In vitro effect of AlCl3 on human erythrocytes: Changes in membrane morphology and functionality

Aluminum belongs to a group of potential toxic elements capable of penetrating the human body. In this paper, the effect of aluminum concentrations on red blood cell membranes using different fluorescent probes able to localize in various parts of the phospholipid bilayer (TMA-DPH, laurdan and pyrene) were studied. Our results confirm that human erythrocytes exposed to aluminum undergo physico-chemical modifications at the membrane level. A decrease in fluorescence anisotropy of TMA-DPH and in the polarity of the lipid bilayer with a concomitant shift toward a gel phase was observed, and the pyrene excimerization coefficient (k_ex) increased.Furthermore, the presence of aluminum induced lipid peroxidation and reduced the activity of erythrocyte antioxidant enzymes (SOD, CAT and GSHPx). Al-induced morphological changes on the erythrocyte membrane surface were monitored using atomic force microscopy. These results provide further information on the target of action of different aluminum amounts.     

Hydrogen sulfide alleviates aluminum toxicity in barley seedlings

Aims

Aluminum (Al) toxicity is one of the major factors that limit plant growth. Low concentration of hydrogen sulfide (H₂S) has been proven to function in physiological responses to various stresses. The objective of this study is to investigate the possible role of H₂S in Al toxicity in barley (Hordeum vulgare L) seedlings.

Methods

Barley seedlings pre-treated with sodium hydrosulfide (NaHS), a H₂S donor, and subsequently exposed to Al treatment were studied for their effects on root elongation, Al accumulation in seedlings, Al-induced citrate secretion and oxidative stress, and plasma membrane (PM) H⁺-ATPase expression.

Results

Our results showed that H₂S had significant rescue effects on Al-induced inhibition of root elongation which was correlated well with the decrease of Al accumulation in seedlings. Meanwhile, Al-induced citrate secretion was also significantly enhanced by NaHS pretreatment. Al-induced oxidative stress as indicated by lipid peroxidation and reactive oxygen species burst was alleviated by H₂S through the activation of the antioxidant system. Moreover, Al-induced reduction in PM H⁺-ATPase expression was reversed by exogenous NaHS.

Conclusions

Altogether, our results suggest H₂S plays an ameliorative role in protecting plants against Al toxicity by inducing the activities of antioxidant enzymes, increasing citrate secretion and citrate transporter gene expression, and enhancing the expression of PM H⁺-ATPase.     

Differential responses of oat genotypes: oxidative stress provoked by aluminum

The phytotoxic effects of aluminum and the mechanisms of genetically-based Al tolerance have been widely investigated, as reported in many papers and reviews. However, investigations on many Al-sensitive and Al-resistant species demonstrate that Al phytotoxicity and Al-resistance mechanisms are extremely complex phenomena. The objective of the present study was to analyze the effects of aluminum on the activity of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), and ascorbate peroxidase (APX). Also was evaluated the lipid peroxidation, H₂O₂ content, levels of ascorbic acid (ASA), non-protein thiols (NPSH) and Al content in three genotypes of oat, Avena sativa L. (UFRGS 930598, UFRGS 17, and UFRGS 280). The genotypes were grown in different concentrations of Al ranging from 90 to 555???M for 5?days. The antioxidant system was unable to overcome toxicity resulting in negative effects such as lipid peroxidation and H₂O₂ content in UFRGS 930598. The results showed that UFRGS 930598 was the most sensitive genotype. UFRGS 17 and UFRGS 280 were more resistant to Al toxicity. These results suggest that UFRGS 17 has mechanisms of external detoxification and UFRGS 280 has mechanisms of internal detoxification. The different behavior of enzymatic and non-enzymatic antioxidants of the genotypes showed that aluminum resistance in UFGRS 17 and UFRGS 280 may be related to oxidative stress.     

扑草净对远志幼苗根系活力及氧化胁迫的影响

以远志(Polygala tenuifolia Willd.)为材料,应用组织化学和生物化学的方法研究不同浓度扑草净(0—400 mg/L)对远志幼苗生长、根系活力、膜脂过氧化、活性氧含量及抗氧化酶活性等的影响。10 mg/L扑草净对远志幼苗根系活力、细胞膜完整性及活性氧的积累几乎无显著影响,而25—400 mg/L扑草净处理则显著增加活性氧的积累,明显抑制根系活力且破坏细胞膜完整性;上述结果进一步被膜脂过氧化、质膜完整性、活性氧产生(O.2-和H2O2)的非损伤组织化学染色所证明。远志幼苗可通过多种抗氧化酶(SOD、POD、CAT、APX等)和非酶抗氧化剂(如脯氨酸)的相互协调作用,清除低浓度扑草净胁迫诱发产生的活性氧,减轻对细胞的伤害。研究结果表明,发芽期是远志对扑草净处理的敏感时期,较为安全的扑草净临界浓度为10 mg/L;25mg/L扑草净处理即引起远志幼苗氧化胁迫和膜脂过氧化,使细胞膜的完整性受到破坏,根系活力下降,抑制了远志幼苗的生长发育。该研究为远志抗除草剂胁迫机制及其栽培过程中除草剂的安全合理使用提供理论依据。     

Distribution and habitat segregation on different spatial scales among diploid, tetraploid and hexaploid cytotypes of Senecio carniolicus (Asteraceae) in the Eastern Alps

MethodsTo evaluate the role of Si in K deficiency-induced inhibition of growth of soybean (Glycine max) seedlings, the effects of K deficiency on shoot and root growth, hydrogen peroxide accumulation, K contents, lipid peroxidation and activities of antioxidant enzymes in the absence and presence of 2 mm sodium silicate (Na₂SiO₃) were investigated.ConclusionsApplication of Si to soybean seedlings grown in K-deficient medium markedly enhanced K use efficiency. Therefore, Si not only increases tolerance to nutrient toxicity, but also ameliorates symptoms associated with deficiency in essential nutrients in plants.     

Effects of exogenous nitric oxide on cadmium toxicity, element contents and antioxidative system in perennial ryegrass

The effects of sodium nitroprusside (SNP, a donor of NO) on cadmium (Cd) toxicity in ryegrass seedlings (Lolium perenne L.) were studied by investigating the symptoms, plant growth, chlorophyll content, lipid peroxidation, H⁺-ATPase enzyme and antioxidative enzymes. Addition of 100???M CdCl₂ caused serious chlorosis and inhibited the growth of ryegrass seedlings, and dramatically increased accumulation of Cd in both shoots and roots, furthermore, the absorption of macro and micronutrients were inhibited. Addition of 50, 100, 200???M SNP significantly decreased the transport of Cd from roots to shoots, alleviated the inhibition of K, Ca, Mg and Fe, Cu, Zn absorption induced by Cd, reduced the toxicity symptoms and promoted the plant growth. The accumulation of reactive oxygen species (ROS) significantly increased in ryegrass seedlings exposed to Cd, and resulted in the lipid peroxidation, which was indicated by accumulated concentration of thiobarbituric acid-reactive substances. Addition of 50, 100, 200???M SNP significantly decreased the level of ROS and lipid peroxidation. Activities of antioxidant enzymes also showed the same changes. Addition of 50, 100, 200???M SNP increased activities of superoxide dismutase, peroxidase, catalase and ascorbate peroxidase in ryegrass seedlings exposed to Cd. Addition of 100???M SNP had the most significant alleviating effect against Cd toxicity while the addition of 400???M SNP had no significant effect with Cd treatment.     

Effects of Oxidative Stress Caused by Hyperoxia and Diquat. A Study in Isolated Hepatocytes

The effects of oxidative stress caused by hyperoxia or administration of the redox active compound diquat were studied in isolated hepatocytes, and the relative contribution of lipid peroxidation, glutathione (GSH) depletion, and NADPH oxidation to the cytotoxicity of active oxygen species was investigated.

The redox cycling of diquat occurred primarily in the microsomal fraction since diquat was found not ' to penetrate into the mitochondria. Depletion of intracellular GSH by pretreatment of the animals with diethyl maleate promoted lipid peroxidation and sensitized the cells to oxidative stress. Diquat toxicity was also greatly enhanced when glutathione reductase was inhibited by pretreatment of the cells with 1,3-bis(2-chloroethyI)-1-nitrosourea. Despite extensive lipid peroxidation, loss of cell viability was not observed, with either hyperoxia or diquat, until the GSH level had fallen below ≈ 6 nmol/10⁶ cells.

The iron chelator desferrioxamine provided complete protection against both diquat-induced lipid peroxidation and loss of cell viability. In contrast, the antioxidant a-tocopherol inhibited lipid peroxidation but provided only partial protection from toxicity. The hydroxy! radical scavenger α-keto-γ-methiol butyric acid, finally, also provided partial protection against diquat toxicity but had no effect on lipid peroxidation.

The results indicate that there is a critical GSH level above which cell death due to oxidative stress is not observed. As long as the glutathione peroxidase – glutathione reductase system is unaffected, even relatively low amounts of GSH can protect the cells by supporting glutathione peroxidase-mediated metabolism of H₂O₂ and lipid hydroperoxides.     

Mitigation of Acute Aluminum Toxicity by Sodium Selenite and N-Acetylcysteine in Adult Male Rats

The objective of this study is to investigate the toxic effects of aluminum and the potential alleviation of selenite and N-acetylcysteine (NAC) on this toxicity. Acute aluminum toxicity was induced by intraperitoneal (i.p.) injection of AlCl₃ (30 mg Al³⁺/kg) for four consecutive days. Al³⁺ damaged the synthetic capability and regeneration power of liver cells and induced inflammation. It also damaged the kidney and disturbed the lipid profile enhancing the total cholesterol level and LDL-cholesterol level increasing the risks of atherosclerosis. Al³⁺ reduced the cellular antioxidant milieu typified by the decrease in reduced glutathione, vitamin E, and four antioxidant enzymes and induced lipid peroxidation (LPO). Selenite at 1 mg Se/kg and NAC at 150 mg/kg injected either simultaneously with or after Al³⁺ mitigated most of these damaging effects probably by the virtue of scavenging the free radicals, binding aluminum and stimulating its excretion and reducing its bioavailability, bolstering the endogenous antioxidant defense systems, stabilizing the cell membrane, and preventing LPO. The beneficial effects of selenite and NAC against aluminum toxicity were also confirmed by the light and electron histopathology study. There were no significant differences between the two regimens used (protection and therapeutic) in the current study probably due to the short time of exposure, and the abrogation of Al³⁺ toxicity offered by selenite was better than that provided by NAC on the histopathology level.     

Prooxidant action of aluminum Ion – Stimulation of iron-mediated lipid peroxidation by aluminum

Prooxidant nature of aluminum ion was analyzed in relation to iron coordination. Aluminum ion effectively enhanced the formation of thiobarbituric acid-reactive substances as a marker of lipid peroxidation of microsomes from rat liver under the acidic conditions, and this metal further attenuated the antioxidant action of flavonoids such as quercetin and baicalein under neutral conditions. Autooxidation of ferrous ion was markedly inhibited by aluminum ion. Aluminum can act as a prooxidant by stabilizing reduced iron the initiating species for lipid peroxidation, and by inhibiting the antioxidant action of flavonoid.     

Endophytic Chaetomium globosum enhances maize seedling copper stress tolerance

This study aims at characterisation of the impact of Chaetomium globosum on copper stress resistance of maize seedlings. Higher levels of copper treatment decreased maize dry weight and induced a marked increase in osmotic solutes, antioxidant enzyme activity and the level of lipid peroxidation. On the other hand, addition of the endophytic C. globosum alleviated the toxic effect of copper on maize growth. The combination of copper sulphate and Chaetomium increased seedling dry weight, osmotic solute content and antioxidant enzyme activity compared to copper sulphate alone, while lipid peroxidation levels were also decreased. The fungal scavenger system might be important for supporting the ability of maize seedlings to resist copper toxicity.     

Oxidation of low-density lipoproteins: effect of antioxidant content,fatty acid composition and intrinsic phospholipase activity on susceptibility to metal ion-induced oxidation

The oxidative modification of low-density lipoprotein (LDL) may play an important role in atherogenesis. Our understanding of the mechanism of LDL oxidation and the factors that determine its susceptibility to oxidation is still incomplete. We have isolated LDL from 45 healthy individuals and studied the relationship between LDL fatty acid, vitamin E and β-carotene composition, intrinsic phospholipase A₂-like activity and parameters of LDL oxidation. LDL was exposed to a copper ion-dependent oxidising system and the kinetics of oxidation studied by monitoring formation of fatty acid conjugated dienes. The length of the lag phase of inhibited lipid peroxidation was measured as well as the rate of lipid peroxidation during the propagation phase. There was no significant correlation between LDL antioxidant vitamin or fatty acid composition and lag time to LDL oxidation. Oleic acid was negatively correlated with the rate of LDL oxidation (r = −0.41, P < 0.01) whilst linoleic acid was significantly correlated with the extent of LDL oxidation measured by the production of total dienes (r = 0.34, P < 0.05). Interestingly, LDL vitamin E content was positively correlated with both the rate (r = 0.28, P < 0.05) and extent of LDL oxidation (r = 0.43, P < 0.01). LDL isolated from this group of subjects showed significant intrinsic phospholipase-like activity. The phospholipase activity, whilst not correlated with lag time, was significantly correlated with both rate (r = 0.43, P < 0.01) and total diene production (r = 0.44, P < 0.01) of LDL oxidation. We conclude that antioxidant content, fatty acid composition and intrinsic phospholipase activity have little influence on the lag time of Cu-induced LDL oxidation. These components do however, significantly influence both the rate and extent of LDL oxidation, with increased vitamin E, linoleic acid content and phospholipase activity associated with faster and more extensive oxidation. The possible pro-oxidant effect of vitamin E has interesting implications for the postulated ‘protective’ effects of vitamin E on atherogenesis.     

Increased oxidative stress and cytotoxicity by hydrogen sulfide in HepG2 cells overexpressing cytochrome P450 2E1

The main objectives of this work were to evaluate the effects of hydrogen sulfide on oxidative stress and cytotoxicity parameters in HepG2 cells and to assess the extent to which cytochrome P450 2E1 (CYP2E1) activity modulates the effects of hydrogen sulfide on oxidative stress and cytotoxicity. Sodium hydrosulfide (NaHS) caused time- and concentration-dependent cytotoxicity in both non-P450-expressing HepG2 cells (C34 cells) and CYP2E1-overexpressing HepG2 cells (E47 cells); however, NaHS-dependent cytotoxicity was higher in E47 than C34 cells. Cytotoxicity by NaHS in C34 and E47 cells was mainly necrotic in nature and associated with an early decrease in mitochondrial membrane potential. NaHS caused increased oxidation of lipophilic (C11-BODIPY^581/591) and hydrophilic (DCFH-DA) probes only in E47 cells, at a time point prior to overt cytotoxicity. Trolox, an amphipathic antioxidant, partially inhibited both the cytotoxicity and the increased oxidative stress detected in E47 cells exposed to NaHS. Cell-permeable iron chelators and CYP2E1 inhibitors significantly inhibited the oxidation of C11-BODIPY^581/591 in E47 cells in the presence of NaHS. NaHS produced lipid peroxidation and cytotoxicity in E47 cells supplemented with a representative polyunsaturated fatty acid (docosahexaenoic acid) but not in C34 cells; these effects were inhibited by α-tocopherol, a lipophilic antioxidant. These data suggest that CYP2E1 enhances H₂S-dependent cytotoxicity in HepG2 cells through the generation of iron-dependent oxidative stress and lipid peroxidation.     

<Emphasis Type="Italic">Terminalia arjuna</Emphasis> bark extract alleviates nickel toxicity by suppressing its uptake and modulating antioxidative defence in rice seedlings

Terminalia arjuna (Ta) bark contains various natural antioxidants and has been used to protect animal cells against oxidative stress. In the present study, we have examined alleviating effects of Ta bark aqueous extract against Ni toxicity in rice (Oryza sativa L.). When rice seedlings were raised for 8 days in hydroponics in Yoshida nutrient medium containing 200 μM NiSO₄, a decline in height, reduced biomass, increased Ni uptake, loss of root plasma membrane integrity, increase in the level of O₂˙^?, H₂O₂ and ˙OH, increased lipid peroxidation, decline in photosynthetic pigments, increase in the level of antioxidative enzymes superoxide dismutase, catalase and glutathione peroxidase and alterations in their isoenzyme profile patterns were observed. Transmission electron microscopy (TEM) showed damage to chloroplasts marked by disorganised enlarged starch granules and disrupted thylakoids under Ni toxicity. Exogenously adding Ta bark extract (3.2 mg ml^?1) to the growth medium considerably alleviated Ni toxicity in the seedlings by reducing Ni uptake, suppressing generation of reactive oxygen species, reducing lipid peroxidation, restoring level of photosynthesis pigments and ultrastructure of chloroplasts, and restoring levels of antioxidative enzymes. Results suggest that Ta bark extract considerably alleviates Ni toxicity in rice seedlings by preventing Ni uptake and reducing oxidative stress in the seedlings.     

Arsenic-induced oxidative stress in the common bean legume,Phaseolus vulgaris L. seedlings and its amelioration by exogenous nitric oxide

The adverse effects of arsenic (As) toxicity on seedling growth, root and shoot anatomy, chlorophyll and carotenoid contents, root oxidizability (RO), antioxidant enzyme activities, H₂O₂ content, lipid peroxidation and electrolyte leakage (EL%) in common bean (Phaseolus vulgaris L.) were investigated. The role of exogenous nitric oxide (NO) in amelioration of As-induced inhibitory effect was also evaluated using sodium nitroprusside (100 μM SNP) as NO donor and 2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (200 μM PTIO) as NO scavenger in different combinations with 50 μM As. As-induced growth inhibition was associated with marked anomalies in anatomical features, reduction in pigment composition, increased RO and severe perturbations in antioxidant enzyme activities. While activity of superoxide dismutase and catalase increased, levels of ascorbate peroxidase, dehydroascorbate reductase and glutathione reductase decreased significantly and guaiacol peroxidase remained normal. The over-accumulation of H₂O₂ content along with high level of lipid peroxidation and electrolyte leakage indicates As-induced oxidative damage in P. vulgaris seedlings with more pronounced effect on the roots than the shoots. Exogenous addition of NO significantly reversed the As-induced oxidative stress, maintaining H₂O₂ in a certain level through balanced alterations of antioxidant enzyme activities. The role of NO in the process of amelioration has ultimately been manifested by significant reduction of membrane damage and improvement of growth performance in plants grown on As + SNP media. Onset of oxidative stress was more severe after addition of PTIO, which confirms the protective role of NO against As-induced oxidative damage in P. vulgaris seedlings.     

Oxidative stress from environmental pollutants

Recently progress has been made on O₂ toxicity and pathology related to numerous environmental contaminants in insects. The pro-oxidants studied included: dioxin, paraquat, and an assorted array of quinones, 8-methoxypsorlen, arsenic, and mercury. The responses to these oxidants are diverse, but they arise from the reactive oxygen species. These pro-oxidants in insects cause lipid peroxidation, protein and enzyme oxidation, and GSH depletion. Potentially, they may also cause DNA oxidation, and form DNA adducts. Oxidative challenge is alleviated by antioxidant compounds, but more importantly by the induction of antioxidant enzymes, which are crucial for the termination of O₂ radical cascade and lipid peroxidation chain reaction. Insects exhibit a wasting syndrome under sub-acute stress. In acute toxicity vital physiological processes impaired are hemolymph melanization and diuresis. Thus, insects resemble vertebrates in both the response to oxidative stress and its pathological consequences. These results raise the prospect that insects may serve as non-mammalian model species for monitoring the oxidative-stress component of environmental toxicity. © 1995 Wiley-Liss, Inc.     

Investigation of synergistic action between coronatine and nitric oxide in alleviating arsenic-induced toxicity in sweet basil seedlings

The phytotoxin coronatine (COR) is a jasmonic acid mimic produced by several pathovars of plant pathogen. In this study, we evaluated the protective effect of COR and nitric oxide (NO) against the toxicity of sodium arsenate in sweet basil (Ocimum basilicum L.). According to the statistical analysis, arsenic had a significant adverse effect on length and biomass of plants. Seedlings that pretreated with COR and sodium nitroprusside (SNP), significantly reversed fresh and dry lose and relative water content decay induced by the metalloid. The protective effects of COR and SNP were indicated by extent of lipid peroxidation, increase glutathione (GSH), ascorbate and thiol (–SH) content, promote antioxidant enzymes and reduce H₂O₂ content in basil seedlings. The present observation suggested that reduction of excess arsenic As-induced toxicity in O. basilicum by COR and NO is through the activation of enzymes involved in ROS detoxification (CAT, SOD, POD, APX, GR) and maintenance contents of molecular antioxidant (GSH, ascorbate, non-protein thiol and protein-thiol). Moreover, the results revealed a mutually amplifying reaction between COR and NO in reducing As-induced damages.     

Antioxidant response of wheat roots to drought acclimation

Wheat (Triticum aestivum L.) seedlings of a drought-resistant cv. C306 were subjected to severe water deficit directly or through stress cycles of increasing intensity with intermittent recovery periods. The antioxidant defense in terms of redox metabolites and enzymes in root cells and mitochondria was examined in relation to membrane damage. Acclimated seedlings exhibited higher relative water content and were able to limit the accumulation of H₂O₂ and membrane damage during subsequent severe water stress conditions. This was due to systematic up-regulation of superoxide dismutase, ascorbate peroxidase (APX), catalase, peroxidases, and ascorbate–glutathione cycle components at both the whole cell level as well as in mitochondria. In contrast, direct exposure of severe water stress to non-acclimated seedlings caused greater water loss, excessive accumulation of H₂O₂ followed by elevated lipid peroxidation due to the poor antioxidant enzyme response particularly of APX, monodehydroascorbate reductase, dehydroascorbate reductase, glutathione reductase, and ascorbate–glutathione redox balance. Mitochondrial antioxidant defense was found to be better than the cellular defense in non-acclimated roots. Termination of stress followed by rewatering leads to a rapid enhancement in all the antioxidant defense components in non-acclimated roots, which suggested that the excess levels of H₂O₂ during severe water stress conditions might have inhibited or down-regulated the antioxidant enzymes. Hence, drought acclimation conferred enhanced tolerance toward oxidative stress in the root tissue of wheat seedlings due to both reactive oxygen species restriction and well-coordinated induction of antioxidant defense.     

Effect of dietary antioxidants and phenobarbital pretreatment on microsomal lipid peroxidation and activation by carbon tetrachloride.

The effect of the dietary antioxidants, vitamin E and selenium, and the effect of phenobarbital pretreatment on $\text{in}$$\text{vitro}$ NADPH-dependent microsomal lipid peroxidation and the activation of microsomal lipid peroxidation by CCl₄ were studied. The rate of microsomal lipid peroxidation decreased as a function of dietary anti-oxidant, while the degree of CCl₄ activation increased. Phenobarbital pretreatment diminished the antioxidant inhibition of microsomal lipid peroxidation found with microsomes from rats fed high levels of antioxidant. Phenobarbital pretreatment lowered the extent of lipid peroxidation as measured by malonaldehyde production but had little effect on the rate of lipid peroxidation as measured by oxygen uptake. The kinetics of lipid peroxidation and the stoichiometry of the reaction were assessed as a function of dietary antioxidant.The findings suggest that at low microsomal antioxidant concentrations, the lipid peroxidation reaction occurs at a maximal rate dependent upon some rate-limiting step, such as the reduction of Fe⁺³, which is unaffected by CCl₄ addition. Conversely, at high microsomal antioxidant concentrations, the antioxidant termination reactions appear to determine the overall reaction rate.     

Mitogenic and Mutagenic Effects of Ionized Air on <Emphasis Type="Italic">Allium fistulosum</Emphasis> L.

In the apical meristem of Allium fistulosum, the relationship between peroxide lipid oxidation, antioxidant activity, proliferative processes, the yield of chromosomal aberrations and duration the exposure to ionized air was studied. Under the influence of air oxygen ions, superoxide dismutase and catalase activities increased, proliferative processes were stimulated, and shifts occurred in the process of lipid peroxidation in cells of A. fistulosum. When these cells were treated with air oxygen for 40 min, hydrogen peroxide and iron sulfate (II) enhanced oxygen biostimulating effect via stimulation of antioxidant enzyme activity and inhibition of lipid peroxidation. Under these conditions, cell proliferation was intensified and the yield of chromosomal aberrations was reduced in A. fistulosum rootlets. When the time of seed treatment with ionized air was increased to 80 min, lipid peroxidation was activated, antioxidant enzyme activity was inhibited, and the yield of chromosomal aberration increased in seedlings. It was concluded that the biostimulating activity of ionized air was mediated by active oxygen species generated in the cell. The accumulation of TBA(thiobarbituric acid)-reactive products was shown to be related to a decrease in antioxidant enzyme activity and an increase in the yield of chromosomal aberrations. It is emphasized that the mutagenic effect of ionized air is associated with generating conditions that support Fenton reaction and OH-radical formation in the cell.     

Cadmium-Induced Hydrogen Accumulation Is Involved in Cadmium Tolerance in Brassica campestris by Reestablishment of Reduced Glutathione Homeostasis

Hydrogen gas (H₂) was recently proposed as a therapeutic antioxidant and signaling molecule in clinical trials. However, the underlying physiological roles of H₂ in plants remain unclear. In the present study, hydrogen-rich water (HRW) was used to characterize the physiological roles of H₂ in enhancing the tolerance of Brassica campestris against cadmium (Cd). The results showed that both 50 μM CdCl₂ and 50%-saturated HRW induced an increase of endogenous H₂ in Brassica campestris seedlings, and HRW alleviated Cd toxicity related to growth inhibition and oxidative damage. Seedlings supplied with HRW exhibited increased root length and reduced lipid peroxidation, similar to plants receiving GSH post-treatment. Additionally, seedlings post-treated with HRW accumulated higher levels of reduced glutathione (GSH) and ascorbic acid (AsA) and showed increased GST and GPX activities in roots. Molecular evidence illustrated that the expression of genes such as GS, GR1 and GR2, which were down-regulated following the addition of Cd, GSH or BSO, could be reversed to varying degrees by the addition of HRW. Based on these results, it could be proposed that H₂ might be an important regulator for enhancing the tolerance of Brassica campestris seedlings against Cd, mainly by governing reduced glutathione homeostasis.