Fructose induced deactivation of antioxidant enzymes: preventive effect of pyruvate

Glycation initiated changes in tissue proteins, which are triggered by the Schiff base formation between the sugar carbonyl and the protein -NH2, have been suggested to play an important role in the development of diabetes-related pathological changes such as the formation of cataracts. While the initial reaction takes place by the interaction of >C=O of the parent sugars with the -NH2 of proteins, reactive oxygen species (ROS) dependent generation of more reactive dicarbonyl derivatives from the oxidation of sugars also plays a significant role in these changes, altering the structural as well as functional properties of proteins. The purpose of this study was to examine whether the activities of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), catalase and superoxide dismutase (SOD) could be affected by the high levels of fructose prevalent in diabetic lenses. Incubation of the enzymes with this sugar led to a significant loss of their activities. GAPDH was inactivated within a day. This was followed by the inactivation of catalase (3-4 days) and SOD (6 days). The loss of the activities was prevented significantly by incorporation of pyruvate in the incubation mixture. The protective effect is ascribable to its ability to competitively inhibit glycation as well as to its ROS scavenging activity. Hence, it could play a significant role in the maintenance of lens physiology and cataract prevention.     

Reactive oxygen species and sugars may be the messengers in kinetin-induced death of field bean root cortex cells

Kinetin-induced programmed cell death of field bean (Vicia faba spp. minor) root cortex cells led to aerenchyma formation. The process was accompanied by appearance of a greater amount of reactive oxygen species (ROS), greater superoxide dismutase (SOD) and catalase (CAT) activities, as well as by thickening cell walls and changes in sugar amounts, particularly in cell wall-bound sugars. The obtained results justify the supposition that ROS scavengers together with an increased amount of sugars (soluble, storage, and cell wall-bound) and thick cell walls protected the cells against death. Thus, kinetin played a dual role because it induced programmed death of chosen cells and simultaneously stimulated protective mechanisms against death in other cells. These results confirm an earlier suggestion that cell death induced by kinetin is a specific process during which its progression is hallmarked by metabolic and morphological features.     

Manganese-excess induces oxidative stress,lowers the pool of antioxidants and elevates activities of key antioxidative enzymes in rice seedlings

Manganese (Mn) is an essential element for plant growth but in excess, specially in acidic soils, it can become phytotoxic. In order to investigate whether oxidative stress is associated with the expression of Mn toxicity during early seedling establishment of rice plants, we examined the changes in the level of reactive oxygen species (ROS), oxidative stress induced an alteration in the level of non-enzymic antioxidants and activities of antioxidative enzymes in rice seedlings grown in sand cultures containing 3 and 6 mM MnCl₂. Mn treatment inhibited growth of rice seedlings, the metal increasingly accumulated in roots and shoots and caused damage to membranes. Mn treated plants showed increased generation of superoxide anion (O₂ ^.−), elevated levels of H₂O₂ and thiobarbituric acid reactive substances (TBARS) and decline in protein thiol. The level of nonprotein thiol, however, increased due to Mn treatment. A decline in contents of reduced ascorbate (AsA) and glutathione (GSH) as well as decline in ratios of their reduced to oxidize forms was observed in Mn-treated seedlings. The activities of antioxidative enzymes superoxide dismutase (SOD) and its isoforms Mn SOD, Cu/Zn SOD, Fe SOD as well as guaiacol peroxidase (GPX) increased in the seedlings due to Mn treatment however, catalase (CAT) activity increased in 10 days old seedlings but it declined by 20 days under Mn treatment. The enzymes of Halliwell-Asada cycle, ascorbate peroxidase (APX) monodehydoascorbate reductase (MDHAR), dehyroascorbate reductase (DHAR) and glutathione reductase (GR) increased significantly in Mn treated seedlings over controls. Results suggest that in rice seedlings excess Mn induces oxidative stress, imbalances the levels of antioxidants and the antioxidative enzymes SOD, GPX, APX and GR appear to play an important role in scavenging ROS and withstanding oxidative stress induced by Mn.     

Plant responses to water stress: Role of reactive oxygen species

Terrestrial plants most often encounter drought stress because of erratic rainfall which has become compounded due to present climatic changes.Responses of plants to water stress may be assigned as either injurious change or tolerance index. One of the primary and cardinal changes in response to drought stress is the generation of reactive oxygen species (ROS), which is being considered as the cause of cellular damage. However, recently a signaling role of such ROS in triggering the ROS scavenging system that may confer protection or tolerance against stress is emerging. Such scavenging system consists of antioxidant enzymes like SOD, catalase and peroxidases, and antioxidant compounds like ascorbate, reduced glutathione; a balance between ROS generation and scavenging ultimately determines the oxidative load. As revealed in case of defence against pathogen, signaling via ROS is initiated by NADPH oxidase-catalyzed superoxide generation in the apoplastic space (cell wall) followed by conversion to hydrogen peroxide by the activity of cell wall-localized SOD. Wall peroxidase may also play role in ROS generation for signaling. Hydrogen peroxide may use Ca2+ and MAPK pathway as downstream signaling cascade. Plant hormones associated with stress responses like ABA and ethylene play their role possibly via a cross talk with ROS towards stress tolerance, thus projecting a dual role of ROS under drought stress.     

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.     

Changes in oxidative balance in rat pericytes exposed to diabetic conditions

Recent data indicate that the oxidative stress plays an important role in the pathogenesis of diabetes and its complications such as retinopathy, nephropathy and accelerated atherosclerosis. In diabetic retinopathy, it was demonstrated a selective loss of pericytes accompanied by capillary basement membrane thickening, increased permeability and neovascularization. This study was designed to investigate the role of diabetic conditions such as high glucose, AGE-Lysine, and angiotensin II in the modulation of antioxidant enzymes activities, glutathione level and reactive oxygen species (ROS) production in pericytes. The activity of antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and total glutathione (GSH) was measured spectrophotometrically. The production of ROS was detected by spectrofluorimetry and fluorescence microscopy after loading the cells with 2'-7' dichlorofluoresceine diacetate; as positive control H2O2 was used. Intracellular calcium was determined using Fura 2 AM assay. The results showed that the cells cultured in high glucose alone, do not exhibit major changes in the antioxidant enzyme activities. The presence of AGE-Lys or Ang II induced the increase of SOD activity. Their combination decreased significantly GPx activity and GSH level. A three times increase in ROS production and a significant impairment of intracellular calcium homeostasis was detected in cells cultured in the presence of the three pro-diabetic agents used. In conclusion, our data indicate that diabetic conditions induce in pericytes: (i) an increase of ROS and SOD activity, (ii) a decrease in GPx activity and GSH level, (iii) a major perturbation of the intracellular calcium homeostasis. The data may explain the structural and functional abnormalities of pericytes characteristic for diabetic retinopathy.     

Does a terminal drought tolerance QTL contribute to differences in ROS scavenging enzymes and photosynthetic pigments in pearl millet exposed to drought?

The control of reactive oxygen species (ROS) and the stability of photosynthetic pigments under stress conditions are hypothesized to contribute to drought tolerance. Here we studied how ascorbic peroxidase (APX), superoxide dismutase (SOD), catalase (CAT) isozyme activities and chlorophyll a, b (Chl a, b) and carotenoids (Car) contents responded to water stress and whether they related to presence of a terminal drought tolerance QTL in pearl millet. We used PRLT2/89-33 (QTL donor), H77/833-2 (sensitive), and near-isogenic lines (QTL-NILs) introgressed with the QTL in H77/833-2 background. Under water stress there was no significant change in the total APX activity; only the proportional APX5 activity increased, with higher band intensity in tolerant genotypes. There were no significant changes in total activities of CAT and SOD under water stress, with similar band intensities in all genotypes, and a new CAT isozyme was induced in all genotypes. The photosynthetic pigment content decreased under water stress, although not differently in any genotype. Under water stress, the activities of most APX, CAT and SOD isozymes were closely related to the total chlorophyll/carotenoids ratio. Overall, besides APX5, water stress did not lead to major changes in the profile of isoenzymes involved in ROS scavenging. Similarly, the pigment content under stress did not discriminate genotypes according to the presence/absence of the QTL. This absence of discrimination for the ROS scavenging enzymes and for the pigment content under stress suggests that these traits may not play a key role in terminal drought tolerance in pearl millet.     

渗透胁迫对黑麦幼苗活性氧和抗氧化酶活性的影响

用20%聚乙二醇(PEG 6000)研究了渗透胁迫对黑麦(Secale cereale L.)幼苗活性氧(reactive oxygen species, ROS)和主要抗氧化酶—— 超氧化物歧化酶(superoxide dismutase, SOD)、过氧化氢酶(catalase, CAT)、抗坏血酸过氧化物酶(ascorbate peroxidase, APX)和谷胱甘肽还原酶(glutathione reductase, GR)活性的影响。结果表明, 与对照相比, PEG处理明显提高了叶子和根中丙二醛(malondialdehyde, MDA)的含量、ROS的水平和以上4种抗氧化酶的活性。渗透胁迫下,叶子和根中MDA和ROS水平变化的规律基本相似, 但抗氧化酶活性在2种器官中表现不完全相同, 叶子中CAT的活性在对照和处理中无显著差异, 但在根中差异明显, 表明叶子中SOD、APX和GR在植物应答渗透胁迫中起重要作用, 而根中这4种抗氧化酶都参与植物对胁迫的反应。GR活性随PEG处理变化幅度显著高于其它抗氧化酶, 表明GR在黑麦应答渗透胁迫中所起作用可能强于其它抗氧化酶。     

Sensitivity of chondrocytes of growing cartilage to reactive oxygen species

Vascular invasion of calcified cartilage, during endochondral ossification, is initiated and sustained by invasive cells (endothelial cells and macrophages) which degrade the tissue by releasing lytic enzymes. Concurrently, reactive oxygen species (ROS) are also released by these cells and we hypothesize that ROS also contribute to the degradation of the tissue. As a preliminary approach to this problem, the antioxidant activities and the effect of ROS on hypertrophic cartilage and chondrocytes (HCs) were investigated. Compared to resting or articular chondrocytes, HCs exhibited higher catalase but lower SOD specific activities and lower PHGPx concentration, thus revealing a defence activity specific against H₂O₂. Moreover, dose-dependent depletion of ATP occurred after few minutes of exposure to ROS, and a long-term treatment (16 h incubation with ROS) promoted the release of LDH activity and a significant variation of the poly- to mono-unsaturated fatty acid ratio. Finally, the incubation of HCs with low ROS doses induced the release of sedimentable alkaline phosphatase activity (matrix vesicles). How the obtained results fit the in vivo occurring events is discussed.     

Role of reactive oxygen species in LPS-induced production of prostaglandin E2 in microglia

We determined the roles of reactive oxygen species (ROS) in the expression of cyclooxygenase-2 (COX-2) and the production of prostaglandin E2 (PGE2) in lipopolysaccharide (LPS)-activated microglia. LPS treatment increased intracellular ROS in rat microglia dose-dependently. Pre-treatment with superoxide dismutase (SOD)/catalase, or SOD/catalase mimetics that can scavenge intracellular ROS, significantly attenuated LPS-induced release in PGE2. Diphenylene iodonium (DPI), a non-specific NADPH oxidase inhibitor, decreased LPS-induced PGE2 production. In addition, microglia from NADPH oxidase-deficient mice produced less PGE2 than those from wild-type mice following LPS treatment. Furthermore, LPS-stimulated expression of COX-2 (determined by RT-PCR analysis of COX-2 mRNA and western blot for its protein) was significantly reduced by pre-treatment with SOD/catalase or SOD/catalase mimetics. SOD/catalase mimetics were more potent than SOD/catalase in reducing COX-2 expression and PGE2 production. As a comparison, scavenging ROS had no effect on LPS-induced nitric oxide production in microglia. These results suggest that ROS play a regulatory role in the expression of COX-2 and the subsequent production of PGE2 during the activation process of microglia. Thus, inhibiting NADPH oxidase activity and subsequent ROS generation in microglia can reduce COX-2 expression and PGE2 production. These findings suggest a potential therapeutic intervention strategy for the treatment of inflammation-mediated neurodegenerative diseases.     

Production of reactive oxygen species and antioxidant enzymes of pea and soybean plants under hypoxia and high CO<Subscript>2</Subscript> concentration in medium

Generation of reactive oxygen species (ROS) and activities of antioxidant enzymes (catalase, peroxidase, ascorbate peroxidase) in pea (Pisum sativum L.) and soybean (Glycine max L.) under hypoxia (3–24 h) and high CO₂ concentration in medium were studied. In sensitive to hypoxia pea seedlings, hypoxia enhanced markedly production of superoxide anion-radical, hydroperoxides, and especially hydrogen peroxide. In more tolerant soybean plants, these changes were less pronounced. During first hours of hypoxia, activity of lipoxygenase in plant cells increased. This allows a suggestion that this enzyme is involved in the processes of hydroperoxide accumulation in plant tissues under oxygen deficit. In pea and soybean plants, a correlation between tolerance to hypoxia, the rate of ROS generation, and antioxidant enzyme activities was established. During the first hours of hypoxia, the catalase activity in soybean plants increased stronger than in sensitive to hypoxia pea plants. At longer exposure to hypoxia (24 h), peroxidases started to play the higher role in cell defense against hypoxia, but only in soybean plants. The medium with the higher CO₂ content induced higher changes in the processes of ROS accumulation and activities of lipoxygenase and antioxidant enzymes. This permits us to refer CO₂, accumulated as a product of respiration in the cells, to low-molecular signal molecules switching on plant adaptation to hypoxic stress.     

Polyamine catabolism influences antioxidative defense mechanism in shoots and roots of five wheat genotypes under high temperature stress

Effect of high temperature stress on polyamine catabolism and antioxidant enzyme activity in relation to glutathione, ascorbate and proline accumulation was studied in five wheat (Triticum aestivum L.) genotypes (differently susceptible to temperature stress). High temperature significantly increased the activities of superoxide dismutase (SOD), catalase (CAT), guaiacol peroxidase (GPX), ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR), glutathione reductase (GR) and glutathione S-transferase (GST) in shoots of all genotypes. Higher activities of GPX in C 306, C 273 and APX in PBW 550, PBW 343 and PBW 534 demonstrate their important role in scavenging H₂O₂. Conversely, high temperature stress led to a significant decline in SOD, CAT, APX and GPX activities of roots with a subsequent increase in diamine oxidase (DAO) and polyamine oxidase (PAO) activities especially in PBW 550 and PBW 343. The concentration of ascorbic acid declined with the imposition of heat stress, however, polyamines responded to high temperature stress by increasing spermidine and spermine levels and decreasing putrescine levels. After exposure to high temperature, proline accumulation was significantly decreased in roots and increased in shoots though maximum concentration was achieved in C 306 genotype. Apparently, the wheat seedlings respond to high temperature mediated increase in reactive oxygen species (ROS) production by altering antioxidative defense mechanism and polyamine catabolism though differentially in five wheat genotypes. Among five genotypes studied, C 306 and C 273 seem to be better protected against temperature stress. The results suggested that shoots were more resistant against the destructive effects of ROS as is indicated by low levels of thiobarbituric acid reactive substances under high temperature stress.     

Protective effect of the octadecaneuropeptide on hydrogen peroxide-induced oxidative stress and cell death in cultured rat astrocytes

Oxidative stress, resulting from accumulation of reactive oxygen species (ROS), plays a critical role on astrocyte death associated with neurodegenerative diseases. Astroglial cells produce endozepines, a family of biologically active peptides that have been implicated in cell protection. Thus, the purpose of the present study was to investigate the potential protective effect of one of the endozepines, the octadecaneuropeptide ODN, on hydrogen peroxide (H(2) O(2) )-induced oxidative stress and cell death in rat astrocytes. Incubation of cultured astrocytes with graded concentrations of H(2) O(2) for 1 h provoked a dose-dependent reduction of the number of living cells as evaluated by lactate dehydrogenase assay. The cytotoxic effect of H(2) O(2) was associated with morphological modifications that were characteristic of apoptotic cell death. H(2) O(2) -treated cells exhibited high level of ROS associated with a reduction of both superoxide dismutases (SOD) and catalase activities. Pre-treatment of astrocytes with low concentrations of ODN dose-dependently prevented cell death induced by H(2) O(2) . This effect was accompanied by a marked attenuation of ROS accumulation, reduction of mitochondrial membrane potential and activation of caspase 3 activity. ODN stimulated SOD and catalase activities in a concentration-dependent manner, and blocked H(2) O(2) -evoked inhibition of SOD and catalase activities. Blockers of SOD and catalase suppressed the effect of ODN on cell survival. Taken together, these data demonstrate for the first time that ODN is a potent protective agent that prevents oxidative stress-induced apoptotic cell death.     

Reduced Superoxide Dismutase in Lung Cells of Patients with Asthma

Lung cells recovered from symptomatic patients with asthma generate increased amounts of reactive oxygen species (ROS). Animal and in vitro studies indicate that ROS can reproduce many of the features of asthma. The ability of ROS to produce the clinical features of asthma may depend on an individual's lung antioxidant defenses. Patients with asthma are reported to have reduced antioxidant defenses in peripheral blood, but little is known about the antioxidant defenses of their lung cells. To define lung cell antioxidant defenses in asthma, the glutathione concentration and the glutathione reductase, glutathione peroxidase, catalase, and superoxide dismutase (SOD) activities were measured in cells recovered by bronchoalveolar lavage (BAL cells) and by bronchial brushing (bronchial epithelial cells, HBEC) from normal subjects and patients with asthma. Superoxide dismutase activity was reduced 25% in BAL cells (p < .05) and nearly 50% in HBEC (p < .02) from patients with asthma. Alterations in the other antioxidants were not identified. A direct relationship was found between airway reactivity to methacholine, measured as PC₂₀FEV₁, and HBEC SOD activity (r² = 89; p < .005), but not between airway reactivity and the other antioxidants. The finding of reduced SOD activity in lung cells of patients with asthma suggests that diminished SOD activity serves as a marker of the inflammation characterizing asthma. Alternatively, it may play a role in the development or severity of the disease. © 1997 Elsevier Science Inc.     

High glucose concentration affects the oxidant-antioxidant balance in cultured mouse podocytes

Hyperglycemia is well-recognized and has long-term complications in diabetes mellitus and diabetic nephropathy. In podocytes, the main component of the glomerular barrier, overproduction of reactive oxygen species (ROS) in the presence of high glucose induces dysfunction and increases excretion of albumin in urine. This suggests an impaired antioxidant defense system has a role in the pathogenesis of diabetic nephropathy. We studied expression of NAD(P)H oxidase subunits by Western blotting and immunofluorescence and the activities of the oxidant enzyme, NAD(P)H, and antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT), in mouse podocytes cultured in a high glucose concentration (30 mM). We found long-term (3 and 5 days) exposure of mouse podocytes to high glucose concentrations caused oxidative stress, as evidenced by increased expression of Nox4 and activities of NAD(P)H oxidase (Δ 182%) and SOD (Δ 39%) and decreased activities of GPx (Δ -40%) and CAT (Δ -35%). These biochemical changes were accompanied by a rise in intracellular ROS production and accumulation of hydrogen peroxide in extracellular space. The role of Nox4 in ROS generation was confirmed with Nox4 siRNA. In conclusion, high glucose concentration affects the oxidant-antioxidant balance in mouse podocytes, resulting in enhanced generation of superoxide anions and its attenuated metabolism. These observations suggest free radicals may play an important role in the pathogenesis of diabetic nephropathy.     

Reduced superoxide dismutase activity in Palaemonetes argentinus (Decapoda, Palemonidae) infected by Probopyrus ringueleti (Isopoda, Bopyridae)

Cellular oxidative stress may promote damage or death in biological systems and may be caused by production of pro-oxidant molecules known as reactive oxygen species (ROS). The aim of this work was to analyze the activity of antioxidant enzymes (catalase [CAT], superoxide dismutase [SOD] and glutathione peroxidase [GPx]) in the shrimp Palaemonetes argentinus Nobili, 1901 infected by Probopyrus ringueleti (Verdi & Schuldt, 1987), a gill chamber parasite known for its capacity to cause host metabolic changes, including changes in oxygen consumption rates. Infested and non-infested shrimp were collected in the Patos Lagoon estuary (southern Brasil), where the prevalence of the parasite may be as high as 70%. No significant differences were observed for either CAT or GPx activities. However, SOD activity was significantly reduced in infected shrimp, suggesting that bopyrid isopod respiratory impairment resulted in reduced SOD enzyme activity.     

Redox Imbalance in the Peripheral Mechanism Underlying the Mirror-Image Neuropathic Pain Due to Chronic Compression of Dorsal Root Ganglion

Reactive oxygen species (ROS) play a critical role in the pathogenesis of neuropathic pain, but few studies have examined the role of oxidative stress in the mirror-image neuropathic pain (MINP). The present study was to investigate the role of ROS in MINP caused by chronic compression of the dorsal root ganglion (DRG) (CCD) in a rat model. SD rats were randomly divided into sham group and CCD group. CCD was conducted to induce MINP. CCD rats were intraperitoneally injected with α-Phenyl-N-tert-butyl-nitrone (PBN) at 7 days after surgery. Paw withdrawal mechanical threshold (PWMT) was measured at ?1, 1, 3, 5 and 7 days after surgery in sham group and CCD group, and at 8 time points after PBN injection. Rats were sacrificed at 3 and 7 days after surgery in sham group and CCD group and at 0.5 and 2 h after PBN injection, and the superoxide dismutase (SOD) and catalase activities, as well as hydrogen peroxide (H₂O₂) and malonaldehyde (MDA) contents were determined in the contralateral DRGs. Results showed bilateral PWMT reduced significantly in sham group and CCD group, but it returned to nearly normal level in sham group. MDA content, H₂O₂ content and SOD activity increased significantly, while catalase activity remained unchanged in CCD rats. PBN at 100 mg/kg significantly attenuated bilateral mechanical hyperalgesia accompanied by the improvement of oxidative stress in the contralateral DRGs. Our results demonstrate that ROS produced in the contralateral DRG are involved in the pathogenesis of CCD induced MINP, and ROS scavenger may be a promising drug for the therapy of MINP.     

Relationship between leaf reddening,ROS and antioxidants in <Emphasis Type="Italic">Buxus microphylla</Emphasis> during overwintering

To provide a theoretical basis for revealing the mechanism of winter leaf reddening in evergreen species, the relationships between winter leaf reddening, reactive oxygen species (ROS) and the antioxidant system of Buxus microphylla ‘Wintergreen’ were studied. The pigment changes, ROS production, lipid peroxidation and antioxidants activities of sun leaves during the reddening and regreening processes were investigated, using green shade leaves as controls. The carotenoids in the sun leaves increased linearly with reddening but decreased with the regreening. There was no significant difference in either the superoxide anions (O ₂ ^?· ) or malondialdehyde (MDA) changes between the sun and shade leaves, and their O ₂ ^?· contents were positively correlated with MDA. In contrast to the shade leaves, the sun leaves showed a trend in which the hydrogen peroxide (H₂O₂) changes were closely related to the reddening process and positively correlated with carotenoids content but not with the MDA content. A similar trend was observed for catalase (CAT) and ascorbate peroxidase (APX) activity between the sun and shade leaves, but superoxide dismutase (SOD) and peroxidase (POD) activity and the ascorbate (AsA) content differed between these two ecotypes. Furthermore, the sun leaves had higher CAT activity and AsA content than the corresponding shade leaves. These results suggested that H₂O₂ might play an important role in the winter reddening of sun leaves by promoting the accumulation of carotenoids. In addition, SOD, POD and AsA probably play a photoprotective role in winter-red sun leaves, while the changes in O ₂ ^?· , CAT and APX were independent of winter leaf reddening and were more likely responses to stress caused by low temperatures.     

Redox status in workers occupationally exposed to long-term low levels of ionizing radiation: A pilot study

Objectives: Reactive oxygen species (ROS), including superoxide (O₂^??), play an important role in the biological effects of ionizing radiation. The human body has developed different antioxidant systems to defend against excessive levels of ROS. The aim of the present study is to investigate the redox status changes in the blood of radiologic technologists and compare these changes to control individuals.

Methods: We enrolled 60 medical workers: 20 occupationally exposed to ionizing radiation (all radiologic technologists), divided in three subgroups: conventional radiography (CR), computerized tomography (CT), and interventional radiography (IR) and 40 age- and gender-matched unexposed controls. Levels of O₂^?? and malondialdehyde (MDA) in blood were measured as an index of redox status, as were the activities of antioxidant enzymes superoxide dismutase (SOD) and catalase. Redox status was also assessed by measuring levels of reduced and oxidized glutathione (GSH, GSSG, respectively).

Results: Levels of O₂^?? and MDA, and SOD activity in the blood of IR and CT-exposed subjects were significantly higher than both the CR-exposed subjects and control individuals. However, there were no statistically significant differences in the levels of catalase, GSH and ratio of GSH/GSSG between exposed workers and control individuals.

Discussion: This study suggests that healthcare workers in CT and IR occupationally exposed to radiation have an elevated circulating redox status as compared to unexposed individuals.