Early-age changes in oxidative stress in brown trout,Salmo trutta

Fish are often used as models for studies investigating the ability of xenobiotics to induce oxidative stress, though age or developmental stage of the individuals studied has been given little attention. Oxidative stress in other organisms is associated with aging as well as with periods of rapid growth, which occurs in young brown trout. We measured protein carbonyls, 20S proteosome activity and glutathione (GSH) levels in farmed Salmo trutta in four different age groups from 5 months to 3 years. We found an increase in protein carbonyls and a decrease in 20S proteosome activity in both brain and liver tissues of the fish with increasing size and age. Total GSH levels in liver tissue declined as fish aged and the GSSG:GSH ratio increased. Five month and 1 year old trout were treated with paraquat (PQ) to induce oxidative stress. Five month old fish showed no changes in the measured parameters while 1 year old fish had both an increase in protein carbonylation in liver tissue and a decrease in 20S proteosome activity in brain tissue. These results indicate that oxidative stress biomarkers are affected by age or rapid growth in brown trout, and that individuals of different ages respond differently to oxidative stress induced by PQ.     

Multi-organ toxicological impact of fungicide propiconazole on biochemical and histological profile of freshwater fish Channa punctata Bloch

Fungicides are a pesticide that particularly kills or destroy fungi responsible for several diseases associated to humans and other living organisms. Assessment of toxic effects and mechanisms of fungicide action is important because humans and domesticated animals get exposed to these pesticides through a wide variety of applications. Several fungicides are being used at the large scale for the crop protection from the fungal invasion. Propiconazole (PCZ), a trazole-containing fungicide, is widely used in China and various Asian countries for food crop protection which made it easily to exposed to the aquatic system. Long term usage of PCZ may contaminate the water bodies, but its toxicity to aquatic organisms is not well studied. In this study, freshwater fish, Channa punctata Bloch was exposed to different sub-lethal concentrations of the fungicide, PCZ (0.5 and 5 ppm) for a period of 96 h. Various biochemical assays and histological alterations were measured to determine the organ toxicity caused by PCZ exposure particularly in liver, kidney and gills of the fishes. Compared to the control group, fish exposed to PCZ (96 h) showed marked dose dependent toxicity. The levels of lipid peroxidation (LPO) and protein carbonyls (PC), oxidative stress biomarker of liver, kidney and gills in the experimental group were significantly higher (P < 0.05 and P < 0.001) compared to the control group. Levels of reduced glutathione (GSH) and non-protein thiols (NP-SH) decreased significantly (P <0.05–0.001) in all analyzed intoxicated organs of the PCZ exposed fishes. Activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx) and catalase (CAT) in fungicide treated groups was significantly lowered (P < 0.05–0.001). In addition, histopathological examination in the organs showed significant changes like atrophy of primary and secondary gill lamellae, infiltrations, inflammation, hepatocyte degeneration, vacuolization and necrotic kidney. Thus, PCZ exposure altered the oxidative stress homeostasis and brought about histopathological changes which may serve as potential biomarkers of the PCZ toxicity in the laboratory set-up for potential risk assessment.     

Selective induction of IL-6 by aluminum-induced oxidative stress can be prevented by selenium

In this study the acute toxic effects of aluminum (Al) on mice have been investigated, including the interactions of Al and selenium (Se). Focus was put on the systemic effects of (co)exposure to Al and Se as a reflection of the redox status in the liver, kidney and brain.Short-term exposure (16 h) to Al resulted in an increase in the systemic inflammation parameters IL-6 and PAI-1, whereas serum levels of TNF-α remained unaffected. The different response pattern of IL-6 and TNF-α probably indicates an increased intracellular oxidative stress and altered redox status in the liver, because the selective increase in IL-6 serves as a protective intrahepatocellular process driven by oxidative stress. The intracellular glutathione concentration GSH_tot decreased significantly upon Al exposure. Both the increase in IL-6 and decrease in glutathione status could be prevented by co-exposure to Se, but not the increase in PAI-1. The redox status of the kidney and brain was not markedly affected.Therefore it was concluded that short-term exposure to Al causes adverse effects on the intracellular oxidative stress processes in the liver, as reflected by the selective increase in the IL-6 concentration. This process can be restored by co-administration of the trace element Se as a part of the glutathione redox system.     

Effectiveness of (PhSe)2 in protect against the HgCl2 toxicity

This work investigated the preventive effect of diphenyl diselenide [(PhSe)₂] on renal and hepatic toxicity biomarkers and oxidative parameters in adult mice exposed to mercury chloride (HgCl₂). Selenium (Se) and mercury (Hg) determination was also carried out. Mice received a daily oral dose of (PhSe)₂ (5.0 mg/kg/day) or canola oil for five consecutive days. During the following five days, the animals were treated with a daily subcutaneous dose of HgCl₂ (5.0 mg/kg/day) or saline (0.9%). Twenty-four hours after the last HgCl₂ administration, the animals were sacrificed and biological material was obtained. Concerning toxicity biomarkers, Hg exposure inhibited blood δ-aminolevulinic acid dehydratase (δ-ALA-D), serum alanine aminotransferase (ALT) activity and also increased serum creatinine levels. (PhSe)₂ partially prevented blood δ-ALA-D inhibition and totally prevented the serum creatinine increase. Regarding the oxidative parameters, Hg decreased kidney TBARS levels and increased kidney non-protein thiol levels, while (PhSe)₂ pre-treatment partially protected the kidney thiol levels increase. Animals exposed to HgCl₂ presented Hg content accumulation in blood, kidney and liver. The (PhSe)₂ pre-treatment increased Hg accumulation in kidney and decreased in blood. These results show that (PhSe)₂ can be efficient in protecting against these toxic effects presented by this Hg exposure model.     

Short term exposure of pendimethalin induces biochemical and histological perturbations in liver,kidney and gill of freshwater fish

Our study was designed to evaluate effects of an herbicide, pendimethalin on biochemical biomarkers and histopathological indices of the freshwater fish Channa punctata Bloch. Fish were acutely exposed (96 h) to sub-lethal concentrations (0.5 and 0.8 ppb of pendimethalin). Various oxidative stress indicators such as thiobarbituric acid reactive substances levels and protein carbonyl content, as well as antioxidant defenses parameters, such as glutathione-S-transferase (GST), catalase (CAT), reduced glutathione (GSH) and non-protein thiols (NP-SH) levels were studied, using the liver, kidney and gill tissues. Pendimethalin exposure increased lipid peroxidation and protein oxidation processes. There was significant inhibition in levels of GSH and NP-SH. The activity of antioxidant enzymes GST and CAT depleted in all the tissues in a dose dependent manner. The histopathological change in the gill showed necrosis and atrophy of primary and secondary gill lamellae. The tissue damages like degeneration of cytoplasm in hepatocytes, atrophy, formation of vacuoles, are some histopathological changes observed in the liver. The changes in histoarchitechture observed in the kidney included necrosis, cellular hypertrophy and granular cytoplasm. The present study demonstrates the disturbances in antioxidant armamentarium and importance of study in the potential risk assessment of herbicides on fish species.     

Effect of gold nanoparticles on glutathione and malondialdehyde levels in liver,lung and heart of rats

We studied the effect of gold nanoparticles (NPs) on oxidative stress markers including reduced glutathione (GSH) and malondialdehyde (MDA) in different organs of rats. Adult male Wistar-Kyoto rats were randomly divided into 3 groups of 5 animals each. One group served as control and received vehicle only. The remaining two groups were treated with 50 μl of 10 nm sized gold NPs, daily for 3 and 7 days, respectively. The rats were sacrificed 24 h after the last injection of NPs. Administration of gold NPs did not cause any significant change in GSH levels in liver, lung and heart on day 3 or day 7. There was no significant effect of gold NPs on MDA levels in lung and heart whereas significant increases in MDA levels were found in the liver of rats treated with gold nanoparticles on both 3 and 7 days post-dosing (ANOVA F = 7.113, P = 0.010). In conclusion, the findings of this preliminary study suggest that gold NPs of 10 nm diameter produce significant lipid peroxidation in rat liver however lungs and heart do not show any oxidative stress. Further studies are warranted to examine the effects of a broader dose range of gold NPs on the levels of free radical indices in different organs of rats.     

Are fish in hot water? Effects of warming on oxidative stress metabolism in the commercial species Sparus aurata

Climate change is disturbing marine biological processes, and impacting goods and services provided to society. Physiological studies are a major contributor to the improvement of biological forecasting in the context of climate change. Oxidative stress biomarkers are useful tools to assess the metabolic status and health of organisms, improving management of wild and cultured populations. The aims of this study were to assess the health status and vulnerability of Sparus aurata juveniles toward ocean warming and heat wave events by (1) exposing fish to a thermal ramp from 18 °C until their Critical Thermal Maximum (≈35 °C) and (2) quantifying oxidative stress biomarkers in several organs, i.e. lipid peroxidation (LPO), catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST), and cytochrome CYP1A. Fish showed signs of oxidative stress in every tissue tested (gills, muscle, liver, brain and intestine), the most affected being muscle and liver, which showed greater increases in LPO. In general, antioxidant enzymes increased their activity: CAT increased in every organ tested, GST increased in every organ except brain (no change) and SOD increased in every organ except intestine (no change) and brain (decrease, probably due to enzyme denaturation). Muscle showed the greatest stress response with a massive increase in GST. Hepatic CYP1A decreased upon warming suggesting that temperature influences detoxifying mechanisms and may affect fish health. These results are significant in the context of climate change and associated impacts on fisheries and aquaculture because over-induction of oxidative stress due to warming can induce health problems, mortality and shortened lifespan.     

Quercetin in vesicular delivery systems: Evaluation in combating arsenic-induced acute liver toxicity associated gene expression in rat model

Arsenic, the environmental toxicant causes oxidative damage to liver and produces hepatic fibrosis. The theme of our study was to evaluate the therapeutic efficacy of liposomal and nanocapsulated herbal polyphenolic antioxidant Quercetin (QC) in combating arsenic induced hepatic oxidative stress, fibrosis associated upregulation of its gene expression and plasma TGF ß (transforming growth factor ß) in rat model.A single dose of Arsenic (sodium arsenite-NaAsO₂, 13 mg/kg b.wt) in oral route causes the generation of reactive oxygen species (ROS), arsenic accumulation in liver, hepatotoxicity and decrease in hepatic plasma membrane microviscosity and antioxidant enzyme levels in liver. Arsenic causes fibrosis associated elevation of its gene expression in liver, plasma TGF ß (from normal value 75.2 ± 8.67 ng/ml to 196.2 ± 12.07 ng/ml) and release of cytochrome c in cytoplasm. Among the two vesicular delivery systems formulated with QC, polylactide nanocapsules showed a promising result compared to liposomal delivery system in controlling arsenic induced alteration of those parameters. A single dose of 0.5 ml of nanocapsulated QC suspension (QC 2.71 mg/kg b.wt) when injected to rats 1 h after arsenic administration orally protects liver from arsenic induced deterioration of antioxidant levels as well as oxidative stress associated gene expression of liver. Histopathological examination also confirmed the pathological improvement in liver. Nanocapsulated plant origin flavonoidal compound may be a potent formulation in combating arsenic induced upregulation of gene expression of liver fibrosis through a complete protection against oxidative attack in hepatic cells of rat liver.     

Elevation of oxidative-damage biomarkers during aging in F2 hybrid mice: Protection by chronic oral intake of resveratrol

Resveratrol (RSV), a naturally occurring phytoalexin that can be found in red wine, berries, and peanuts, has been shown to extend both mean and maximum life span in model organisms. RSV has also been reported to shift the physiology of middle-aged mice on a high-calorie diet toward that of mice on a standard diet. These beneficial effects of RSV have been suggested to resemble caloric restriction. Our study in F2 four-way cross-hybrid mice was the first to evaluate the effects of aging and long-term RSV treatment (14.09 ± 3.4 mg/L in drinking water for 6 or 12 months) on biomarkers of oxidative damage to DNA, 8-hydroxy-2′-deoxyguanosine (8OHdG); lipid, 8-iso-prostaglandin_2α (8-iso-PGF_2α); and protein, protein carbonyl content (PCC). There was a significant age-dependent accumulation of oxidative damage to DNA, lipid, and protein as well as a clear increase in urine 8-iso-PGF_2α levels in the majority of mouse tissues. Rates of age-dependent increases in damage biomarkers varied between tissues. Chronic RSV treatment elevated total RSV plasma levels and reduced the observed age-dependent accumulation of (1) 8OHdG in liver and heart, (2) 8-iso-PGF_2α in heart and urine, and (3) PCC in liver and kidney. However, a 12-month RSV intake resulted in significant elevation of 8-iso-PGF_2α and PCC in kidney. Our studies demonstrate that RSV treatment consistently attenuated oxidative damage in tissues where age-related oxidative damage accumulation was prominent, but also suggested that chronic RSV treatment may induce nephrotoxicity.     

Synergistic effect of Se-methylselenocysteine and vitamin E in ameliorating the acute ethanol-induced oxidative damage in rat

The present study was conduced to investigate the synergistic effects of combined treatments with Se-methylselenocysteine (SeMSC) and vitamin E (Vit E) in reversing oxidative stress induced by ethanol in serum and different tissues of rats. Sixty female rats were randomly divided into six groups for 30 days’ consecutive pretreatments as followed: control (I), physiological saline (II), 2.8 μg kg⁻¹ Se as SeMSC (III), 2.8 μg kg⁻¹ Se as sodium selenite (Na₂SeO₃, IV), 5 mg kg⁻¹ α-tocopherol as α-tocopherol acetate (Vit E, V), 5 mg kg⁻¹ α-tocopherol as α-tocopherol acetate and 2.8 μg kg⁻¹ Se as SeMSC (VI). All animals in groups II–VI were treated by ethanol treatment to cause oxidative stress. After 6 h of ethanol treatment, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), the contents of total antioxidant capacity (T-AOC), malondialdehyde (MDA), glutathione (GSH) and carbonyl protein (CP) in the serum, liver, heart and kidney were measured. The result showed that the individual SeSMC, Na₂SeO₃ and vitamin E could effectively increase the SOD, T-AOC, GSH-Px and GSH contents as well as significantly decrease the MDA and CP concentrations in the tissues of ethanol-induced rats. At the same dose on different forms of Se, SeMSC showed greater antioxidant activity than Na₂SeO₃. Moreover, group VI (SeMSC and α-tocopherol acetate) showed much better antioxidant activity than individual group III (SeMSC) and V (α-tocopherol acetate) due to the synergistic effect.     

Propiconazole induced toxicological alterations in brain of freshwater fish Channa punctata Bloch

Fungicides are a class of pesticides which are used indiscriminately in large amounts and pose a serious threat to the environment. Propiconazole (PCZ) is a systemic foliar fungicide with a broad range of activity. The potential of this fungicide to induce toxicity has not been fully explored. The present study was designed to investigate the dose dependent neurotoxic effect of propiconazole (PCZ), with Channa punctata Bloch as a model organism. Effect of PCZ on the brain specific enzyme activity such as acetylcholinesterase (AChE), monoamine oxidase (MAO) and Na⁺-K⁺-ATPase was determined in the fish brain tissue exposed to sub-lethal concentrations (0.5 and 5 ppm) for 96 h. Also, levels of oxidative stress reflected by various enzymatic and non-enzymatic antioxidants were measured. Neurotransmitter (epinephrine) level was also assessed. PCZ exposure induced oxidative stress as reflected by the significant increase in fish brain lipid peroxidation and protein carbonyl content with decrease in reduced glutathione levels, as well as the significant inhibition of glutathione dependent metabolizing enzymes and CAT activities. In addition, AChE, MAO and Na⁺-K⁺-ATPase activities were significantly lowered along with reduction in epinephrine levels in PCZ exposed fishes than those of the control in a dose dependent manner. Also, histopathological alterations were observed in fish brain of the treated fishes. The results point towards the potential neurotoxicity in the fish caused by PCZ exposure but the application of these findings will need more detailed study before they can be established as special biomarkers for toxicity monitoring the aquatic environment.     

Antioxidative effects of Panax notoginseng saponins in brain cells

Oxidative stress resulting from accumulation of reactive oxygen species (ROS) is involved in cell death associated with neurological disorders such as stroke, Alzheimer's disease and traumatic brain injury. Antioxidant compounds that improve endogenous antioxidant defenses have been proposed for neural protection. The purpose of this study was to investigate the potential protective effects of total saponin in leaves of Panax notoginseng (LPNS) on oxidative stress and cell death in brain cells in vitro. Lactate dehydrogenase (LDH) assay indicated that LPNS (5 μg/ml) reduced H₂O₂-induced cell death in primary rat cortical astrocytes (23 ± 8% reduction in LDH release vs. control). Similar protection was found in oxygen and glucose deprivation/reoxygenation induced SH-SY5Y (a human neuroblastoma cell line) cell damage (78 ± 7% reduction vs. control). The protective effects of LPNS in astrocytes were associated with attenuation of reactive oxygen species (ROS) accumulation. These effects involved activation of Nrf2 (nuclear translocation) and upregulation of downstream antioxidant systems including heme oxygenase-1 (HO-1) and glutathione S-transferase pi 1 (GSTP1). These results demonstrate for the first time that LPNS has antioxidative effects which may be neuroprotective in neurological disorders.     

Allometric scaling of fatty acyl chains in fowl liver,lung and kidney,but not in brain phospholipids

The phospholipid (PL) fatty acyl chain (FA) composition (mol%) was determined in the kidney, liver, lung and brain of 8 avian species ranging in body mass from 150 g (Japanese quail, Coturnix coturnix japonica) to 19 kg (turkey, Meleagris gallopavo). In all organs except the brain, docosahexaenoic acid (C22:6 n3, DHA) was found to show a negative allometric scaling (allometric exponent: B = ? 0.18; ? 0.20 and ? 0.24, for kidney, liver and lung, respectively). With minor inter-organ differences, smaller birds had more n3 FAs and longer FA chains in the renal, hepatic and pulmonary PLs. Comparing our results with literature data on avian skeletal muscle, liver mitochondria and kidney microsomes and divergent mammalian tissues, the present findings in the kidney, liver and lung PLs seem to be a part of a general relationship termed “membranes as metabolic pacemakers”. Marked negative allometric scaling was found furthermore for the tissue malondialdehyde concentrations in all organs except the brain (B = ? 0.17; ? 0.13 and ? 0.05, respectively). In the liver and kidney a strong correlation was found between the tissue MDA and DHA levels, expressing the role of DHA in shaping the allometric properties of membrane lipids.     

Ganoderma atrum polysaccharide attenuates oxidative stress induced by d-galactose in mouse brain

AimsGanoderma atrum polysaccharide (PSG-1), the main constituent of G. atrum, has been reported to attenuate oxidative stress in vitro. The aim of this study was to investigate whether PSG-1 has a protective effect on the brain against oxidative stress induced by d-galactose (D-gal) in vivo.Main methodsMice were intraperitoneally (i.p.) injected with D-gal (100 mg/kg body weight) once daily for 10 weeks. From the seventh week, D-gal-treated mice received PSG-1 (50, 100, or 150 mg/kg body weight) once daily for the last 4 weeks. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GSH-Rd), and the contents of glutathione (GSH), glutathione disulfide (GSSG) and malondialdehyde (MDA) in the brain were measured using different biochemical methods to evaluate the changes of the antioxidant ability in the PSG-1 treated mice. Apoptosis, reactive oxygen species (ROS) and calcium levels were determined by flow cytometry.Key findingsAdministration of PSG-1 significantly reduced apoptosis in the mouse brain in a dose-dependent manner. PSG-1-evoked reduction of apoptosis was associated with the decrease of MDA and GSSG contents, and the increase of SOD, CAT, GPx and GSH-Rd activities, and GSH contents. PSG-1 treatment was also found to attenuate ROS production and calcium accumulation.SignificancePSG-1 has a potential to be used as a novel therapeutic agent for the protection of aging brain tissue against oxidative damage by modifying the redox system and maintaining calcium homeostasis.     

A combination of ascorbic acid and α-tocopherol or a combination of Mg and Zn are both able to reduce the adverse effects of lindane-poisoning on rat brain and liver

The purpose of this study, carried out on male Wistar rats, was to evaluate the beneficial effects of supplementation with ascorbic acid (Vit C) and α-tocopherol (Vit E) or with Mg and Zn upon lindane-induced damages in liver and brain. Under our experimental conditions, lindane poisoning (5 mg/kg body weight per day for 3 days) resulted in (1) an increased level of plasma glucose, cholesterol and triglycerides, (2) an increased activity of LDH, ALP, AST, ALT, (3) an oxidative stress in liver and brain as revealed by an increased level of lipids peroxidation (TBARS) and a decrease of glutathione-peroxidase, superoxide dismutase and catalase activities in liver and brain. In conclusion, both Vit C + E or Mg + Zn treatments display beneficial effects upon oxidative stress induced by lindane treatment in liver and brain.     

Lactating and non-lactating rats differ in sensitivity to HgCl2: Protective effect of ZnCl2

This work investigated zinc (Zn) and mercury (Hg) effects on oxidative parameters, markers of toxicity and metal levels in different tissues from non-lactating rats (NLR) and lactating rats (LR). Adult NLR and LR received ZnCl₂ (27 mg/kg) or saline (0.9%) subcutaneously and after 24 h they received HgCl₂ (5 mg/kg) or saline (0.9%). Twenty four hours later, they were sacrificed and the preparation of biological material and biochemical analyses were performed. With respect to oxidative parameters, Hg exposure decreased kidney total SH levels from NLR and LR and hepatic catalase activity (not statistically significant) in NLR. Zinc pre-treatment partly prevented the decrease of kidney total SH levels in LR. Zinc per se increased hepatic non-protein SH levels of NLR and LR. Regarding toxicity markers, Hg exposure inhibited the δ-aminolevulinic acid dehydratase (δ-ALA-D) activity from kidney and liver of NLR, inhibited serum alanine aminotransferase (ALT) activity of LR and increased serum creatinine and urea levels of NLR and LR. Zinc pre-exposure prevented the enzymatic alterations caused by Hg. NLR and LR Hg exposed presented accumulation of mercury in the kidney, liver, blood and urine. Zinc pre-treatment prevented this accumulation partly in NLR liver and blood and completely in LR kidney and liver. These results show that NLR and LR are differently sensitive to HgCl₂ and that ZnCl₂ showed a promising effect against Hg toxicity.     

Protective effect of Piper betle leaf extract against cadmium-induced oxidative stress and hepatic dysfunction in rats

The present study was undertaken to examine the attenuative effect of Piper betle leaf extract (PBE) against cadmium (Cd) induced oxidative hepatic dysfunction in the liver of rats. Pre-oral supplementation of PBE (200 mg/kg BW) treated rats showed the protective efficacy against Cd induced hepatic oxidative stress. Oral administration of Cd (5 mg/kg BW) for four weeks to rats significantly (P > 0.05) elevated the level of serum hepatic markers such as serum aspartate transaminase (AST), serum alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma-glutamyl transpeptidase (GGT), bilirubin (TBRNs), oxidative stress markers viz., thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH), protein carbonyls (PC) and conjugated dienes (CD) and significantly (P > 0.05) reduced the enzymatic antioxidants viz., superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PD) and non-enzymatic antioxidants Viz., reduced glutathione (GSH), total sulfhydryls (TSH), vitamin C and vitamin E in the liver. Pre-oral supplementation of PBE (200 mg/kg BW) in Cd intoxicated rats, the altered biochemical indices and pathological changes were recovered significantly (P > 0.05) which showed ameliorative effect of PBE against Cd induced hepatic oxidative stress. From the above findings, we suggested that the pre-administration of P. betle leaf extract exhibited remarkable protective effects against cadmium-induced oxidative hepatic injury in rats.     

Oxidative stress and antioxidant defense responses of Etroplus suratensis to acute temperature fluctuations

Fishes are always exposed to various environmental stresses and the chances of succumbing to such stresses are of great physiological concern. Any change in temperature from the ambient condition can induce various metabolic and physiological changes in the body. The present study evaluates the effects of temperature induced stress on the antioxidant profile of Etroplus suratensis such as superoxide dismutase, catalase, glutathione peroxidase and lipid peroxidation. Fishes of same size were kept in a thermostatized bath at three different temperature regimes viz 16 °C, 27 °C (ambient temperature) and 38 °C for 72 h. These temperatures were selected based on the CT Max (Critical Thermal Maximum) and CT Min (Critical Thermal Minimum) exhibited by E. suratensis. Superoxide dismutase and catalase activity was found maximum in brain and muscle respectively during the 48th hour of exposure in fishes kept at 38 °C. At 16 °C the antioxidant response of glutathione peroxidase was maximum in muscles, whereas the lipid peroxidation rate was found to be high in gills compared to other tissues. The profound increase in the levels of oxidative stress related biomarkers indicate that the thermal stressors severely affected oxidative state of E. suratensis by the second day of experiment. Such down-regulation of redox state accompanied with the induction of oxidative stress cascade may lead to physiological damage in various tissues in fishes, in vivo. However current data indicate that a transition to low and high temperature environment from ambient condition severely affected the levels and profile of the antioxidant markers overtime in E. suratensis.     

Brassica napus subjected to copper excess: Phospholipases C and D and glutathione system in signalling

Brassica napus plants were subjected to an oxidative stress by incubating them with 100 μM CuSO₄ for different times. The early response to copper stress was evaluated studying changes at both root and leaf level in the putative lipid and antioxidative signals diacylglicerol (DAG), phosphatidic acid (PA) and glutathione, in order to achieve elucidation on how these two kind of signals are related to each other. Activation of phospholipases C (PLC) and D (PLD) was studied in roots and leaves whereas increases in the levels of total and reduced glutathione (GSH) and changes in its redox status were evaluated in roots, leaves and chloroplast stroma. PLC and PLD were measured by studying the production of DAG, PA and phosphatidylbutanol (PtdButOH). PA, PtdButOH as well as DAG increased in roots already after 1 min of the treatment whereas in leaves, where no translocation of the metal occurred, any increase in PA and DAG was observed and no PtdButOH was formed. Roots were affected by oxidative stress showing decreases in glutathione reductase (GR), in total glutathione (GSH + GSSG) and GSH, and increases in oxidised glutathione (GSSG). In leaves, GR was induced during the whole stress period and both GSH + GSSG and GSH showed a peak at 5 min of the treatment. In the stroma, the maximum presence in GSH + GSSG and GSH occurred with a time shift of 25 min compared with total leaf extract.