Antioxidant enzymes activities in obese Tunisian children.

BACKGROUND: The oxidant stress, expected to increase in obese adults, has an important role in the pathogenesis of many diseases. It results when free radical formation is greatly increased or protective antioxidant mechanisms are compromised. The main objective of this study is to evaluate the antioxidant response to obesity-related stress in healthy children. METHODS: A hundred and six healthy children (54 obese and 52 controls), aged 6-12 years old, participated in this study. The collected data included anthropometric measures, blood pressure, fasting glucose, total cholesterol, triglycerides and enzymatic antioxidants (Superoxide dismutase: SOD, Catalase: CAT and Glutathione peroxidase: GPx). RESULTS: The first step antioxidant response, estimated by the SOD activity, was significantly higher in obese children compared with normal-weight controls (p < 0.05). Mean activities of anti-radical GPx and CAT enzymes were not affected by the BMI increase. Although, total cholesterol levels were statistically higher in the obese group, there was no significant association with the SOD activity. CONCLUSIONS: The obesity-related increase of the oxidant stress can be observed even in the childhood period. In addition to the complications of an increased BMI, obesity itself can be considered as an independent risk factor of free radical production resulting in an increased antioxidant response.

Reduced antioxidant defense systems in schizophrenia and bipolar I disorder.

Numerous evidence and proofs suggest that the oxidative stress contributes to the pathogenesis of schizophrenia (SZ) and bipolar disorder (BD). The aim of this study is to determine the glutathione levels and the antioxidant enzyme activities in blood samples of patients suffering from SZ and patients with bipolar disorder in comparison with the healthy controlled subjects. It was a case-controlled study carried on upon three groups: forty-six SZ patients (41 men and 5 women, mean age=33.2±7years), thirty BD patients (25 men and 5 women, mean age=31.3±8years) and forty healthy controls (33 men and 7 women, mean age=32.3±7years). The glutathione levels are the total glutathione (GSHt), the reduced glutathione (GSHr), and the oxidized glutathione (GSSG) and the antioxidant enzyme activities that are the superoxide dismutase (SOD), the glutathione peroxidase (GPx), and the catalase (CAT) are determined by the spectrophotometer. We noticed that the GSHt and the GSHr levels significantly decreased in both SZ and BD patients in comparison with the healthy control subjects. As for SOD and CAT activities they remained lower for the patients with SZ when compared both with the controls or the BD patients. We noticed as well that the CAT activity was significantly lower in the BD group than that in the control group, whereas, GPx activity showed no significant change in each group. Hence, this report of the decreased plasma levels of GSHt and GSHr, and the impaired antioxidant enzyme activities in SZ and BD patients aims at highlighting the GSH deficit that seems to be contributing to these disorders, and showing that it may be an important indirect biomarker of the oxidative stress for the SZ and BD.

The prolongation of the lifespan of rats by repeated oral administration of [60]fullerene.

Countless studies showed that [60]fullerene (C(60)) and derivatives could have many potential biomedical applications. However, while several independent research groups showed that C(60) has no acute or sub-acute toxicity in various experimental models, more than 25 years after its discovery the in vivo fate and the chronic effects of this fullerene remain unknown. If the potential of C(60) and derivatives in the biomedical field have to be fulfilled these issues must be addressed. Here we show that oral administration of C(60) dissolved in olive oil (0.8 mg/ml) at reiterated doses (1.7 mg/kg of body weight) to rats not only does not entail chronic toxicity but it almost doubles their lifespan. The effects of C(60)-olive oil solutions in an experimental model of CCl(4) intoxication in rat strongly suggest that the effect on lifespan is mainly due to the attenuation of age-associated increases in oxidative stress. Pharmacokinetic studies show that dissolved C(60) is absorbed by the gastro-intestinal tract and eliminated in a few tens of hours. These results of importance in the fields of medicine and toxicology should open the way for the many possible -and waited for- biomedical applications of C(60) including cancer therapy, neurodegenerative disorders, and ageing.

Influence of cadmium exposure on growth and fecundity of freshwater mosquitofish Gambusia affinis: in situ and in vivo studies.

This study aims to investigate the effect of cadmium (Cd) exposure on growth and fecundity of mosquitofish Gambusia affinis. For this purpose, two natural populations of pregnant females of G. affinis captured from two sites were differently contaminated with Cd (S1 present Cd levels 5-fold higher than S2) and a sublethal exposure to 0.4 mg CdCl(2)/L (10% of LC(50)) during 56 days was conducted in vivo. The length-weight regression revealed a significant difference in the growth between these two populations. A significant difference in fecundity was also noted between the two populations. Indeed, the embryo numbers in pregnant females captured from S1 are significantly higher than those noted in pregnant females from S2 (21.17±5 and 7.97±2.12, respectively; p<0.05). Following Cd exposure, we noted a growth perturbation resulting in lower values of both indices BWG and SGR following 7 and 21 days (-5.21 and -1.18 for BWG, and -2.09 and -0.46 for SGR, respectively) and a recuperation of growing weight at 42 and 56 days (1.32 and 1.71 for BWG, and 0.45 and 0.54 for SGR, respectively). For CF index, we observed a significant difference (p<0.05) between control and Cd groups at 7 and 21 days of exposure, and at 21 and 56 days respectively for HSI and GSI indices. Furthermore, Cd contents in both tissues (liver and yolk sac) and fractions (cytosolic and membrane) are significantly different between groups during experimentation. In addition, the Cd contents noticed in the liver membrane fraction are significantly higher than those noted in the yolk sac tissue. The MTs levels revealed a significant difference between the control and Cd groups. In liver tissue, a significant difference was noted, in MTs levels, during the Cd exposure (7, 21, 42, and 56 days) while in the yolk sac tissue the difference was noted at 42 days of exposure. Taken together, these results imply the potential negative effect of Cd on physiological status of G. affinis as evidenced by decreasing growth and fecundity rate.

Impact of seminal trace element and glutathione levels on semen quality of Tunisian infertile men.

BACKGROUND: Growing evidence indicates that oxidative stress can be a primary cause of male infertility. Non-enzymatic antioxidants play an important protective role against oxidative damages and lipid peroxidation. Human seminal plasma is a natural reservoir of antioxidants. The aim of this study was to determine glutathione (GSH) concentrations, trace element levels (zinc and selenium) and the lipid peroxidation end product, malondialdehyde (MDA), in the seminal plasma of men with different fertility potentials. METHODS: Semen samples from 60 fertile men (normozoospermics) and 190 infertile patients (74 asthenozoospermics, 56 oligozoospermics, and 60 teratozoospermics) were analyzed for physical and biochemical parameters. Zinc (Zn) and selenium (Se) levels were estimated by atomic absorption spectrophotometry. Total GSH (GSHt), oxidized GSH (GSSG), reduced GSH (GSHr) and MDA concentrations were measured spectrophotometrically. RESULTS: Zn and Se concentrations in seminal plasma of normozoospermics were more elevated than the three abnormal groups. Nevertheless, only the Zn showed significant differences. On the other hand, Zn showed positive and significant correlations with sperm motility (P = 0.03, r = 0.29) and count (P < 0.01, r = 0.49); however Se was significantly correlated only with sperm motility (P < 0.01, r = 0.36). GSHt, GSSG and GSHr were significantly higher in normozoospermics than in abnormal groups. We noted a significant association between seminal GSHt and sperm motility (P = 0.03). GSSG was highly correlated to sperm motility (P < 0.001) and negatively associated to abnormal morphology (P < 0.001). GSHr was significantly associated to total sperm motility (P < 0.001) and sperm count (P = 0.01). MDA levels were significantly higher in the three abnormal groups than in normozoospermics. Rates of seminal MDA were negatively associated to sperm motility (P < 0.01; r = -0.24) and sperm concentration (P = 0.003; r = -0.35) Meanwhile, there is a positive correlation between seminal lipid peroxidation and the percentage of abnormal morphology (P = 0.008). CONCLUSIONS: This report revealed that decreased seminal GSH and trace element deficiencies are implicated in low sperm quality and may be an important indirect biomarker of idiopathic male infertility. Our results sustain that the evaluation of seminal antioxidant status in infertile men is necessary and can be helpful in fertility assessment from early stages.

Decreased glutathione levels and impaired antioxidant enzyme activities in drug-naive first-episode schizophrenic patients.

BACKGROUND: The aim of this study was to determine glutathione levels and antioxidant enzyme activities in the drug-naive first-episode patients with schizophrenia in comparison with healthy control subjects. METHODS: It was a case-controlled study carried on twenty-three patients (20 men and 3 women, mean age = 29.3 ± 7.5 years) recruited in their first-episode of schizophrenia and 40 healthy control subjects (36 men and 9 women, mean age = 29.6 ± 6.2 years). In patients, the blood samples were obtained prior to the initiation of neuroleptic treatments. Glutathione levels: total glutathione (GSHt), reduced glutathione (GSHr) and oxidized glutathione (GSSG) and antioxidant enzyme activities: superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) were determined by spectrophotometry. RESULTS: GSHt and reduced GSHr were significantly lower in patients than in controls, whereas GSSG was significantly higher in patients. GPx activity was significantly higher in patients compared to control subjects. CAT activity was significantly lower in patients, whereas the SOD activity was comparable to that of controls. CONCLUSION: This is a report of decreased plasma levels of GSHt and GSHr, and impaired antioxidant enzyme activities in drug-naive first-episode patients with schizophrenia. The GSH deficit seems to be implicated in psychosis, and may be an important indirect biomarker of oxidative stress in schizophrenia early in the course of illness. Finally, our results provide support for further studies of the possible role of antioxidants as neuroprotective therapeutic strategies for schizophrenia from early stages.

Cadmium-induced ovarian pathophysiology is mediated by change in gene expression pattern of zinc transporters in zebrafish (Danio rerio).

This study explored the potential for expression pattern of genes encoding zinc (Zn) transporters to be involved in the cadmium (Cd)-induced reproductive toxicity in female of zebrafish. For this purpose, oocytes maturity and ovarian histology as well as Cd, Zn and metallothioneins (MTs) accumulation and expression of genes encoding Zrt-,Irt-related protein 10 (ZIP10), Zn transporter 1 (ZnT1) and zebrafish metallothionein (zMT) were examined in ovaries of adult zebrafish exposed to 0.4 mg/L Cd in water and supplemented with Zn (5 mgkg(-1)) in their diet for 21 days. Cd-exposure decreased the expression of ZnT1 and caused up-regulation of ZIP10 and zMT gene expression. These changes were accompanied by increased Cd and MTs accumulation, decreased Zn contents as well as by histopathological damages in ovarian tissues. The co-exposure of fish to Cd and Zn abolished ZnT1 down-regulation and rendered a persistently increased ZIP10 mRNA level. This treatment also decreased Cd and MTs accumulation, reversed Cd-induced Zn depletion and partially restored Cd-induced histological changes in ovarian tissues. These results imply that the downregulation of ZnT1 as well as the overexpression of ZIP10, in responses to the ovarian Zn depletion induced by Cd, play a major role in Cd accumulation and consequently in its toxicity. The protective effect of dietary Zn supplementation against Cd-induced toxicity is mediated, at least in part, by the increase of Zn availability and subsequently the induction of ZnT1 gene expression.

Mechanisms underlying the protective effect of zinc and selenium against cadmium-induced oxidative stress in zebrafish Danio rerio.

The present study was designed to elucidate the protective effect mechanism of Zinc (Zn) and Selenium (Se) on cadmium (Cd)-induced oxidative stress in zebrafish. For this purpose we investigate the response of oxidative stress markers, metallothionein accumulation and gene expression in liver and ovary of female zebrafish exposed to 0,4 mg/l Cd in water and supplemented with Zn (5 mg kg(-1)) and/or Se (2 mg kg(-1)) for 21 days in their diet. Liver and ovary Cd uptake was evaluated after the exposure period. Cd exposure significantly inhibited the antioxidant enzyme activities termed as catalase (CAT), superoxide dismutase (SOD) and glutathione peroxydase (GPx) and caused a pronounced malondialdehyde (MDA) accumulation in both organs. Co-administration of Zn and Se reversed the Cd-induced toxicity in liver and ovary measured as MDA accumulation. Interestingly, gene expression patterns of Cat, CuZnSod and Gpx were up-regulated when related enzymatic activities were altered. Zebrafish metallothionein transcripts (zMt) significantly decreased in tissues of fish supplemented with Zn and/or Se when compared to Cd-exposed fish. Our data would suggest that Zn and Se protective mechanism against Cd-induced oxidative stress is more depending on the correction of the proteins biological activities rather than on the transcriptional level of related genes.

Effects of zinc pre-treatment on blood glutathione, serum zinc and kidney histological organisation in male rats exposed to cadmium.

The effects of sub-chronic exposure to cadmium (Cd) on the blood glutathione, serum zinc and on the kidney histological organisation in rats as well as the possible protective role of zinc (Zn) are the object of this study. For this purpose, 60 male Wistar rats (8 weeks old) were divided into three groups: the first group was exposed to Cd in the form of CdCl(2), administered in five doses (each of 0.4 mg Cd/kg b.w.) on days 5, 10, 15, 20 and 25, giving a total dose of 2mg Cd/kg b.w., i.p.; the second group was simultaneously exposed to Zn and Cd with the same timeline and the same doses of Cd as the first group but with, in addition, injections of Zn in the form of ZnCl(2), administered in doses of 0.8 mg Zn/kg b.w., giving a total dose of 4 mg Zn/kg b w, i.p.; a control group received 0.5 mL of physiological saline in an identical manner. Intoxication with Cd was followed by a significant decrease in blood glutathione, increase in oxidized glutathione as well as histological damage in kidneys. Pre-treatment with Zn exhibited a protective role against Cd toxicity with a significant decrease in serum zinc content. This fact may be explained by an excessive use of zinc in metallothionein synthesis as a cadmium detoxification agent.

Involvement of selenoprotein P and GPx4 gene expression in cadmium-induced testicular pathophysiology in rat.

To investigate the effect of co-exposure to cadmium (Cd) and selenium (Se) on selenoprotein P (SelP) and phospholipid hydroperoxide glutathione peroxidase (GPx4) gene expression in testis and to evaluate their possible involvement in Cd-induced testicular pathophysiology, male rats received either tap water, Cd or Cd+Se in their drinking water for 5 weeks. Cd exposure caused a down-regulation of SelP and GPx4 gene expression and a significant decrease in plasma and testicular concentrations of Se. These changes were accompanied by decreased plasma testosterone level, sperm count and motility, GSH content, protein-bound sulfhydryl concentration (PSH), enzymatic activities of catalase (CAT) and glutathione peroxidase (GSH-Px) as well as by increased glutathione-S-transferase (GST) activity, lipid peroxidation (as malondialdehyde, MDA) and proteins carbonyls (PC). The decrease of testicular SelP and GPx4 gene expression under Cd influence was significantly restored in Cd+Se group. Co-treatment with Cd and Se also totally reversed the Cd-induced depletion of Se, decrease in plasma testosterone level and partially restored Cd-induced oxidative stress and decrease in sperm count and motility. Taken together, these data suggest that down-regulation of SelP and GPx4 gene expression induces plasma and testicular Se depletion leading, at least in part, to Cd-induced testicular pathophysiology.

Influence of combined treatment with zinc and selenium on cadmium induced testicular pathophysiology in rat.

The present study was conducted to evaluate the potential benefit of combined treatment with zinc (Zn) and selenium (Se) in reversing cadmium (Cd)-induced testicular pathophysiology compared to Se or Zn treatment alone in rats. For this purpose, male rats received either tap water, Cd, Cd+Zn, Cd+Se or Cd+Zn+Se in their drinking water, for 35 days. Cd exposure caused a significant decrease in plasma and testicular concentrations of Se and Zn which was accompanied by decreased plasma testosterone level, sperm count and motility, enzymatic activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) as well as by increased lipid peroxidation (as malondialdehyde, MDA). With Se or Zn administration, during exposure to Cd, only partial corrective effects on depletion of testicular and plasma Se and Zn levels, sperm characteristics and oxidative stress have been observed. The combined treatment of Cd-exposed animals with Se and Zn assured a more significant decrease in plasma and testicular Cd concentrations and a more efficient protection against the observed testicular damage as evidenced by the total prevention of both Se and Zn deprivation and by the entire restoration of the sperm motility and the testicular antioxidant status.

Metallothionein gene expression in liver of rats exposed to cadmium and supplemented with zinc and selenium.

Cadmium (Cd), one of the most widely distributed heavy metals, is highly toxic to humans and animals. It is well known that zinc (Zn) and selenium (Se) administration reduce the Cd-induced toxicity and that metallothioneins can have a protective effect to mitigate Cd toxicity in biological systems. In this study we report the expression analysis of the two metallothioneines gene classes MT-1 and MT-2 as well as the total metalloprotein content in the liver of rats exposed to Cd (200 ppm), Cd + Zn (200 ppm + 500 ppm), Cd + Se (200 ppm + 0.1 ppm) or Cd + Zn + Se (200 ppm + 500 ppm + 0.1 ppm) in their drinking water for 35 days. Metals accumulation was quantified in rat liver. Cd decreased significantly the hepatic concentrations of Se and increased those of Zn. The treatment of Cd-exposed rats with Se alone or combined with Zn reversed the Cd-induced depletion of Se concentrations in the liver. However, Zn or Zn + Se administration significantly increased the liver Cd uptake and had no effect on the Cd-induced increase in hepatic concentrations of Zn. The molecular assay showed a decreasing trend of MT-1 relative gene expression levels in animals supplemented with Zn (6.87-fold), Se (3.58-fold), and their combination (1.69-fold) when compared to Cd-treated animals (16.22-fold). Upregulation of the MT-2 expression were recorded in all conditions, although fold induction levels were less pronounced than MT-1 expressions. Our data suggest that the well-established protective effect of Zn and Se against Cd-induced toxicity passes through non-MT gene expression mechanisms, being more dependent on the oxidative stress status of the cell.

Evaluation of involvement of testicular metallothionein gene expression in the protective effect of zinc against cadmium-induced testicular pathophysiology in rat.

To investigate the effects of exposure to Cd and Zn on testicular MT-1 and MT-2 gene expression and evaluate their involvement in Zn protection against Cd-induced testicular pathophysiology, male rats received either tap water, Cd or Cd+Zn in their drinking water for 35 days. Cd induced histopathological changes in testicular tissues were accompanied by decreased plasma testosterone level, plasma and testicular Zn concentrations, oxidative stress, and by increased MT-1 and MT-2 gene expression. Co-treatment with Cd and Zn reversed the Cd-induced decrease testosterone level and SOD activity, decreased testicular Cd accumulation and partially restored Cd-induced histological changes, lipid peroxidation, and Zn depletion. The increase of testicular MT-1 and MT-2 gene expression under Cd influence was significantly reduced in Cd+Zn group. These data suggest that Zn enhances the protection against Cd-induced testicular pathophysiology through non-MT gene expression mechanisms but essentially by preventing Cd accumulation, Zn deprivation and by ameliorating the testicular antioxidant status.

Influence of high temperature on cadmium-induced skeletal deformities in juvenile mosquitofish (Gambusia affinis).

The aim of this study was to assess the effect of high temperature on cadmium (Cd)-induced skeletal deformities in juvenile Mosquitofish, Gambusia affinis. For this purpose, 188 juveniles (1 day old) were equally divided into the control group, which was maintained in Cd-free water at 24 degrees C, and three treated groups exposed either to Cd (0.4 mg/l as Cd Cl(2)) at 24 degrees C, to high temperature (32 degrees C), or to Cd at 32 degrees C for 30 days. The results showed that Cd exposure at 24 degrees C significantly increased the Cd accumulation (P < 0.0001) in the whole tissues of juveniles as well as the incidence of skeletal deformities (P < 0.01) compared with control animals. Exposure to high temperature also led to a significant increase in the incidence of skeletal deformities (P < 0.01) with respect to the control group. Interestingly, our results showed that the combined exposure to Cd and high temperature led to a more significant increase in Cd accumulation and in the frequency of spinal deformities than exposure to Cd or high temperature alone. These results confirm that temperature increases Cd toxicity and needs to be taken into account for the accurate prediction and assessment of Cd-induced spinal deformities in fish.

Reversal of cadmium-induced oxidative stress in rat erythrocytes by selenium, zinc or their combination.

The aim of this study was to evaluate the potential benefit of combined treatment with zinc (Zn) and selenium (Se) in reversing cadmium (Cd)-induced oxidative stress in erythrocytes, compared to Se or Zn treatment alone in rats exposed to Cd. For this purpose, 30 adult male Wistar albino rats were equally divided into control and four treated groups received either 200ppm Cd (as CdCl(2)), 200ppm Cd+500ppm Zn (as ZnCl(2)), 200ppm Cd+0.1ppm Se (as Na(2)SeO(3)), or 200ppm Cd+500ppm Zn+0.1ppm Se in their drinking water for 35 days. Marked alterations of antioxidative system were found in Cd-treated rats. Activities of catalase (CAT) and glutathione peroxidise (GSH-Px) as well as the total glutathione (GSH) contents in erythrocytes were significantly decreased, whereas the activity of total superoxide dismutase (SOD) was significantly increased. The treatment of Cd-exposed rats with Se alone had no significant effect on the Cd-induced increase in the SOD activity but increased significantly the CAT and GSH-Px activities and partially reversed Cd-induced depletion of GSH levels in erythrocytes. The treatment of Cd-exposed animals with Zn alone partially reversed Cd-induced increase in SOD activity and Cd-induced decrease in GSH-Px activity. The combined treatment of Cd-exposed animals with Se and Zn was more effective than that with either of them alone in reversing Cd-induced decrease in CAT and GSH-Px activities and Cd-induced increase in SOD activity. This treatment also partially restored Cd-induced depletion of GSH. These results could be important for the further development of better treatments for people and/or animals exposed to Cd.

Cadmium bioaccumulation in three benthic fish species, Salaria basilisca, Zosterisessor ophiocephalus and Solea vulgaris collected from the Gulf of Gabes in Tunisia.

To select a marine teleost fish which can be used as a bioindicator of cadmium (Cd) pollution in the Gulf of Gabes in Tunisia, Cd concentrations in liver and gill were compared in three benthic fish species including Salaria basilisca, Zosterisessor ophiocephalus and Solea vulgaris. Fish samples were collected from three selected sites in the Gulf of Gabes, with different degrees of Cd contamination: the industrialized coast of Sfax (S1), the coast of Douar Chatt (S2) and the coast of Luza (S3). The results shows that Cd concentrations in both sediment and water collected from S1 were significantly higher (p < 0.0001) than those from S2 and S3. For each species, Cd concentrations, in both liver and gill, showed the decreasing order: S1 > S2 > S3. The highest concentration of Cd was detected in the liver of S. basilisca, and only S. basilisca showed bioaccumulation factors (BAF) greater than 1 in all studied sites. In S1 and S2, BAF values respect the following order: S. basilisca > Z. ophiocephalus > S. vulgaris. These results of significant bioaccumulation of Cd, in terms of hepatic concentrations and bioaccumulation factors, indicated that S. basilisca can be used as bioindicator to evaluate the evolution of Cd pollution in the Gulf of Gabes.

Decreased glutathione levels and antioxidant enzyme activities in untreated and treated schizophrenic patients.

There is substantial evidence found in the literature that supports the fact that the presence of oxidative stress may play an important role in the physiopathology of schizophrenia. Previous studies have reported the occurrence of impairments in the glutathione levels and the activities of the antioxidant enzymes in patients suffering from schizophrenia. However, most of these studies were performed on treated patients. The present study evaluated treated schizophrenic patients (n=52) along with neuroleptic-free or untreated schizophrenic patients (n=36) and healthy controls (n=46). The blood glutathione levels: total glutathione (GSHt), reduced glutathione (GSHr), and oxidized glutathione (GSSG) as well as the activities of the antioxidant enzymes: superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were measured. The psychopathology of the patients was assessed through the Clinical Global Impressions-severity (CGI-severity). The tests revealed that in comparison with the healthy controls, the schizophrenic patients showed significantly lower levels of GSHr, SOD, and CAT. Among the schizophrenic patients, the activities of the antioxidant enzymes SOD and CAT were recorded to be significantly lower in untreated patients than in the treated ones. In addition, the levels of both GSHt and GSHr were found to be inversely correlated with the obtained CGI-severity score. These results evidently suggest that a decrease in the glutathione levels and the activities of the antioxidant enzymes in patients diagnosed with schizophrenia is not related to neuroleptic treatment and could be considered as a biological indicator of the degree of severity of the symptoms of schizophrenia.

Protective effects of selenium, zinc, or their combination on cadmium-induced oxidative stress in rat kidney.

The present study was conducted to investigate whether the combined treatment with Se and Zn offers more beneficial effects than that provided by either of them alone in reversing Cd-induced oxidative stress in the kidney of rat. For this purpose, 30 adult male Wistar albino rats, equally divided into control and four treated groups, received either 200 ppm Cd (as CdCl(2)), 200 ppm Cd + 500 ppm Zn (as ZnCl(2)), 200 ppm Cd + 0.1 ppm Se (as Na(2)SeO(3)), or 200 ppm Cd + 500 ppm Zn + 0.1 ppm Se in their drinking water for 35 days. The results showed that Cd treatment decreased significantly the catalase (CAT) and glutathione peroxidase (GSH-Px) activities, whereas the superoxide dismutase (SOD) activity and the renal levels of lipid peroxidation (as malondialdehyde, MDA) were increased compared to control rats. The treatment of Cd-exposed rats with Se alone had no significant effect on the Cd-induced increase in the MDA concentrations but increased significantly the CAT activities and reversed Cd-induced increase in SOD activity. It also partially prevented Cd-induced decrease in GSH-Px activity. The treatment of Cd-exposed animals with Zn alone increased significantly the CAT activity and partially protected against Cd-induced increase in the MDA concentrations, whereas it had no significant effect on the Cd-induced increase in SOD activity and decrease in GSH-Px activity. The combined treatment of Cd-exposed animals with Se and Zn was more effective than that with either of them alone in reversing Cd-induced decrease in CAT and GSH-Px activities and Cd-induced increase in MDA concentrations. Results demonstrated beneficial effects of combined Se and Zn treatment in Cd-induced oxidative stress in kidney and suggest that Se and Zn can have a synergistic role against Cd toxicity.

Comparative study of the sensitivity to cadmium of two populations of Gambusia affinis from two different sites.

This study aims to demonstrate the influence of animals' origin on their sensitivity toward heavy metals. For this purpose, we compared LC(50) of cadmium in two populations of Gambusia affinis captured in two geographically isolated environments in the east of Tunisia; Oued El Gsil in the city of Monastir (S2) and Oued Chenini in the region of Gabes (S1). Although physicochemical parameters of the water (pH, dissolved oxygen and salinity) are similar in the two studied sites, cadmium concentrations in water, sediments and fish tissues from S1 are significantly higher (P < 0.01) than those from S2, 48-h and 96-h LC(50) of the (S1) population are significantly higher than those from S2. In the same way, the offspring of the polluted site (S1) population exhibit 48-h and 96-h LC(50) values much higher than those of the reference site (S2) population. These results show that the population of the Gabes region is more resistant to cadmium than that of the Monastir region and that this resistance could have a genetic basis. These results indicate the influence of the origin of animals that has to be taken into account not only in laboratory toxicity tests, but also in field ecotoxicological studies.

Oxidative stress: correlation with Behçet's disease duration, activity and severity.

OBJECTIVE: To study the oxidant/antioxidant status in Behçet's disease (BD) patients and the potential link between antioxidant enzymatic defences impairment and the disease duration, activity and severity. METHODS: 40 BD patients (27 males, 13 females; mean age: 38.8 years) were prospectively enrolled in the study and compared to a sex and age matched control group. Plasma malondialdehyde (MDA), the reduced glutathione (GSH)/oxidised glutathione (GSSG) ratio, erythrocyte superoxide dismutase, catalase and glutathione peroxidase (GSH-PX) were analysed in both groups. A correlation analysis was performed between these parameters and disease duration, activity and severity. Activity and severity of BD were assessed meaning two respective clinical scores. RESULTS: When compared to controls MDA was increased and GSH/GSSG reduced in BD patients (respectively p<0.005). Superoxide dismutase (SOD) was significantly lower while catalase was significantly higher in BD than in controls. Correlation analysis showed that SOD activity was significantly and negatively correlated to disease duration and activity but not to severity. Other oxidant/antioxidant markers were not significantly linked to neither disease duration nor activity and severity. CONCLUSION: Our study confirm the existence of an oxidative stress (OS) state in BD as shown by the increase of MDA and the diminution of GSH/GSSG ratio which can be used as another index of OS. Despite this OS state, the activity of antioxidant enzymes and especially of SOD is impaired and negatively correlated to the disease duration and activity. We think that a rational strengthening of antioxidant defences should be part of an optimal treatment strategy.