Hyperglycemia is known to cause oxidative stress that leads mainly to enhanced production of mitochondrial reactive oxygen species (ROS). It has been demonstrated that hyperbaric oxygen (HBO) treatment also increases the formation of ROS. There are, however, no comprehensive evaluations of such oxidative effects in diabetes which requires HBO treatment. The purpose of this study is to investigate the influence of a clinically-recommended HBO treatment on glucose homeostasis and oxidative stress in rats with streptozotocin (STZ)-induced diabetes. Under the clinically-used HBO exposure protocol, the levels of blood glucose, thiobarbituric acid reactive substances (TBARS) as a lipid peroxidation marker, and the activity of superoxide dismutase (SOD) as an antioxidant enzyme marker were investigated in the erythrocytes, liver, pancreas, skeletal muscle, and brain of rats with STZ-induced diabetes. The levels of blood glucose and TBARS increased significantly (p<0.05), and the activity of SOD decreased significantly (p<0.05) in the erythrocytes and all organs of rats with diabetes subjected to HBO exposure. These results suggested that HBO exposure might boost glucose autoxidation and increase ROS production in STZ-induced diabetes as side-effects of administering HBO treatment for the first time., T. Matsunami ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Despite the demonstrated exercise -induced increase in reactive oxygen species (ROS) production, growing epidemiological evidence indicates that habitual, moderate physical activity reduces the incidence of several oxidative stress-based diseases. This apparent paradox can be explained taking into account that ROS produced during repeated ex ercise bouts may act as mild stressors able to trigger physiological and biomolecular hormetic responses through a number of redox-sensitive transcription pathways. Unfortunately, much more limited information is available from general population-based research, which could better reflect the condition of common people interested in achieving and maintaining good fitness levels. The present work aimed at investigatin g whether and how exercise-related habits in non-professional regular runners (n=33) can affect the systemic anti-oxidative capacity, and the resting serum levels of typical lipid peroxidation-related by-products and oxidatively- damaged proteins, in comparison with untrained sedentary individuals (n=25). We also anal yzed in both groups the redox response elicited by a modified Bruce-based maximal exercise test on the same parameters. Our findings indicated that long- term regular and moderate practice of aerobic physical activity can increase antioxidant defense systems, lower the resting protein oxidation processes and reduce the immediate up- regulation of lipid-targeting oxidative stress in response to an acute bout of exercise., S. Falone, A. Mirabilio, A. Pennelli, M. Cacchio, A. Di Baldassarre, S. Gallina, A. Passerini, F. Amicarelli., and Obsahuje bibliografii
The effects of enhanced ultraviolet-B (UV-B, 0.4 W m-2) irradiance and nickel (Ni, 0.01, 0.10 and 1.00 mM; Ni0.01, Ni0.10, Ni1.00, respectively) treatment, singly and in combination, on growth, photosynthetic electron transport activity, the contents of reactive oxygen species (ROS), antioxidants, lipid peroxidation, and membrane leakage in soybean seedlings were evaluated. Ni0.10 and Ni1.00 and UV-B declined the growth and chlorophyll content, which were further reduced following combined exposure. Contrary to this, Ni0.01 stimulated growth, however, the effect together with UV-B was inhibitory. Carotenoids showed varied response to both the stresses. Simultaneous exposure of UV-B and Ni as well as UV-B alone reduced the activities of photosystems 1 and 2 (PS1 and PS2) and whole chain activity significantly, while Ni individually, besides strongly inhibiting PS2 and whole chain activity, stimulated the PS1 activity. Both the stresses, alone and together, enhanced the contents of superoxide radical (O2⋅-), hydrogen peroxide (H2O2), malondialdehyde (MDA), electrolyte leakage, and proline content, while ascorbate content declined over control. Individual treatments increased the activities of catalase (CAT), peroxidase, and superoxide dismutase (SOD), but Ni1.00 declined SOD activity significantly. Combined exposure exhibited similar response, however, CAT activity declined even more than in control. Compared to individual effects of UV-B and Ni, the simultaneous exposure resulted in strong inhibition of photosynthetic electron transport and excessive accumulation of ROS, thereby causing severe damage to soybean seedlings. and S. M. Prasad, R. Dwivedi, M. Zeeshan.
Environmental stresses, such as cold, heat, salinity, and drought, induce ethylene production and oxidative stress and cause damage in plants. On the other hand, studies have shown that salicylic acid (SA) induced resistance to environmental stresses in plants. In this research, the effects of ethylene on chlorophyll (Chl), carotenoid (Car), anthocyanin, flavonoids, ascorbic acid, dehydroascorbic acid, total ascorbate, lipid peroxidation, and ethylene production in leaves of canola pretreated with SA were studied. The plants were grown in pots until they have four leaves. Leaves were sprayed for two days with three different concentrations of SA (0, 0.5, and 1 mM). The plants were treated for three days with three concentrations of ethylene (0, 50, and 100 ppm). At the end of the ethylene treatments, all examined parameters were measured. The results showed that the ethylene treatments induced lipid peroxidation, while SA mitigated this effect. The ethylene treatment lowered significantly Chl and Car contents and anthocyanin accumulation, but SA alleviated these effects. SA induced an increase in ascorbic acid content in canola plants after the ethylene treatments. Therefore, we concluded that SA played an important role in the alleviation of damages caused by stress conditions. and M. M. Tirani, F. Nasibi, Kh. M. Kalantari.
Hypothalamic paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) play an important role in brain control of blood pressure (BP). One of the important mechanisms involved in the pathogenesis of hypertension is the elevation of reactive oxygen species (ROS) production by nicotine adenine dinucleotide phosphate (NADPH) oxidase. The aim of our present study was to investigate NADPH oxidase -mediated superoxide (O 2 - ) production and to search for the signs of lipid peroxidation in hypothalamus and medulla oblongata as well as in renal medulla and cortex of hypertensive male rats transgenic for the murine Ren -2 renin gene (Ren -2 TGR) and their age -matched normotensive controls ‒ Hannover Sprague Dawley rats (HanSD) . We found no difference in the activity of NADPH oxidase measured as a lucigenin -mediated O 2 - production in the hypothalamus and medulla oblongata. However, we observed significantly elevated NADPH oxidase in both renal cortex and medulla of Ren -2 TGR com pared with HanSD. Losartan (LOS) treatment (10 mg/kg body weight/day) for 2 months (Ren -2 TGR+LOS) did not change NADPH oxidase -dependent O 2 - production in the kidney. We detected significantly elevated indirect m arkers of lipid peroxidation measured as th iobarbituric acid -reactive substance s (TBARS) in Ren -2 TGR, while they were significantly decreased in Ren -2 TGR +LOS. In conclusion, the present study shows increased NADPH oxidase activities in renal cortex and medulla with significantly increased TBARS in renal cortex. No significant changes of NADPH oxidase and markers of lipid peroxidation were detected in the studied brain regions., M. Vokurková, H. Rauchová, L. Řezáčová, I. Vaněčková, J. Zicha., and Obsahuje bibliografii