-derived neurotrophic factor: Role of 67-kDa laminin receptor and hydrogen peroxide

Delivery of optimal amounts of brain-derived neurotrophic factor (BDNF) to regions of the brain affected by neurodegenerative diseases is a daunting task. Using natural products with neuroprotective properties, such as green tea polyphenols, would be a highly useful complementary approach for inexpensive long-term treatment of these diseases. In this study, we used PC12(TrkB) cells which ectopically express TrkB, a high affinity receptor for BDNF. They differentiate and induce neurite outgrowth in response to BDNF. Using this model, we show for the first time that treatment with extremely low concentrations (<0.1 μg/ml) of unfractionated green tea polyphenols (GTPP) and low concentrations (<0.5 μM) of their active ingredient, epigallocatechin-3-gallate (EGCG), potentiated the neuritogenic ability of a low concentration (2 ng/ml) of BDNF. A synergistic interaction was observed between GTPP constituents, where epigallocatechin and epicatechin, both individually lacking this activity, promoted the action of EGCG. GTPP-induced potentiation of BDNF action required the cell-surface associated 67 kDa laminin receptor (67LR) to which EGCG binds with high affinity. A cell-permeable catalase abolished GTPP/EGCG-induced potentiation of BDNF action, suggesting the possible involvement of H₂O₂ in the potentiation. Consistently, exogenous sublethal concentrations of H₂O₂, added as a bolus dose (5 μM) or more effectively through a steady-state generation (1 μM), potentiated BDNF action. Collectively, these results suggest that EGCG, dependent on 67LR and H₂O₂, potentiates the neuritogenic action of BDNF. Intriguingly, this effect requires only submicromolar concentrations of EGCG. This is significant as extremely low concentrations of polyphenols are believed to reach the brain after drinking green tea.     

Changes in biochemical parameters in rabbits blood after oral exposure to diphenyl diselenide for long periods

The concept that selenium-containing molecules may be better antioxidants than classical antioxidants, has led to the design of synthetic organoselenium compounds. The present study was conducted to evaluate the potential toxicity of long time oral exposure to diphenyl diselenide (PhSe)2 in rabbits. Male adult New Zealand rabbits were divided into four groups, group I served as control; groups II, III and IV received 0.3, 3.0 and 30 ppm of (PhSe)2 pulverized in the chow for 8 months. A number of parameters were examined in blood as indicators of toxicity, including delta-aminolevulinate dehydratase (delta-ALA-D), catalase, glutathione peroxidase (GPx), alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, creatinine, TBARS, non-protein-SH, ascorbic acid and selenium. The results demonstrated that 6 and 8 months of 30 ppm (PhSe)2 intake caused a significant increase in blood delta-ALA-D activity. Erythrocyte non-protein thiol levels were significantly increased after 2 months of 30 ppm (PhSe)2 intake and then return to control levels after prolonged periods of intake. Ingestion of 3.0 ppm of (PhSe)2 for 8 months significantly increased catalase activity in erythrocytes. Conversely, no alterations in GPx, ALT, AST, TBARS and selenium levels were observed in rabbit serum, conversely, selenium levels in peri-renal adipose tissue were significantly increased after 8 months of 30 ppm (PhSe)2 intake, indicating its great lipophylicity. The present results suggest that diphenyl diselenide was not hepato- or renotoxic for rabbits, but caused some biochemical alterations that can be related to some pro-oxidant activity of the compound (particularly the reduction in Vitamin C).     

Diphenyl diselenide and diphenyl ditelluride: neurotoxic effect in brain of young rats, in vitro

This study examined whether maturity of rat brain may be relevant for the sensitivity to diphenyl diselenide (PhSe)₂ and diphenyl ditelluride (PhTe)₂ on [³H]glutamate uptake and release, in vitro. Brain synaptosomes were isolated from young (14- and 30-day-old) and adult rats and incubated at different concentrations of (PhSe)₂ or (PhTe)₂. The results demonstrated that the highest concentration (100 μM) of (PhSe)₂ and (PhTe)₂ inhibited the [³H]glutamate uptake by synaptosomes of brain at all ages. In the adult brain, (PhSe)₂ did not inhibit the [³H]glutamate uptake at the lowest concentration (10 μM). The highest concentration of (PhTe)₂ inhibited the [³H]glutamate uptake more in the 14-day-old than in the 30-day-old rats or adult rats. In the 30-day-old animals, the highest concentration of (PhSe)₂, and the lowest concentration of (PhTe)₂, increased the basal [³H]glutamate release. At the highest concentration, (PhTe)₂ increased the basal and K⁺-stimulated glutamate release on all ages evaluated. The results suggest that (PhSe)₂ and (PhTe)₂ caused alterations on the homeostasis of the glutamatergic system at the pre-synaptic level. These alterations were age-, concentration-, and compound-dependent. The maturity of rat brain is relevant for the glutamatergic system sensitivity to (PhSe)₂ and (PhTe)₂ .     

The Influence of Sulphate Deposition on the Seasonal Variation of Peat Pore Water Methyl Hg in a Boreal Mire

In this paper we investigate the hypothesis that long-term sulphate (SO₄ ²⁻) deposition has made peatlands a larger source of methyl mercury (MeHg) to remote boreal lakes. This was done on experimental plots at a boreal, low sedge mire where the effect of long-term addition of SO₄ ²⁻ on peat pore water MeHg concentrations was observed weekly throughout the snow-free portion of 1999. The additions of SO₄ ²⁻ started in 1995. The seasonal mean of the pore water MeHg concentrations on the plots with 17 kg ha⁻¹ yr⁻¹ of sulphur (S) addition (1.3±0.08 ng L⁻¹, SE; n = 44) was significantly (p<0.0001) higher than the mean MeHg concentration on the plots with 3 kg ha⁻¹ yr⁻¹ of ambient S deposition (0.6±0.02 ng L⁻¹, SE; n = 44). The temporal variation in pore water MeHg concentrations during the snow free season was larger in the S-addition plots, with an amplitude of >2 ng L⁻¹ compared to +/−0.5 ng L⁻¹ in the ambient S deposition plots. The concentrations of pore water MeHg in the S-addition plots were positively correlated (r² = 0.21; p = 0.001) to the groundwater level, with the lowest concentrations of MeHg during the period with the lowest groundwater levels. The pore water MeHg concentrations were not correlated to total Hg, DOC concentration or pH. The results from this study indicate that the persistently higher pore water concentrations of MeHg in the S-addition plots are caused by the long-term additions of SO₄ ²⁻ to the mire surface. Since these waters are an important source of runoff, the results support the hypothesis that SO₄ ²⁻ deposition has increased the contribution of peatlands to MeHg in downstream aquatic systems. This would mean that the increased deposition of SO₄ ²⁻ in acid rain has contributed to the modern increase in the MeHg burdens of remote lakes hydrologically connected to peatlands.     

New examples of the exploitation of intermediary ligands in the synthesis of polymeric (μ-Se)Hg-clusters

(PhSe)₂Hg reacts initially with HgX₂ (X = Cl, I) and further with triphenylphosphine/DMF to give [(PhSe)₇Hg₄ClPy]_n (1) and [(PhSe)₇Hg₄I(DMF)]_n (2), polymeric assemblies of (μ-Se)Hg clusters obtained through coordinating intermediary ligands. Each single adamantoid molecule of 1 and 2 presents the Hg^II ions with a distorted tetrahedral configuration linked through asymmetric [μ-(Ph)Se]⁻ bridges. [(PhSe)₇Hg₄ClPy]_n and [(PhSe)₇Hg₄I(DMF)]_n are further examples of extended one-dimensional chains of closed anisotropic ME (E = S, Se, Te) systems. In these reactions the features of the intermediary ligands should determine the template which leads to single adamantane moieties or to fused ones.     

Involvement of non-enzymatic antioxidant defenses in the protective effect of diphenyl diselenide on testicular damage induced by cadmium in mice

The involvement of non-enzymatic antioxidant defenses in the protective effect of diphenyl diselenide (PhSe)₂ on testicular damage caused by cadmium in mice was investigated. Mice received a single dose of CdCl₂ (5 mg/kg, intraperitoneally). Thirty minutes after the CdCl₂ injection, they received a single oral dose of (PhSe)₂ (400 μmol/kg). Twenty-four hours after CdCl₂ administration, blood samples were collected and mice were killed and had their testes dissected. Parameters in plasma (aspartate (AST) and alanine (ALT) aminotransferases and lactato dehydrogenase (LDH) activities as well as creatinine levels) were determined. The activity of δ-aminolevulinate dehydratase (δ-ALA-D), the levels of thiobarbituric acid-reactive substances (TBARS), ascorbic acid and nonprotein thiols (NPSH) and histological analysis were determined in collected samples. Results demonstrated that (PhSe)₂ protected against toxicity induced by CdCl₂ on δ-ALA-D activity, ascorbic acid and NPSH levels. (PhSe)₂ protected against the increase in plasma AST, ALT and LDH activities caused by CdCl₂. Testes of mice exposed to CdCl₂ showed marked histopathological alterations that were ameliorated by administration of (PhSe)₂. (PhSe)₂ protected against toxicity induced by CdCl₂ in testes of mice. Ascorbic acid and NPSH, non-enzymatic antioxidant defenses, are involved in the protective effect of (PhSe)₂ against testicular damage caused by CdCl₂ in mice.