The intracellular levels of antioxidant and free radical scavenging enzymes are gradually altered during the aging process. An age-dependent increase of oxidative stress occurring throughout the lifetime is hypothesized to be the major cause of aging. The current study examined the effects of L-malate on oxidative stress and antioxidative defenses in the liver and heart of aged rats. Sprague-Dawley male rats were randomly divided into four groups, each group consisting of 6 animals. Group Ia and Group IIa were young and aged control rats. Group Ib and Group IIb were young and aged rats treated with L-malate (210 mg/kg body weight per day). L-malate was orally administrated via intragastric canula for 30 days, then the rats were sacrificed and the liver and heart were removed to determine the oxidant production, lipid peroxidation and antioxidative defenses of young and aged rats. Dietary L-malate reduced the accumulation of reactive oxygen species (ROS) and significantly decreased the level of lipid peroxidation in the liver and heart of the aged rats. Accordingly, L-malate was found to enhance the antioxidative defense system with an increased activity of antioxidant enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) and increased glutathione (GSH) levels in the liver of aged rats, a phenomenon not observed in the heart of aged rats. Our data indicate that oxidative stress was reversed and the antioxidative defense system was strengthened by dietary supplementation with L-malate., J.-L. Wu, Q.-P. Wu, X.-F. Yang, M.-K. Wei, J.-M. Zhang, Q. Huang, X.-Y. Zhou., and Obsahuje bibliografii a bibliografické odkazy
Morpho-physiological and biochemical analyses were carried out in eight diverse indigenous muskmelon (Cucumis melo L.) genotypes exposed to different degrees of water deficit (WD). The ability of genotypes MM-7, and especially MM-6, to counteract better the negative effect of WD was associated with maintaining higher relative water content (RWC), photosynthetic rate, efficiency of PSII, and photosynthetic pigments compare to other genotypes. Furthermore, MM-6 showed a better ability to maintain cellular homeostasis than the others. It was indicated by a stimulated antioxidative defense system, i.e., higher activities of antioxidant enzymes, accumulation of nonenzymatic antioxidants together with lower concentration of reactive oxygen species and malondialdehyde. However, the genotypes MM-2 and MM-5 suffered greatly due to WD and showed reduced RWC, photosynthetic rates, pigment content, and exhibited higher oxidative stress observed as lower antioxidant enzyme activities., W. A. Ansari, N. Atri, B. Singh, P. Kumar, S. Pandey., and Obsahuje bibliografii
A common problem in management of polytrauma – a simultaneous injury to more than one organ or organ system, at least one of them lethal without intervention – is a discrepancy between a relatively good initial state and a serious subsequent development. Since nitric oxide (NO) is produced in high quantities during tissue injury, we assumed that serum levels of NO (and its oxidation products, NOx) might serve as a prognostic marker of polytrauma severity. However, we found recently that NOx was increased in polytrauma, but not in the most severe cases. The present study was undertaken to test the hypothesis that serum NOx is reduced in severe polytrauma by concomitant overproduction of reactive oxygen species (ROS). Polytrauma was induced in rats under anesthesia by bilateral fracture of femurs and tibiae plus incision of the right liver lobe through
laparotomy. Serum NOx was measured by chemiluminescence after hot acidic reduction. The role of ROS was assessed by treatment with an antioxidant, N-acetyl-L-cysteine (NAC). Experimental polytrauma elevated NOx from 11.0±0.7 to 23.8±4.5 ppb. This was completely prevented by NAC treatment (9.1±2.2 ppb). Serum NOx is elevated in severe polytrauma, and this is not reduced by ROS. On the contrary, ROS are necessary for the NOx elevation, probably because ROS produced by inflammatory cells activated by the polytrauma induce massive NO production.
This review concerns the role of nitric oxide (NO) in the pathogenesis of different models of experimental hypertension (NO-deficient, genetic, salt-dependent), which are characterized by a wide range of etiology. Although the contribution of NO may vary between different models of hypertension, a unifying characteristic of these models is the presence of oxidative stress that participates in the maintenance of elevated arterial pressure and seems to be a common denominator underlying endothelial dysfunction in various forms of experimental hypertension. Besides the imbalance between the endothelial production of vasorelaxing and vasoconstricting compounds as well as the relative insufficiency of vasodilator systems to compensate augmented vasoconstrictor systems, there were found numerous structural and functional abnormalities in blood vessels and heart of hypertensive animals. The administration of antihypertensive drugs, antioxidants and NO donors is capable to attenuate blood pressure elevation and to improve morphological and functional changes of cardiovascular system in some but not all hypertensive models. The failure to correct spontaneous hypertension by NO donor administration reflects the fact that sympathetic overactivity plays a key role in this form of hypertension, while NO production in spontaneously hypertensive rats might be enhanced to compensate increased blood pressure. A special attention should be paid to the modulation of sympathetic nervous activity in central and peripheral nervous system. These results extend our knowledge on the control of the balance between NO and reactive oxygen species production and are likely to be a basis for the development of new approaches to the therapy of diseases associated with NO deficiency., J. Török., and Obsahuje bibliografii a bibliografické odkazy
In order to assess its response to the herbicide, sethoxydim (SEY), seedlings of two foxtail millet (Setaria italica) hybrids were exposed to 0.75, 1.5, 3, and 6 L(SEY active ingredient, ai) ha-1 for 7 and 15 d. Our results showed that SEY reduced photosynthesis and oxidative stress in the hybrid millet (Zhangza) at the dosage below 1.5 L(ai) ha-1 (i.e., recommended dosage), whereas it caused death of Jingu 21 at all treatment dosages. In addition, we further explored the effect of SEY on PSI and PSII; the hybrid millet showed a greater tolerance to SEY and also the ability to recover. In conclusion, the hybrid millet seems to possess certain photosynthetic protection mechanisms which could reduce or eliminate the herbicide stress by increasing nonphotochemical quenching for dissipating excessive light energy under SEY-induced oxidative stress., M. J. Guo, Y. G. Wang, S. Q. Dong, Y. Y. Wen, X. E. Song, P. Y. Guo., and Obsahuje bibliografii
We investigated the physiological effect of night chilling (CN) on potted seedlings of two tropical tree species, Calophyllum polyanthum and Linociera insignis, in Xishuangbanna, southwest China. Seedlings grown under 8, 25, and 50 % daylight for five months were moved to a 4-6 °C cold storage house for three consecutive nights, and returned to the original shaded sites during the day. CN resulted in strong suppression of photosynthesis and stomatal conductance for L. insignis, and reduced photorespiration rates, carboxylation efficiency, and maximum photochemical efficiency of photosystem 2 (PS2) at dawn and midday for both species. CN increased dawn and midday rates of non-photochemical quenching, and the contents of malondialdehyde and H2O2 for both species. CN also induced inactivation or destruction of PS2 reaction centres. The impacts of CN on tropical seedlings increased with the number of CN. Shading could significantly mitigate the adverse effects of CN for both species. After 3-d-recovery, gas exchange and fluorescence parameters for both species returned to pre-treatment levels in most cases. Thus CN induced mainly stomatal limitation of photosynthesis for L. insignis, and non-stomatal limitation for C. polyanthum. C. polyanthum was more susceptible to CN than L. insignis. Fog, which often occurs in Xishuangbanna, could be beneficial to chilling sensitive tropical seedlings in this area through alleviating photoinhibition or photodamage by reducing sunlight. and Y.-L. Feng, K.-F. Cao.
Glyphosate herbicide caused oxidative stress and exhibited negative effects on photosynthesis and gas exchange of peanut [Arachis hypogaea L. cv. Giza (G) 5 and 6] leaves. We demonstrated that glyphosate caused various morphological symptoms, such as chlorosis, yellowing, and appearance of curly edges in leaves treated with high doses of herbicide in both cultivars; however, the G5 cultivar was more sensitive and showed severer symptoms. Glyphosate lowered photosynthesis and reduced contents of pigments and proteins as well as free amino acids in both cultivars. The gas-exchange parameters, such as photosynthetic (P N) and transpiration rate (E), were highly altered by the glyphosate application. For example, P N and E were reduced by 65 and 61%, respectively, in G5 treated with high dose of glyphosate compared with control. Antioxidant enzymes, such as peroxidase, catalase, ascorbate peroxidase, and superoxide dismutase were induced by both low and high concentrations in the glyphosate-treated leaves. Moreover, the level of lipid peroxidation, indicated by a malondialdehyde content, as well as the hydrogen peroxide content increased in the glyphosate-treated leaves. However, an increase in total antioxidant activity was detected in leaves and this reflected changes in the antioxidant status and accumulation of antioxidants as a defense mechanism against glyphosate toxicity in peanut., D. E. M. Radwan , K. A. Fayez., and Obsahuje seznam literatury
The aim of our study was to answer whether any positive correlation exists between K+ uptake and salt tolerance in wheat. We carried out a sand-culture experiment with salt-tolerant, DK961 (ST), and salt-sensitive, JN17 (SS), wheat cultivars, where photosynthesis, the K+/Na+ ratio, growth, and the biomass yield were examined. The seeds were exposed for four weeks to six NaCl concentrations (50, 100, 150, 200, 250, and 300 mM), which were embodied in the Hoagland solution. Salinity-induced decrease of K+ or increase in the Na+ content was much smaller in ST than that in SS. The reductions in the light-saturated photosynthetic rate (P Nmax) and chlorophyll content caused by salinity were smaller in the ST compared to SS. Stomatal conductance decreased in both cultivars under saline conditions; nevertheless, it was lower in SS than in ST. The antioxidative capacity was higher in ST than that in SS under saline conditions. Significant positive correlations were observed in both cultivars between K+ contents and P Nmax/biomass yields. We suggest that higher-affinity K+ uptake might play a key role in higher salt tolerance and it might be a reliable indicator for breeding new species of salt-tolerant wheat., D. Cheng, G. Wu, Y. Zheng., and Obsahuje seznam literatury
Proper renal blood flow (RBF) and glomerular filtration rate (GFR)
are critical for maintaining normal blood pressure, kidney
function and water and electrolyte homeostasis. The renal
microvasculature expresses a multitude of receptors mediating
vasodilation and vasoconstriction, which can influence glomerular
blood flow and capillary pressure. Despite this, RBF and GFR
remain quite stable when arterial pressure fluctuates because of
the autoregulatory mechanism. ATP and adenosine participate in
autoregulatory control of RBF and GFR via activation of two
different purinoceptor families (P1 and P2). Purinoceptors are
widely expressed in renal microvasculature and tubules.
Emerging data show altered purinoceptor signaling in
hypertension-associated kidney injury, diabetic nephropathy,
sepsis, ischemia-reperfusion induced acute kidney injury and
polycystic kidney disease. In this brief review, we highlight recent
studies and new insights on purinoceptors regulating renal
microvascular function and renal hemodynamics. We also
address the mechanisms underlying renal microvascular injury
and impaired renal autoregulation, focusing on purinoceptor
signaling and hypertension-induced renal microvascular
dysfunction. Interested readers are directed to several excellent
and comprehensive reviews that recently covered the topics of
renal autoregulation, and nucleotides in kidney function under
physiological and pathophysiological conditions (Inscho 2009,
Navar et al. 2008, Carlstrom et al. 2015, Vallon et al. 2020).
Enhanced production of superoxide radicals by nicotinamideadenine dinucleotide phosphate (NADPH) oxidase in the brain and/or kidney of salt hypertensive Dahl rats has been proposed to participate in the pathogenesis of this form of experimental hypertension. Most information was obtained in young Dahl saltsensitive (DS) rats subjected to high salt intake prior to sexual maturation. Therefore, the aim of our study was to investigate whether salt hypertension induced in adult DS rats is also accompanied with a more pronounced oxidative stress in the brain or kidney as compared to Dahl salt-resistant (DR) controls. NADPH oxidase activity as well as the content of thiobarbituric acid-reactive substances (TBARS) and conjugated dienes (oxidative index), which indicate a degree of lipid peroxidation, were evaluated in two brain regions (containing either hypothalamic paraventricular nucleus or rostral ventrolateral medulla) as well as in renal medulla and cortex. High salt intake induced hypertension in DS rats but did not modify blood pressure in DR rats. DS and DR rats did not differ in NADPH oxidase-dependent production of ROS, TBARS content or oxidative index in either part of the brain. In addition, high-salt diet did not change significantly any of these brain parameters. In contrast, the enhanced NADPH oxidase-mediated ROS production (without significant signs of increased lipid peroxidation) was detected in the renal medulla of salt hypertensive DS rats. Our findings suggest that there are no signs of enhanced oxidative stress in the brain of adult Dahl rats with salt hypertension induced in adulthood., M. Vokurková, H. Rauchová, L. Řezáčová, I. Vaněčková, J. Zicha., and Obsahuje bibliografii