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Aim: To investigate the emphasis of oxidative stress in the pathogenesis of vitiligo through an evaluation of ischemia-modified albumin (IMA). Results/methodology: IMA was of higher statistical significance in patients than in the control group (IMA: 0.57 ± 0.2 vs 0.52 ± 0.2 ΔABSU; p < 0.0001). IMA (p < 0.0001; OR: 8.9; 95% CI = 3.1-26.1) was found as an independent predictor of oxidative stress. Increases in affected body surface area and age were found to be independent risk factors for IMA. The sensitivity, specificity and positive and negative predictive values and capacity of IMA were higher than other studied biomarkers., Discussion/conclusion: IMA can be detected in the condition of oxidative stress in vitiligo; it has great potential as a biomarker of said condition, when compared with other studied biomarkers.

This study aimed to understand the molecular mechanisms of nitrogen dioxide (NO 2 )-induced toxicity and cell death in plants. Exposure of Arabidopsis to high concentrations of NO 2 induced cell death in a dose-dependent manner. No leaf symptoms were visible after fumigation for 1 h with 10 parts per million (ppm) NO 2 However, 20 ppm NO 2 caused necrotic lesion formation and 30 ppm NO 2 complete leaf collapse, which had already started during the 1 h fumigation period. NO 2 fumigation resulted in a massive accumulation of nitrite and in protein modifications by S-nitrosylation and tyrosine nitration. Nitric oxide (NO) at 30 ppm did not trigger leaf damage or any of the effects observed after NO 2 fumigation. The onset of NO 2 -induced cell death correlated with NO and hydrogen peroxide (H 2 O 2 ) signaling and a decrease in antioxidants. NO- and H 2 O 2 -accumulating mutants were more sensitive to NO 2 than wild-type plants. Accordingly, experiments with specific scavengers confirmed that NO and H 2 O 2 are essential promoters of NO 2 -induced cell death. Leaf injection of 100 mM nitrite caused an increase in S-nitrosylation, NO, H 2 O 2 , and cell death suggesting that nitrite functioned as a mediator of NO 2 -induced effects. A targeted screening of phytohormone mutants revealed a protective role of salicylic acid (SA) signaling in response to NO 2 It was also shown that phytohormones were modulators rather than inducers of NO 2 -induced cell death. The established experimental set-up is a suitable system to investigate NO 2 and cell death signaling in large-scale mutant screens., (© The Author 2016. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Background/aim: Plumbago indica (PI) L. and its active constituent, plumbagin, has been traditionally claimed for several pharmacological activities; however, there is little information regarding their toxicity. The present study aims to examine the effects of plumbagin and PI extract (PI) on hepatic histomorphology and antioxidative system in mice., Materials and Methods: Adult male intelligent character recognition mice were intragastrically administered plumbagin (1, 5, and 15 mg/kg/day) or PI (20, 200, and 1,000 mg/kg/day) consecutively for 14 days. Hepatic histomorphology was examined. Plasma alanine transaminase (ALT) and aspartate transaminase (AST) levels, hepatic lipid peroxidation, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, and the ratio of reduced to oxidized glutathione (GSH/GSSG) were determined., Results: Plumbagin and PI concentration-dependently induced hepatic injury based on histopathological changes via imbalance of antioxidative system. Plumbagin and PI significantly increased plasma ALT and AST levels, hepatic lipid peroxidation, and GPx activity but significantly decreased hepatic SOD and CAT activities. The GSH/GSSG ratio was significantly reduced by plumbagin., Conclusion: Plumbagin and PI caused hepatotoxic effects in the mice by unbalancing of the redox defense system. Therefore, plumbagin and PI-containing supplements should be used cautiously, especially when consumed in high quantities or for long periods.

The necrotrophic fungus Botrytis cinerea is a major threat to grapevine cultivation worldwide. A screen of 41 Vitis genotypes for leaf resistance to B. cinerea suggested species independent variation and revealed 18 resistant Chinese wild Vitis genotypes, while most investigated V. vinifera, or its hybrids, were susceptible. A particularly resistant Chinese wild Vitis, "Pingli-5" (V. sp. [Qinling grape]) and a very susceptible V. vinifera cultivar, "Red Globe" were selected for further study. Microscopic analysis demonstrated that B. cinerea growth was limited during early infection on "Pingli-5" before 24 h post-inoculation (hpi) but not on Red Globe. It was found that reactive oxygen species (ROS) and antioxidative system were associated with fungal growth. O[Formula: see text] accumulated similarly in B. cinerea 4 hpi on both Vitis genotypes. Lower levels of O[Formula: see text] (not H2O2) were detected 4 hpi and ROS (H2O2 and O[Formula: see text]) accumulation from 8 hpi onwards was also lower in "Pingli-5" leaves than in "Red Globe" leaves. B. cinerea triggered sustained ROS production in "Red Globe" but not in "Pingli-5" with subsequent infection progresses. Red Globe displayed little change in antioxidative activities in response to B. cinerea infection, instead, antioxidative activities were highly and timely elevated in resistant "Pingli-5" which correlated with its minimal ROS increases and its high resistance. These findings not only enhance our understanding of the resistance of Chinese wild Vitis species to B. cinerea, but also lay the foundation for breeding B. cinerea resistant grapes in the future.

Seed heteromorphism provides plants with alternative strategies for survival in unfavourable environments. However, the response of descendants from heteromorphic seeds to stress has not been well documented. Suaeda aralocaspica is a typical annual halophyte, which produces heteromorphic seeds with disparate forms and different germination characteristics. To gain an understanding of the salt tolerance of descendants and the impact of seed heteromorphism on progeny of this species, we performed a series of experiments to investigate the plant growth and physiological parameters (e.g. osmolytes, oxidative/antioxidative agents and enzymes), as well as expression patterns of corresponding genes. Results showed that osmolytes (proline and glycinebetaine) were significantly increased and that excess reactive oxygen species ([Formula: see text] H2O2) produced under high salinity were scavenged by increased levels of antioxidant enzymes (superoxide dismutase, ascorbate peroxidase and glutathione reductase) and corresponding antioxidants (ascorbic acid and glutathione). Moreover, enhancement of phosphoenolpyruvate carboxylase activity at high salt intensity had a positive effect on photosynthesis. The descendants from heteromorphic seeds presented no significant difference in performance with or without salinity. In conclusion, we found that high salinity induced the same active physiological responses in plants from heteromorphic seeds of S. aralocaspica, there was no carry-over of seed heteromorphism to plants: all the descendants required salinity for optimal growth and adaptation to their natural habitat., (Published by Oxford University Press on behalf of the Annals of Botany Company.)

Imidacloprid is a neonicotinoid insecticide that can have negative effects on nontarget animals. The present study was conducted to assess the toxicity of various imidacloprid doses (0.3, 1.25, and 5 mg/mL) on zebrafish sampled after 7, 14, 21, and 28 days of exposure. The levels of catalase (CAT), superoxide dismutase (SOD), reactive oxygen species (ROS), glutathione-S-transferase (GST), and malondialdehyde (MDA) and the extent of DNA damage were measured to evaluate the toxicity of imidacloprid on zebrafish. SOD and GST activities were noticeably increased during early exposure but were inhibited toward the end of the exposure period. In addition, the CAT levels decreased to the control level following their elevation during early exposure. High concentrations of imidacloprid (1.25 and 5 mg/L) induced excessive ROS production and markedly increased MDA content on the 21st day of exposure. DNA damage was dose- and time-dependent. In conclusion, the present study showed that imidacloprid can induce oxidative stress and DNA damage in zebrafish.

This study investigated the influence of different durations of aerobic exercise on fuel utilization, lactate levels and antioxidative status in trained rats. Forty rats underwent physical training (T, n = 20) or non- training (NT, n = 20) for 6 weeks. For physical training, animals exercised on a treadmill for 30 min 5 days per week. At the end of week 6, the animals in each group were subdivided into BE, DE-0.5, DE-1 and DE-2, which were sacrificed at the end of week 6 without having performed exercise or after exercise on a treadmill for 0.5h, 1h and 2h, respectively, immediately before being sacrificed. The plasma glucose level in DE-2 of the NT group was significantly lower than in the other groups. Muscle and liver glycogen levels were significantly lower in DE-1 and DE-2, but there were no significant differences between DE-1 and DE-2 in the T group. Liver protein in DE-2 of the NT group was significantly lower. Muscle TG levels were decreased in DE-0.5 of the T group, while those of the NT group were decreased in DE-1. FFA levels were increased in DE-0.5 of the T group and in DE-1 of the NT group. Lactate levels were increased in DE-0.5 of the NT group, while they were increased in DE-1 of the T group. Catalase activity of the T group was lower in BE but higher in DE-0.5, DE-1 and DE-2. SOD activities were higher in trained rats, while the GSH/GSSG ratios were higher in BE, DE-0.5 and DE-1 in the T group, and there was no difference in that of DE-2. There were no differences in MDA levels in BE and DE-0.5, but they were significantly lower in DE-1 and DE-2 of the T group. Overall, the results of this study, suggest that training may improve exercise performance by facilitating the mobilization and oxidation of fat and conserving limited carbohydrate storage, and that it may delay the onset of fatigue and enhance the antioxidative defense system, but cannot support two hours of vigorous exercise.

When melatonin was injected into the liver of rats with toxic hepatitis, there was a reduction in the rate of free radical processes and in the mobilization of the antioxidative system, as estimated by the parameters of biochemiluminescence and the level of α-tocopherol, which is likely to be accounted for by the antioxidative effect of this hormone. The administration of melatonin to intact animals causes a reduction in the activity of aconitate hydratase and an increase in the level of citrate, which reflects the enhancement of the antioxidative potential as it promotes the decreased hydroxyl radical formation in the Fenton reaction. Metatonin-induced elevations in citrate levels and changes in the activity of aconitate hydratase were observed in the liver of animals with toxic hepatitis as compared with those not receiving the hormone, which seems to be associated with the less mobilization of the antioxidative system in the presence of melatonin that is able to produce an antioxidative effect.

The purpose of the present study was to elucidate the influence of sessions of intermittent hypoxic training (IHT) alone and in combination with high-intensity chronic exercise on lipid peroxidation and antioxidative defense system in rat heart. High-intensity chronic exercise was performed as swimming training with load that corresponded to ~ 75% VO 2max (30 min/day, 5 days/wk, for 4 wk). IHT consisted of repeated episodes of hypoxia (12% O 2 , 15 min), interrupted by equal periods of recovery (5 sessions/day, for 2wk). Sessions of IHT were applied during the first two weeks and during the last two weeks of chronic exercise. It was shown that long-term training was accompanied by the accumulation of thiobarbituric acid reactive substances (TBARS) in myocardium. IHT attenuated the increase in TBARS content caused by high-intensity chronic exercise and it enhanced myocardial reduced glutathione concentration, activities of superoxide dismutase, catalase, and glutathione peroxidase in comparison with trained animals only. No significant changes were found in glutathione reductase, glucose-6-phosphate dehydrogenase activities. Our results suggest that intermittent hypoxic stimuli may induce a state of preconditioning that protects the heart from oxidative stress evoked by high-intensity chronic exercise.

The aim of the present study was to examine the influence of intermittent hypoxia at rest and in combination with long-term high-intensity swimming exercise on lipid peroxidation and antioxidant defense system adaptation in skeletal muscles differing in fiber type composition. High-intensity chronic exercise was performed as swimming training with load that corresponded to ~ 75 % VO2max (30 min·day(-1), 5 days·wk(-1), for 4 wk). Intermittent hypoxic training (IHT) consisted of repeated episodes of hypoxia (12%O2, 15 min), interrupted by equal periods of recovery (5 sessions/day, for 2 wk). Sessions of IHT were used during the first two weeks and during the last two weeks of chronic exercise. Oxidative (red gastrocnemius and soleus, mix) and glycolytic (white gastrocnemius) muscles were sampled. Our results indicated that high-intensity swim training in combination with sessions of IHT induced more profound antioxidative adaptations in skeletal muscles than the exercise training only. This adaptation has muscle fiber type specificity and is reflected in significantly elevated superoxide dismutase and catalase activities in highly oxidative muscle only. Training adaptation of GSH system (reduced glutathione content, activities of glutathione reductase, glutathione peroxidase, NADPH-supplying enzyme glucose-6-phosphate dehydrogenase) occurred both in slow- and fast-twitch muscles. However, this process was more effective in oxidative muscles. IHT attenuated the increase in TBARS content induced by high-intensity swimming training. The test on exercise tolerance demonstrated a significant elevation of the swimming time to exhaustion after IHT at rest and after IHT in conjunction with high-intensity exercise in comparison with untrained and chronically exercised rats. These results confirmed that sessions of IHT might improve exercise tolerance and increase maximal work capacity. Key PointsSingle high-intensity exercise induces a significant increase in TBARS content, decreases in GPx, GR activities and GSH content in both fast- and slow-twitch muscles.Intermittent hypoxic training (IHT) may improve exercise tolerance and maximal work capacity.Antioxidant enzyme response to chronic exercise is highly muscle fiber specific.IHT induces no significant change in TBARS content in both slow- and fast-twitch muscles in comparison with normoxic rats.IHT promotes an adaptation of GSH system as well as antioxidant enzymes in skeletal muscle, however the biochemical mechanisms underlying the muscle fiber specific GSH adaptation to hypoxic training is not clear.