Gender related differences in the oxidative stress response to PCB exposure in an endangered goodeid fish (Girardinichthys viviparus)

Polychlorinated biphenyls (PCBs) are persistent xenobiotics within aquatic environments, which elicit diverse toxic effects such as induction of oxidative stress. Despite numerous earlier studies, no detailed information exists on the toxic response by different sexes in fish. The aim of this study was to determine sex-linked differences in oxidative stress response and antioxidant defenses in Girardinichthys viviparus, an endangered fish endemic to Mexico, when exposed to sub-lethal concentrations of waterborne PCBs. The biological markers evaluated were lipid peroxidation (LPOX), superoxide dismutase (SOD) and catalase (CAT) activity. Adult eight-month-old specimens born in the laboratory were exposed to ½ of the LC₀ (0.92 mg PCBs/L) in semi-hard synthetic water and sacrificed on days 1, 2, 4, 8 and 16 for biomarker assays. Sex-linked differences were observed in the control fish with respect to all three factors assayed. PCBs elicited significant (p < 0.01) time- and sex-dependent LPOX levels which were higher in the case of males. In PCB-treated G. viviparus, SOD activity was depressed in both sexes and appears to return to pre-exposure levels after 16 days in males only. In contrast, CAT was significantly induced (p < 0.01) in both sexes. This enzyme may be responsible for balancing oxidative stress and antioxidant defenses under experimental conditions. PCBs at sub-lethal concentrations are hazardous to both sexes of G. viviparus since these compounds are able to induce liver LPOX and changes in the antioxidant defense activities. The relationship between these biomarkers and cytochrome P450 and CYP1A induction is also discussed.     

Estrogenic, anti-estrogenic and cytotoxic effects elicited by water from the type localities of the endangered goodeid fish Girardinichthys viviparus

Girardinichthys viviparus is a Mexican endangered endemic fish species living only in Lake Texcoco (LTX), one of two extant type localities for this species. The other type locality is Lake Zumpango (LZ). LTX and LZ are fed by wastewater treated at secondary level that contains several endocrine disrupting chemicals. Our goal was to assess the estrogenic and anti-estrogenic effects elicited in G. viviparus by water from the two type localities and by these same matrices enriched with PCBs in order to understand potential damage due to increased xenobiotic levels. Estrogenic and anti-estrogenic effects were evaluated in vitro by E-screen assay in MCF-7 cells and cytotoxicity by MTT assay. PCBs were quantified in type localities. In vivo vitellogenin (VTG) induction was determined by a hybrid ELISA in adult laboratory-born fish exposed during 1, 2, 4, 8 and 16 days to LTX or LZ water in static exposure systems, and by the same matrices enriched with PCBs. We found PCBs only in LTX, but the water from both type localities elicit estrogenic and anti-estrogenic effects in vitro. Cytotoxicity was not observed in MCF-7 cells exposed to LTX or LZ water. VTG induction was higher with LTX water than with LZ water; also the response of males was greater than in females. In the PCB-enriched matrices, VTG induction in both sexes exposed to LTX water was reduced compared to un-enriched matrices. Thus, the sublethal increases in PCB levels may be hazardous to both sexes since they are linked probably to hepatotoxicity.     

Investigation of Cadmium-Induced Genotoxicity and Oxidative Stress Response in Indian Major Carp,Labeo rohita

We investigated genotoxicity and oxidative stress in the gills of Labeo rohita exposed to 33.6, 67.1, and 100.6 mg L^–1of cadmium chloride at 96 h. Genotoxicity was assessed using single cell gel electrophoresis whereas oxidative stress was monitored through lipid peroxidation induction and antioxidant response parameters, namely reduced glutathione (GSH), glutathione peroxidase, glutathione-S-transferase, superoxide dismutase, and catalase (CAT) activities. Significant (p < .05) effect of both concentration and time of exposure was observed on the extent of DNA damage in treated fish. Similarly, malondialdehyde content, level of GSH, and activities of antioxidant enzymes were significantly elevated in treated groups, except CAT. The increased DNA damage and lipid peroxidation (LPO) content along with fluctuation in antioxidant defense system in fish indicated the interaction of cadmium (Cd) with DNA repair processes and production of reactive oxygen species. Thus, Cd is liable for induction of LPO, alteration of antioxidant defenses, and DNA damage in gills of L. rohita.     

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.     

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.     

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.     

Antioxidant defenses and biochemical changes in pacu (Piaractus mesopotamicus) in response to single and combined copper and hypoxia exposure

The effect of combined-factors (hypoxia+copper) on the biochemical parameters and antioxidant defenses were studied in the neotropical fish Piaractus mesopotamicus. Fish were exposed for 48 h to 0.4 mg Cu(2+) L(-1) (0.4Cu), hypoxia=50 mm Hg (Hpx), and 0.4 mg Cu(2) L(-1)+hypoxia=50 mm Hg (0.4CuHpx). The exposure to 0.4Cu increased the reactive oxygen species (ROS) in the liver, accompanied by increases in superoxide dismutase (SOD) and decreases in catalase (CAT) activity, showing the influence of copper in this protection. The exposure to Hpx decreased the activity of glutathione peroxidase (GSH-Px) and CAT. Exposure to a combined-factor caused an increase in the ROS production followed by an increase in SOD and a decrease in GSH-Px and CAT. At 0.4Cu, fish presented a reduction in CAT, while in Hpx decreases in SOD, CAT and GSH-Px were observed in red muscles. Single-factors were insufficient to cause ROS production. In combined-factors, increased ROS formation and decreased SOD, CAT and GSH-Px were observed. RBC increased in all groups, but only under combined-factors was there an increase in hemoglobin. Copper plasma concentration increased in groups exposed to copper. Na(+)/K(+)-ATPase activity in gills decreased in 0.4Cu and 0.4CuHpx, and increased in Hpx. Metallothionein concentration in gills increased under combined-factors. Combined-factors caused significant disturbances in the antioxidant defenses and biochemical parameters than single-factors.     

The role of Acanthamoeba castellanii (T4 genotype) antioxidant enzymes in parasite survival under H2O2-induced oxidative stress

Acanthamoeba castellanii (A. castellanii) is an important opportunistic parasite. Induction of oxidative stress by the host immune system is one of the most important defense strategies against parasites. Hence, parasites partly deal with oxidative stress by different mechanisms. Identifying resistance mechanisms of A. castellanii parasites against oxidative stress is important to achieve a new therapeutic approach. Thus, this study aimed to understand the resistance mechanisms of A. castellanii, against oxidative stress. Trophozoites of A. castellanii were treated with different concentrations of H₂O₂. The half maximal inhibitory concentration (IC₅₀) of H₂O₂ was determined using the MTT assay. The induction of oxidative stress was confirmed by flow cytometer. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR) were determined. The gene expression levels of CAT and SOD were measured by qRT-PCR. Furthermore, 3-amino-1:2:4-triazole (3-AT) and potassium cyanide (KCN) were used as specific inhibitors of CAT and SOD, respectively. Cell cycle assay and the apoptosis were evaluated by flow cytometer. The activities of SOD, CAT, GR, and GPx, showed an increase in oxidative stress. The cell cycle analysis revealed that most of the cellular population was in G0 and G1 phases. The apoptosis increased in oxidative stress conditions. Moreover, the apoptosis significantly increased after the specific inhibition of CAT and SOD under oxidative stress. The gene expression levels of CAT and SOD significantly increased under oxidative stress. A. castellanii can resist the host immune system through various mechanisms, including evoking its antioxidant enzymes. Therefore, by reducing or inhibiting the activity of the parasite's antioxidant enzymes such as SOD and CAT, it is possible to cope with A. castellanii.     

Neurotoxicological assessment of pendimethalin in freshwater fish Channa punctata Bloch

Over the years, indiscriminate usage of pesticides has resulted in situations which are not conducive for a good environment. In aquatic toxicology, fishes have been developed as established models for studying toxic responses of xenobiotics including pesticides. Pendimethalin (PD), an herbicide, is widely present in the aquatic environment, but little is known regarding its potential neurotoxicity in fish. The present study was conducted on Channa punctata Bloch exposed to sub-lethal doses of PD (0.5 and 0.8 ppb) for 96 h. The exposure resulted in alterations in epinephrine levels in the fish brain. Epinephrine levels decreased significantly in a dose dependent manner with increase in the PD exposure. A marked decrease in the activity of acetylcholinesterase along with reduction in Na⁺-K⁺-ATPase and monoamine oxidase activity was also observed. In comparison with the corresponding controls, the sub-lethal doses of PD also caused significant changes in the oxidative stress markers (lipid peroxidation and carbonyl derivatives of protein oxidative destruction levels) and antioxidant defenses (reduced glutathione levels, catalase, glutathione-s-transferase activity) in brain tissue. Our results reflect that a detailed investigation is warranted regarding the toxicity potential of PD.     

Effects of phenol in antioxidant metabolism in matrinxã, Brycon amazonicus (Teleostei; Characidae)

Parameters of the antioxidant defense systems of Brycon amazonicus (matrinx?--a neotropical fish) exposed to phenol for 96 h plus the recovery over 1 and 2 weeks were studied in erythrocytes and liver. Hematocrit increase was observed during phenol exposure and recovery for 1 week. Total superoxide dismutases (SOD), glutathione peroxidase (GPx) and reduced glutathione (GSH) did not change during phenol exposure. Erythrocyte glucose-6-phosphate dehydrogenase (G6PDH) increased during that period while catalase (CAT) activity decreased during phenol exposure and recovery for 2 weeks. In the liver, SOD and CAT did not change, whereas GPx increased in the first week of recovery and decreased after 2 weeks. A late response was observed for G6PDH activity which increased only at the second week. Ascorbate concentration in the brain decreased during phenol exposure and increased over recovery. From our results it appears that the oxidative stress was limited in matrinx? exposed to phenol, but seemed to occur during the recovery period.     

Age-related changes in antioxidant enzyme activities and lipid peroxidation in lungs of control and sulfur dioxide exposed rats

Antioxidant defenses within the lung are pivotal in preventing damage from oxidative toxicants. There have also been several reports with conflicting results on the antioxidant system during aging. In this study, we attempted to investigate age-related alterations in both antioxidant enzyme activities and thiobarbituric acid-reactive substances (TBARS), a product of lipid peroxidation, in the whole lung of control and sulfur dioxide (SO₂) exposed rats of different age groups (3-, 12-, and 24-months-old). Swiss-Albino Male rats were exposed to 10 ppm SO₂ 1 hr/day, 7 days/week for 6 weeks. The antioxidant enzymes examined include Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione S-transferase (GST). A mixed pattern of age-associated alterations in antioxidant activities was observed. SOD, GSH-Px and GST activities were increased with age, but CAT activity was decreased. Lung SOD, GSH-Px and GST activities were also increased in response to SO₂. The level of TBARS was increased with age. SO₂ exposure stimulated lipid peroxide formation in the lung as indicated by an increase in the level of TBARS. These findings suggest that both aging and SO₂ exposure may impose an oxidative stress to the body. We conclude that the increase in the activities of the antioxidant enzymes of the lung during aging, could be interpreted as a positive feedback mechanism in response to rising lipid peroxidation.     

Age-related changes in antioxidant enzyme activities and lipid peroxidation in lungs of control and sulfur dioxide exposed rats

Antioxidant defenses within the lung are pivotal in preventing damage from oxidative toxicants. There have also been several reports with conflicting results on the antioxidant system during aging. In this study, we attempted to investigate age-related alterations in both antioxidant enzyme activities and thiobarbituric acid-reactive substances (TBARS), a product of lipid peroxidation, in the whole lung of control and sulfur dioxide (SO₂) exposed rats of different age groups (3-, 12-, and 24-months-old). Swiss-Albino Male rats were exposed to 10 ppm SO₂ 1 hr/day, 7 days/week for 6 weeks. The antioxidant enzymes examined include Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione S-transferase (GST). A mixed pattern of age-associated alterations in antioxidant activities was observed. SOD, GSH-Px and GST activities were increased with age, but CAT activity was decreased. Lung SOD, GSH-Px and GST activities were also increased in response to SO₂. The level of TBARS was increased with age. SO₂ exposure stimulated lipid peroxide formation in the lung as indicated by an increase in the level of TBARS. These findings suggest that both aging and SO₂ exposure may impose an oxidative stress to the body. We conclude that the increase in the activities of the antioxidant enzymes of the lung during aging, could be interpreted as a positive feedback mechanism in response to rising lipid peroxidation.     

镉对长江华溪蟹肝胰腺抗氧化酶活力的影响

重金属对环境的污染已成为全球面临的首要问题之一,其中镉(Cd2 )是一种广泛存在的毒性污染物,能通过消化道和呼吸道进入生物体,对机体造成损伤(Zyadah and Abdel-Baky,2000)。研究表明,Cd2 可以通过Ca2 通道穿过细胞膜进入机体(Roesijadi and Robinson,1994),诱导产生大量自由基和活性氧(ROS),从而形成氧胁迫(Toppi andGabbrielli,1994;Hegedus et al.,2001)。ROS可以与体内脂质、蛋白质和核酸反应,导致脂质过氧化、细胞膜损伤并且影响多种酶的活力,对生物体造成威胁。由于在水生生态系统中生物富集污染物的作用明显,故相对于陆地生…     

Cathepsin B differential expression and enzyme processing and activity during Fundulus heteroclitus embryogenesis

The present study aimed to test the effects of melatonin on oxidative stress in the yellowtail clownfish, Amphiprion clarkii, as produced by light emitting diodes (LEDs): red, green, and blue. We investigated the effects of the different LEDs on oxidative stress by measuring the mRNA expression of arylalkylamine N-acetyltransferase (AANAT2), the expression and activities of antioxidant enzymes (superoxide dismutase, SOD (EC 1.15.1.1); and catalase, CAT (EC 1.11.1.6)), and plasma H2O2 and plasma melatonin levels. In red light, the expression of AANAT2, SOD, and CAT mRNA was significantly higher than those under the other light spectra. SOD and CAT activities and plasma H2O2 and melatonin levels were also significantly higher for the red spectra than those for the other light spectra. These results indicate that red light induces oxidative stress. To investigate the effects of melatonin on oxidative stress, we injected melatonin into live fish (in vivo) or treated cultured pineal organ (in vitro) with melatonin. We found that AANAT2, SOD, and CAT mRNA expression levels, SOD and CAT activities, and plasma H2O2, lipid peroxidation (LPO) and melatonin levels were significantly lower than those for the controls. Therefore, our results indicate that red light induces oxidative stress and melatonin plays the role of a strong antioxidant in yellowtail clownfish.     

Alterations in Antioxidant Enzymes During Aging in Humans

The oxidative stress theory of aging offers the best mechanistic elucidation of the aging phenomenon and other age-related diseases. The susceptibility of an individual depends on the antioxidant status of the body. In humans, the antioxidant system includes a number of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT), nonenzymatic antioxidants such as glutathione (GSH), protein –SH, ascorbic acid, and uric acid, and dietary antioxidants. Antioxidant enzymes form the first line of defense against reactive oxygen species. In an earlier report, we showed that the plasma antioxidant potential in humans decreases as a function of age and that there are compensatory mechanisms operating in the body which are induced to maintain the antioxidant capacity during aging. In the present study, we report the relationship between human aging and antioxidant enzymes SOD and CAT; we also correlate the activity of these enzymes with the antioxidant capacity of the plasma. Our results show a significantly higher plasma SOD and CAT activity in older individuals than in younger individuals. The induction in activity of SOD and CAT during human aging may be a compensatory response of the individual to an increased oxidative stress.     

Cloning and mRNA expression of antioxidant enzymes in the Pacific oyster, Crassostrea gigas in response to cadmium exposure

Cadmium (Cd) is one of the most toxic heavy metal pollutants in the aquatic environment and can induce the formation of reactive oxygen species (ROS) that cause oxidative stress. In present study, we cloned catalase (CAT) and glutathione peroxidase (GPX) cDNA, and investigated its time- and dose-related effects of three Cd concentrations (0.01, 0.05 or 0.1 ppm) on mRNA levels of antioxidant enzymes (superoxide dismutase (SOD), CAT, GPX) in the gill and changes enzyme levels in the hemolymph of the Pacific oyster, Crassostrea gigas. The cDNA indentified encoded proteins of 516 and 244 amino acids corresponding to CAT and GPX, respectively. BLAST analysis from other species indicated that the residues essential to the enzymatic function of CAT and GPX proteins of C. gigas are highly conserved. Cd treatment significantly increased antioxidant enzyme mRNA expression in the gill in a time- and dose-dependent manner. The mRNA expression at 0.1 ppm Cd concentration increased up to 3 days (CAT, GPX) or 7 days (SOD) and then decreased by 7 days (CAT, GPX) or 11 days (SOD). Aspartate aminotransferase, alanine amintransferase and hydrogen peroxide (H(2)O(2)) concentrations levels increased significantly with exposure to 0.05 or 0.1 ppm Cd for 7 days. These results suggest that antioxidant enzymes play important roles in the physiological changes related to metabolism and cell protection that occur in Pacific oysters exposed to Cd.     

mRNA expression of antioxidant enzymes (SOD, CAT and GSH-Px) and lipid peroxidative stress in liver of Atlantic salmon (Salmo salar) exposed to hyperoxic water during smoltification

The mRNA levels of three antioxidant genes, Cu/Zn superoxide dismutase (SOD), catalase (CAT) and phospholipid hydroperoxide glutathione peroxidase (GSH-Px), were quantified with real-time qRT-PCR in liver of Atlantic salmon Salmo salar exposed to 80% (normoxia), 105% and 130% O2 saturation for 54 days. The salmon were then translocated and exposed to 90% and 130% O2 saturation for additional 72 days during smoltification. TBARS and vitamin E levels in liver and the levels of oxidized glutathione (GSSG), total glutathione (GSH) and the resulting oxidative stress index (OSI) in blood were quantified as traditional oxidative stress markers. No significant mean normalized expression (MNE) differences of SOD, CAT or GSH-Px were found in liver after hyperoxia exposure at the two sampling times. Significantly decreased OSI was found in smolt exposed to 130% O2 saturation after 126 days (n = 18, P < 0.0001), indicating hyperoxia-induced oxidative stress. No effects were seen on growth, or on the levels of thiobarbituric reactive substances (TBARS) and vitamin E in liver after the exposure experiment. Overall, the mRNA expression of SOD, CAT and GSH-Px in liver related poorly with the hyperoxic exposure regimes, and more knowledge are needed before the expressed levels of these antioxidant genes can be applied as biomarkers of hyperoxia in Atlantic salmon.     

Lethal and sublethal effect of heat shock on Phenacoccus solenopsis Tinsley (Hemiptera: Pseudococcidae)

Temperature is an important abiotic environmental factor, and is responsible for various kinds of behavioral and physiological changes in living organisms. Induced heat shock is associated with feeding behaviour, reproduction and reactive oxygen species (ROS) generation that causes oxidative damage. In this experiment, we examined the lethal and sublethal effects of heat shock on reproduction, feeding behaviour and antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD) and peroxidases (POD) in P. solenopsis. Results showed that males were highly susceptible to heat shock treatments than females, as LTemp₅₀ values were 43.8 °C for males and 45.11 °C for females. Heat shock events non-significantly affected the fecundity in female only treated adults and significantly affected the both sexes heat treated adults, it increased the xylem feeding duration, percentage of xylem feeding adults and reduce the phloem feeding duration and percentage of phloem feeding adults. Similarly it alter the antioxidant enzymes activities, an increase of CAT, SOD and POD activities were noticed in response to highest intensity of heat shock while a reduction of CAT and SOD activity were noticed in response to lowest intensity of heat shock compared to control (30 °C). These results suggest that heat shock may result in loss of body water and induce oxidative stress in P. solenopsis. However, antioxidant enzymes play a significant role in overcoming the oxidative damage.     

Oxidants and antioxidants in aquatic animals.

1. Oxidative stress, potentially, is experienced by all aerobic life when antioxidant defenses are overcome by prooxidant forces, and is the basis of many physiological abberations. 2. Environmental contaminants may enhance oxidative stress in aquatic organisms, e.g. highly elevated rates of ideopathic lesions and neoplasia among fish inhabiting polluted environments is increasingly related to oxidative stress associated with environmental pollution. 3. Metabolism of redox cycling xenobiotics in aquatic organisms is very similar to that of mammals suggesting similarities in the health consequences of exposure to such compounds. 4. The expression of specific lesions known to arise specifically from oxidative stress, e.g. lipid peroxidation, oxidized bases in DNA and accumulation of lipofuscin pigments are present in many aquatic animals exposed to contaminants. 5. Aquatic organisms contain the major antioxidant enzymes SOD, catalase and glutathione peroxidase, albeit there are marked quantitative differences among the various species reported.     

Effect of chronic cadmium exposure on antioxidant defense system in some tissues of rats: protective effect of selenium

The effects of selenium (Se) on antioxidant defense system in liver and kidneys of rats with cadmium (Cd)-induced toxicity were examined. Cd exposure (15 mg Cd/kg b.m./day as CdCl(2) for 4 weeks) resulted in increased lipid peroxidation (LP) in both organs (p<0.005 and p<0.01). Vitamin C (Vit C) was decreased in the liver (p<0.005), whereas vitamin E (Vit E) was increased in the liver and kidneys (p<0.005 and p<0.05) of Cd-exposed animals. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were decreased in both tissues (p<0.05 and p<0.005), whereas catalase (CAT) activity was decreased only in liver (p<0.005). Glutathione S-transferase (GST) increased in both tissues (p<0.005 and p<0.01). Treatment with Se (0.5 mg Se/kg b.m./day as Na(2)SeO(3) for 4 weeks) significantly increased liver and kidneys SOD and GSH-Px activities (p<0.05 to p<0.005), as well as CAT and GST activities only in the liver (p<0.01). In animals exposed to Se, both the concentrations of Vit C (p<0.01) and Vit E (p<0.005) were increased in both tissues. Co-treatment with Se resulted in reversal of oxidative stress with significant decline in analyzed tissues Cd burden. Our results show that Se may ameliorate Cd-induced oxidative stress by decreasing LP and altering antioxidant defense system in rat liver and kidneys and that Se demonstrates the protective effect from cadmium-induced oxidative damage.