Cadmium-induced Oxidative Stress Research Articles

Ascorbic acid, garlic extract and taurine alleviate cadmium-induced oxidative stress in freshwater catfish ( Clarias batrachus)

An experiment was conducted to investigate bioaccumulation potential of cadmium (Cd) and changes in oxidative stress indices in liver and kidney tissues from Cd-exposed catfish ( Clarias batrachus) with or without simultaneous treatment of water with ascorbic acid, garlic extract or taurine. C. batrachus ( n = 324) with average length of 20 ± 4 cm and weight of 86 ± 5 g were used for the present investigation. Fishes were divided into nine groups (I to IX) each comprising 36 fishes. The fishes of groups II, III, IV and V were challenged with 5 ppm of cadmium chloride monohydrate (CdCl 2.H 2O), whereas groups VI, VII, VIII and IX were exposed to 10 ppm CdCl 2.H 2O solution for a period of 45 days. Group I was kept as negative control and the fishes of this group were maintained in water containing no added Cadmium. Group II and VI were maintained as Cd exposed non treated control to serve as positive controls. Fishes of III and VII, IV and VIII, V and IX received ascorbic acid (5 ppm), extract of dried garlic (5 ppm) or taurine (5 ppm), respectively during the entire experiment period. The concentrations of Cd in liver and kidney increased significantly following exposure to Cd and the level continued to rise with the increase in exposure duration. Treatment of tank water with ascorbic acid, garlic or taurine significantly reduced the Cd concentrations in tissues compared to the positive control group, but the level in Cd exposed groups was greater than the negative control group. Fishes exposed to Cd and treated with ascorbic acid, garlic or taurine had reduced oxidative stress as evidenced from lower concentration of lipid peroxides and higher activities of superoxide dismutase and catalase in liver, kidney and erythrocytes compared to fishes exposed to Cd. The reduction in Cd induced oxidative stress was highest in ascorbic acid treated group followed by garlic and taurine treatment. The results suggest that ascorbic acid, garlic and taurine have potential to reduce tissue accumulation of Cd and associated oxidative stress in freshwater catfish.

Arabidopsis acyl-CoA-binding protein 2 enhances tolerance to cadmium-induced oxidative stress in transgenic plants

Arabidopsis acyl-CoA-binding protein 2 enhances tolerance to cadmium-induced oxidative stress in transgenic plants

Antioxidant Activity of the Yeast Mitochondrial One-Cys Peroxiredoxin Is Dependent on Thioredoxin Reductase and Glutathione In Vivo

Peroxiredoxins are ubiquitous enzymes which protect cells against oxidative stress. The first step of catalysis is common to all peroxiredoxins and results in oxidation of a conserved peroxidatic cysteine residue to sulfenic acid. This forms an intermolecular disulfide bridge in the case of 2-Cys peroxiredoxins, which is a substrate for the thioredoxin system. 1-Cys Prx's contain a peroxidatic cysteine but do not contain a second conserved cysteine residue, and hence the identity of the in vivo reduction system has been unclear. Here, we show that the yeast mitochondrial 1-Cys Prx1 is reactivated by glutathionylation of the catalytic cysteine residue and subsequent reduction by thioredoxin reductase (Trr2) coupled with glutathione (GSH). This novel mechanism does not require the usual thioredoxin (Trx3) redox partner of Trr2 for antioxidant activity, although in vitro assays show that the Trr2/Trx3 and Trr2/GSH systems exhibit similar capacities for supporting Prx1 catalysis. Our data also indicate that mitochondria are a main target of cadmium-induced oxidative stress and that Prx1 is particularly required to protect against mitochondrial oxidation. This study demonstrates a physiological reaction mechanism for 1-Cys peroxiredoxins and reveals a new role in protection against mitochondrial heavy metal toxicity.

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 CdCl2), 200ppm Cd+500ppm Zn (as ZnCl2), 200ppm Cd+0.1ppm Se (as Na2SeO3), 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-induced oxidative stress and antioxidative mechanisms in germinating Indian mustard ( Brassica juncea L.) seeds

Cadmium, known as a non-essential heavy metal, can cause oxidative stress in plants. In this study we tried to find out whether oxidative changes could be measured in the early stages of ontogenesis in Indian mustard ( Brassica juncea L.) seeds exposed to Cd stress. Cadmium-caused oxidative stress and antioxidative responses were investigated with respect to both time- and concentration-dependence. Parameters that were measured were follows: total antioxidant capacity (ferric reducing ability of plasma (FRAP)), glutathione (GSH) content, level of lipid peroxidation (LP), total protein content, and glutathione-S-transferase (GST, EC 2.5.1.18) activity. Seeds were germinated in vitro at 0, 50, 100 and 200 mg/L Cd concentrations in dark for 12, 24, 48 and 96 h. Oxidative stress occurred in the seeds due to Cd treatment, the level of LP was high at the beginning of the germination at all concentrations used, but it attenuated later on. FRAP showed concentration-dependent increase during 24 h, but it decreased later on. GSH content was also elevated by increasing concentrations of Cd, which referred to the activity of non-enzymatic antioxidant system. The GST activity induced with germination only after 24 h at the highest Cd concentration. The results show that FRAP is a suitable parameter with which to assess the antioxidant capacity of heavy metal-stressed germinating seeds.

Cadmium-induced oxidative stress in two potato cultivars

A hydroponic experiment was carried out to characterize the oxidative stress responses of two potato cultivars (Solanum tuberosum L. cvs. Asterix and Macaca) to cadmium (Cd). Plantlets were exposed to four Cd levels (0, 50, 100, 150 and 200 microM) for 7 days. Cd concentration was increased in both roots and shoot. Number of sprouts and roots was not decreased, whereas Cd treatment affected the number of nodal segments. Chlorophyll content and ALA-D activity were decreased in both cultivars, whereas carotenoids content was decreased only in Macaca. Cd caused lipid peroxidation in roots and shoot of both cultivars. Protein oxidation was only verified at the highest Cd level. H(2)O(2) content was increased in roots and shoot of Asterix, and apparently, a compensatory response between roots and shoot of Macaca was observed. SOD activity was inhibited in roots of Asterix at all Cd treatments, whereas in Macaca it was only increased at two highest Cd levels. Shoot SOD activity increased in Asterix and decreased in Macaca. Root CAT activity in Asterix decreased at 100 and 150 microM, whereas in Macaca it decreased only at 50 microM. Shoot CAT activity was decreased in Macaca. Root AsA content in Macaca was not affected, whereas in shoot it was reduced at 100 microM and increased at 200 microM. Cd caused increase in NPSH content in roots and shoot. Our results suggest that Cd induces oxidative stress in both potato cultivars and that of the two cultivars, Asterix showed greater sensitivity to Cd levels.

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.

Changes In Antioxidant Status in HepG2, 1321N1 and HEK 293 Cells In Response To Cadmium Induced-oxidative Stress

Cadmium (Cd) has been implicated in a number of pathological diseases and oxidative stress has been proposed as one of its mechanisms of toxicity. In this present study, the toxic effect of 5, 10 and 50 μM of cadmium as cadmium chloride was investigated in three human cell lines: human hepatocellular liver carcinoma cells (HepG2), human astrocytoma cells (1321N1) and human embryonic kidney cells (HEK 293). Antioxidant defence responses of these cells were determined in order to evaluate the extent of oxidative stress induced by this metal after 24hrs exposure. Results indicate that CdCl2 decreases the viability of all three cells in a dose-dependent manner in agreement with earlier reports of Fotakis and Timbrell (2006). However it is clear that HepG2 cells are more sensitive (EC50 = 13.96 μM) than 1321N1 (EC50 = 19.92 μM) and HEK293 (EC50 = 221.8 μM) cells. This may be related to increased uptake, as it has been observed that Cd preferentially accumulates in liver cells in vivo. Increase LDH leakage has earlier been reported to be associated with CdCl2 induced toxicity (Bradley et al., 1987). Table 1 shows a significant increase in LDH leakage in all the three cells at 50 μM. An increase in Reactive Oxygen Species (ROS) was also significant in HepG2 cells but was not significant in 1321N1 and HEK 293 cells .This implies that ROS production may not be involve in CdCl2 induced toxicity in 1321N1 and HEK 293 cells. The results also show that CdCl2 does not deplete GSH in HepG2 cells but does deplete GSH in 1321N1 and HEK 293 cells (Table 1). There was a significant increase in malondialdehyde MDA levels at 50 μM exposure in all the three cells. The results also show a significant increase in the activities of the antioxidant enzymes; GST, GPx, SOD and catalase in the three cell lines at 50 μM CdCl2 with the exception of glutathione reductase in HepG2 cells and catalase in 1321N1 cells. Overall this suggests an adaptive response by the three cells to the CdCl2 insult and this is investigated further by Western blot analysis.

Activation of Nrf2 in Defense against Cadmium-Induced Oxidative Stress

Exposure to cadmium (Cd) elicits a range of adverse responses including oxidative damage and cancer. The molecular targets of Cd remain largely unidentified. Here, we analyzed the function and signal transduction of transcription factor Nrf2 in protection against Cd-induced oxidative stress. Wild-type (Nrf2 (+/+)) mouse embryonic fibroblasts (MEF) produced reactive oxygen species (ROS) at a low level, whereas treatment with Cd significantly increased the ROS production. On the other hand, Nrf2 knockout (Nrf2 (-/-)) MEF cells exhibited an elevated level of ROS under a basal condition, and Cd dramatically increased the ROS production at concentrations as low as 2 microM, resulting in increased sensitivity to Cd-induced cell death. Cd induced the basal and inducible expression of cytoprotective enzymes NQO1 and HO1 in WT MEF cells, but induction was lost in Nrf2 (-/-) MEF cells. Induction of the genes required antioxidant response elements (ARE) as Cd drove ARE-dependent reporter expression and Cd-activated Nrf2 bound to endogenous AREs in mouse hepa1c1c7 cells. Activation of Nrf2 by Cd involved stabilization of the Nrf2 protein, increased formation of Nrf2/Keap1 complex in the cytoplasm, translocation of the complex into the nucleus, and subsequently disruption of the complex. Lastly, Nrf2 was found ubiquitinated in the cytoplasm but deubiquitinated in the nucleus. The study provided a mechanistic transcriptional model in which Cd activates Nrf2 through a metal-activated signaling pathway involving a dynamic interplay between ubiquitination/deubiquitination and complex formation/dissociation of Nrf2 and Keap1.

Cadmium-induced oxidative stress and DNA damage in kidney of pregnant female rats

In the present study, we have investigated the influence of sub-acute treatment with cadmium (Cd) on some parameters indicative of oxidative stress and DNA damage in tissues of pregnant female rats. Pregnant female rats ( n = 6 ) were injected subcutaneously, daily with a dose of cadmium chloride of 3 mg/kg body weight (b.w.) from day 6 to day 19 of pregnancy, and they were allowed to deliver normally. MDA level and GPx, CAT and SOD activities were used as markers of oxidative stress in liver and kidney. The 8-oxo-dG level was measured by the HPLC-EC system. Cd treatment increased MDA (+116%, p < 0.01 ) in kidney. Moreover, Cd treatment also decreased CuZn-SOD (−11%, p < 0.05 ) and GSH level (−52%, p < 0.05 ) in kidney. Treated rats displayed an increase of the liver metallothionein (MT) level. Induction of MT in liver was probably implicated in the detoxification of Cd. The high level of Cd (3 mg/kg) used in the present study is partially neutralized by MT in liver, whereas the free fraction could be implicated in the oxidative stress and DNA oxidation observed in kidney. Cd treatment failed to alter 8-oxodGuo, indicating the absence of DNA oxidation in liver; by contrast, the same treatment increased the 8-oxodGuo level (+51%, p < 0.05 ) in the kidney of pregnant female rats, indicating an oxidative stress associated with DNA damage only in kidney. To cite this article: S. Chater et al., C. R. Biologies 331 (2008).

The effects of Panax ginseng and Spirulina platensis on hepatotoxicity induced by cadmium in rats

Cadmium is an environmental and industrial cumulative pollutant that affects many organs, specially the liver. The protective effect of Spirulina platensis and Panax ginseng on cadmium-induced oxidative stress and hepatotoxicity was evaluated in adult female Wistar albino rats. At the end of the 1-month experimental period, all animals were fasted for 12h and liver samples were taken for the determination of malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD) and nitric oxide (NO) levels. S. platensis and P. ginseng treatments showed marked decrease lipid peroxidation and increase of the endogenous antioxidants levels. The cadmium-induced histopathological changes were also minimized with the tested extracts. These results suggest that S. platensis and P. ginseng might play a role in reducing the toxic effect of cadmium and its antioxidant properties seem to mediate such a protective effect.

Preventive Effect of Zinc Against Cadmium-induced Oxidative Stress in the Rat Testis

The aim of this study was to investigate the antioxidant role of zinc (Zn) in the Cd-exposed testes of Wistar rats. Subchronic exposure to Cd (CdCl(2), 40 mg/l, per os) for 30 days resulted in a significant reduction in growth rate (-11%) and relative weights of testes (-36%) and seminal vesicles (-80%). Treated rats displayed a decrease in testicular and plasma testosterone levels, respectively (-70%, P<0.05; -48%, P<0.05), epididymal sperm count (-22%, P<0.05), and spermatozoa motility (-35%, P<0.05). In contrast, Cd increased the malondialdehyde (+46%, P<0.05), metallothionein (+200%, P<0.05), and 8-oxodGuo concentrations (+71%, P<0.05) in the testis. In the gonad, Cd decreased the GPx (-30%, P<0.05), CAT (-32%, P<0.05), mitochondrial Mn-SOD (-34%, P<0.05), and cytosolic CuZn-SOD (-32%, P<0.05) activities. Zinc supplementation (ZnCl(2), 40 mg/l, per os) in the Cd-exposed rats restored the activities of GPx, CuZn-SOD, and Mn-SOD in the testes to the levels of the control group. Moreover, zinc administration was capable of reducing the elevated levels of malondialdehyde in the testis. Interestingly, zinc supplementation attenuated DNA oxidation induced by Cd in the gonad and restored the testosterone level and sperm count to the levels of the control group. Zinc administration minimized oxidative damage and reversed the impairment of spermatogenesis and testosterone production induced by Cd in the rat testis.

The Protective Effects of Ethanolic Extract of Garlic and Ascorbic Acid on Cadmium-Induced Oxidative Stress

The Protective Effects of Ethanolic Extract of Garlic and Ascorbic Acid on Cadmium-Induced Oxidative Stress

Role of respiration and glutathione in cadmium-induced oxidative stress in Escherichia coli K-12

Cadmium is a widespread pollutant that has been associated with oxidative stress, but the mechanism behind this effect in prokaryotes is still unclear. In this work, we exposed two glutathione deficient mutants (DeltagshA and DeltagshB) and one respiration deficient mutant (DeltaubiE) to a sublethal concentration of cadmium. The glutathione mutants show a similar increase in reactive oxygen species as the wild type. Experiments performed using the DeltaubiE strain showed that this mutant is more resistant to cadmium ions and that Cd-induced reactive oxygen species levels were not altered. In the light of these facts, we conclude that the interference of cadmium with the respiratory chain is the cause of the oxidative stress induced by this metal and that, contrary to previously proposed models, the reactive oxygen species increase is not due to glutathione depletion, although this peptide is crucial for cadmium detoxification.

The hepatoprotective effects of selenium against cadmium toxicity in rats

Exposure to cadmium and other pollutants is a major environmental problem. Cadmium is causing acute liver injury but the mechanism of hepatotoxicity is poorly understood. The present study aimed to assess the possible reasons by which cadmium causes liver toxicity. Furthermore, the protective role of selenium against this toxicity was investigated. The hepatic level of lipid peroxidation (malondialdehyde, MDA), the antioxidant system (reduced glutathione, glutathione peroxidase, and thioredoxin reductase), as well as the levels of different lipid classes and the fatty acids pattern were determined in three groups of rats of 15 each. The first group (control group) received saline solution intraperitoneal (i.p.) daily for 10 days. The second group (cadmium chloride-treated group) received 2 mg/kg body weight cadmium chloride solution i.p. for a period of 10 days. The third group (cadmium chloride/sodium selenite-treated group) received cadmium chloride as in the second group and received i.p. sodium selenite (1 mg/kg body weight) at the first and sixth day of treatment (two separate injections within 10 days). The results showed that cadmium treatment increased the hepatic level of malondialdehyde (MDA) and the mean percent of total saturated fatty acid in all lipid classes, whereas the levels of antioxidant system, the levels of hepatic cholesterol esters, triglycerides, total phospholipids, mono- and polyunsaturated fatty acids in all lipid classes were decreased compared to control rats. These changes resulting from Cd-treatment were prevented due to treatment of rats with selenium since the levels of reduced glutathione, glutathione peroxidase, and thioredoxin reductase were induced in Se/Cd-treated group compared with either Cd-treated or control group. In addition, selenium maintained the low levels of cholesterol esters, triglycerides, total phospholipids, mono- and polyunsaturated fatty acids in all lipid classes caused by cadmium to their normal levels. It is concluded that cadmium-induced oxidative stress by increasing the levels of free radicals and by decreasing antioxidants level. This oxidative stress could be the primary cause of Cd-induced hepatotoxicity. Also, selenium can be used as a protective agent against Cd-toxicity. This study could provide a possible explanation to hepatotoxicity resulting from exposure to cadmium in the environment. In addition, selenium could ameliorate cadmium-induced hepatotoxicity since it reduced MDA levels and increased the activities of antioxidant enzymes in this tissue.

Glutathione synthesis inhibitor increases cadmium-induced oxidative stress and cytotoxicity in glomerular kidney cells

Glutathione synthesis inhibitor increases cadmium-induced oxidative stress and cytotoxicity in glomerular kidney cells

Role of α-tocopherol in cadmium-induced oxidative stress in Wistar rat's blood, liver and brain

Cadmium (Cd) a highly toxic metal is considered to be a multitarget toxicant, and it accumulates principally in the liver and kidney after absorption. In vivo studies of mouse and rat liver have shown that apoptosis plays a primary role in Cd-induced hepatotoxicity. However, the detailed mechanisms by which toxic metals such as Cd produce their effects are still largely unknown. The present study aimed at investigating the consequences of exposure to Cd, α-tocopherol and their combination on stress biochemical parameters (lipoperoxidation and protein carbonyls levels). Male albino Wistar rats (1 month old) were treated intravenously with cadmium (2 mg CdCl 2/kg body weight/day), and α-tocopherol (100 mg/kg body weight/day), or with α-tocopherol + Cd (100 mg Vit E/kg body weight, 2 mg CdCl 2/kg). The lipoperoxidation was measured by the thiobarbituric acid reactive substances (TBARS) method and oxidatively generated damage to proteins by determining carbonyl (DNPH) levels. Among the hematological parameters measured the haematocrit value and haemoglobin concentration were significantly decreased in the blood of Cd-treated rats. A significant increase was observed in the level of malondialdehyde (MDA) and protein carbonyls in the cadmium exposed group compared to control group ( p < 0.001), and these values were decreased after administration of α-tocopherol (group 4). The activity of lactate dehydrogenase in rat liver and brain showed a significant increase as compared to that found in the control group and significant decrease of catalase and superoxide dismutase activities. In the liver of the Cd-treated group the contents of reduced glutathione were decreased. Our results suggest that cadmium induces an oxidation of cellular lipids and proteins and that administration of α-tocopherol can reduce Cd-induced oxidative stress and improve the glutathione level together with other biochemical parameters.

Effects of Selenium and Vitamin E, in Addıtıon to Melatonin, Against Oxidative Stress Caused by Cadmium in Rats

The present study was carried to evaluate the protective effects of melatonin alone and vitamin E with selenium combination against high dose cadmium-induced oxidative stress in rats. The control group received subcutaneous physiological saline. The first study group administered cadmium chloride (CdCl2) by subcutaneous injection of dose of 1 mg/kg. The second study group administered cadmium plus vitamin E with selenium (1 mg/kg sodium selenite with 60 mg/kg vitamin E); the third study group administered cadmium plus 10 mg/kg melatonin (MLT); the fourth study group administered CdCl2 plus a combination of melatonin in addition to vitamin E and selenium for a month. Determination levels of plasma malondialdehyde (MDA), glutathione peroxidase (GSH-Px), blood superoxide dismutase (SOD), creatinine alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), blood urea nitrogen (BUN), and urea were measured in serum. In only CdCl2 administered group, the MDA, creatinine, ALT, AST, ALP, and urea levels in the serum were significantly higher than the control group (p < 0.05). Whereas in all other groups, this values were significantly lower than the only CdCl2 administered group (p < 0.05). Erythrocytes GSH-Px, serum SOD activities of only CdCl2 received group were significantly lower than the control group (p < 0.05). In conclusion, vitamin E + Se, melatonin and vitamin E, and Se, in addition to MLT combinations, had protective effects against high dose cadmium-induced oxidative damage.

Cadmium-induced oxidative stress and response of the ascorbate–glutathione cycle in Bechmeria nivea (L.) Gaud

Bechmeria nivea (L.) Gaud. (ramie) seedlings subjected to a series of cadmium (Cd) concentrations (0, 1, 3 and 7 mg l −1) over a 10 d period were investigated with regard to the uptake and distribution of Cd, its effect on membrane lipid and chlorophyll synthesis, and response of the ascorbate–glutathione cycle in both leaves and roots. Increased Cd level in the medium resulted in a significant enhancement of Cd concentration in tested plants, with most accumulation in roots. Ramie under Cd stress exhibited increased level of lipid peroxidation, as was evidenced by the increased malondialdehyde content (MDA, an index of lipid peroxidation) in leaves and roots. Shorter exposure to lower Cd concentrations (1 and 3 mg l −1) led to a stimulation of chlorophyll synthesis, while longer exposure and higher Cd concentration (7 mg l −1) led to a remarkable breakdown of chlorophyll, suggesting that Cd caused oxidative stress in ramie. The antioxidant system as represented by the ascorbate–glutathione pathway was clearly activated following Cd exposure. An overall increase in the metabolite levels and major constituting enzyme activities (ascorbate peroxidase APX and glutathione reductase GR) was observed in ramie treated with 1 and 3 mg l −1 Cd throughout the entire experimental period, while prolongation of exposure to 7 mg l −1 Cd resulted in decrease of GR activity and GSH pool in roots which may limit the operation of the whole cycle. Results suggest that Cd-induced oxidative damage in ramie is closely associated with the efficiency of its intrinsic antioxidant mechanisms and the accelerated operation of ascorbate–glutathione cycle provides ramie with enhanced Cd-stress tolerance.

Endogenous salicylic acid potentiates cadmium-induced oxidative stress in Arabidopsis thaliana

To better understand the role of endogenous salicylic acid (SA) in plants exposed to abiotic stresses known to generate oxidative damage, the response to cadmium treatment of a wild Arabidopsis thaliana ecotype and a SA-deficient transgenic line was investigated. After 5 days of Cd treatment, chlorophyll content was significantly reduced and TBARS significantly increased in wild type seedlings but not in the SA-deficient line. Leaves of wild type plants exposed to the metal showed accumulation of H 2O 2 and increased oxidized glutathione content, resulting in decreased GSH/GSSG ratios. After Cd treatment, transgenic plants displayed a significantly decreased SOD activity (about 50% of control) which may have contributed to prevent H 2O 2 increase. The activity of several H 2O 2-detoxyfing enzymes diminished in wild type seedlings exposed to the metal (27–35% decrease). In SA-deficient plants ascorbate peroxidase and glutathione peroxidase activities slightly decreased, but guaiacol peroxidase and catalase activities significantly increased. CAT1 isoform was found to be particularly abundant in wild type Arabidopsis plants exposed to Cd, but scarcely expressed and almost unaffected by the metal addition in the transgenic line. Even when protective effects of SA have been extensively reported for several plant species, our results suggest that endogenous SA may function in A. thaliana as a signaling molecule necessary to generate, to sustain or to amplify Cd-induced oxidative stress.