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Objective: Hydroxytyrosol (HT) is a polyphenol with a wide range of biological activities. Excessive drinking can lead to oxidative stress and inflammation in the liver, which usually develop into alcohol liver disease (ALD). At present, there is no specific drug to treat ALD. In this paper, the protection effect of HT on ALD and the underline mechanism were studied. Methods: HepG2 cells were exposed to ethanol in vitro and C57BL/6J mice were fed with a Lieber-DeCarli ethanol liquid diet in vivo. Results: triglyceride (TG) level in serum and the expression of fatty acid synthase (FASN) were reduced significantly by the treatment with HT The acetaldehyde dehydrogenase (ALDH) activity was increased, the serum level of malondialdehyde (MDA) was decreased, catalase (CAT) and glutathione (GSH) were increased, suggesting that HT may reduce its oxidative damage to the body by promoting alcohol metabolism. Furthermore, according to the mRNA levels of tnf-α, il-6 and il-1β, HT inhibited ethanol-induced inflammation significantly. The anti-inflammatory mechanism of HT may be related to suppress the STAT3/iNOS pathway. Dissussion: Our study showed that HT could ameliorate ethanol-induced hepatic steatosis, oxidative stress and inflammation and provide a new candidate for the prevention and treatment of ALD. [ABSTRACT FROM AUTHOR]

The present endeavor has demonstrated the impacts of different sources of silicon (Si) such as potassium silicate (K2SiO3) and calcium silicate (CaSiO3) during the in vitro axillary shoot multiplication of carnation. For the Si treatments, nodal explants were cultured onto the Murashige and Skoog's medium fortified with 1.0 mg L-1 of 6-benzyladenine and 0.5 mg L-1 indole-3- acetic acid with or without K2SiO3 and CaSiO3 in three different concentrations (0, 1.8, or 3.6 mM). After six weeks, the shoot induction ratio, number of shoots produced per explant, expression of photosystem (PS) I and II core proteins, and activities of antioxidant enzymes were examined. Among the Si sources, K2SiO3 application enhanced the axillary shoot multiplication and the uptake of Si on comparison with CaSiO3. Both forms of Si resulted in the enhancement of stomatal density, and PSrelated protein such as PsaA and PsbA illustrating the apparent involvement of Si on the photosynthetic process. Nevertheless, addition of Si improved the antioxidant capacity during the in vitro shoot multiplication. Overall, the outcomes of the present study suggested that Si can be utilized as a supplementary source during the in vitro propagation of carnation. [ABSTRACT FROM AUTHOR]

With devastating increase in population there is a great necessity to increase crop productivity of staple crops but the productivity is greatly affected by various abiotic stress factors such as drought, salinity. An attempt has been made a brief account on abiotic stress resistance of major cereal crops viz. In spite of good successes obtained on physiological and use molecular biology, the benefits of this high cost technology are beyond the reach of developing countries. This review discusses several morphological, anatomical, physiological, biochemical and molecular mechanisms of major cereal crops related to the adaptation of these crop to abiotic stress factors. It discusses the effect of abiotic stresses on physiological processes such as flowering, grain filling and maturation and plant metabolisms viz. photosynthesis, enzyme activity, mineral nutrition, and respiration. Though significant progress has been attained on the physiological, biochemical basis of resistance to abiotic stress factors, very little progress has been achieved to increase productivity under sustainable agriculture. Therefore, there is a great necessity of inter-disciplinary research to address this issue and to evolve efficient technology and its transfer to the farmers’ fields. [ABSTRACT FROM AUTHOR]

Aminoethylcysteine ketimine decarboxylated dimer (AECK-DD) is a natural sulphur compound present in human plasma and urine and in mammalian brain. Recently, it has been detected in many common dietary vegetables. The aim of the present study was to evaluate the ability of AECK-DD to affect cellular response of U937 human monocytic cells to tert -butyl hydroperoxide-induced oxidative stress. AECK-DD was incorporated into cells, as confirmed by GC-MS analyses, without any cytotoxic effect. A 24 h treatment with 50 and 250 μM AECK-DD resulted in the incorporation of 0.10±0.01 and 0.47±0.08 ng AECK-DD × 10 6 cells, respectively. U937 cells pretreated with AECK-DD (in the range 4-100 μM) showed an increased resistance to tert -butyl hydroperoxide-induced necrotic death, as revealed by a higher percent of survival measured at all incubation times with respect to control cells. Moreover, the protective effect exhibited by AECK-DD is significantly stronger with respect to that obtained with other common antioxidants ( N -acetyl cysteine and trolox) and comparable, although somewhat higher, to that of vitamin E. This effect seems to be due to the ability of AECK-DD to reduce glutathione depletion and to inhibit lipid peroxidation during tert -butyl hydroperoxide treatment. It can be concluded that AECK-DD protects cultured human monocytic cells against tert -butyl hydroperoxide-induced oxidative stress and subsequent cell death, likely through an antioxidant action inside the cell. Due to its presence in both human plasma and urine, AECK-DD may play a role in the modulation of oxidative processes in vivo . [ABSTRACT FROM AUTHOR]

Nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) mediated generation of reactive oxygen species (ROS) was originally identified as the powerful host defense machinery against microorganism in phagocytes. But recent reports indicated that some non-phagocytic cells also have the NADPH oxidase activity, and the ROS produced by it may act as cell signal molecule. But as far as today, whether the NADPH oxidase also plays similar role in phagocyte has not been paid much attention. Utilizing the undifferentiated HL-60 promyelocytic leukemia cells as a model, the aim of the present study was to determine whether NADPH oxidase plays a role on ROS generation in undifferentiated HL-60, and the ROS mediated by it was essential for cell's survival. For the first time, we verified that the release of ROS in undifferentiated HL-60 was significantly increased by the stimulation with Calcium ionophore or opsonized zymosan, which are known to trigger respiration burst in phagocytes by NADPH oxidase pathway. Diphenylene iodonium (DPI) or apocynin (APO), two inhibitors of NADPH oxidase, significantly suppressed the increasing of ROS caused by opsonized zymosan. Cell survival assay and fluorescence double dyeing with acridine orange and ethidium bromide showed that DPI and APO, as well as superoxide dismutase (SOD) and catalase (CAT) concentration-dependently decreased the viability of undifferentiated HL-60 cells, whereas exogenous H2O2 can rescue the cells from death obviously. Our results suggested that the ROS, generated by NADPH oxidase play an essential role in the survival of undifferentiated HL-60 cells. [ABSTRACT FROM AUTHOR]

The effect of high dietary intake of animal fat and an increased fat energy intake on colon and liver genotoxicity and on markers of oxidative damage and antioxidative defence in colon, liver and plasma was investigated in Big Blue rats. The rats were fed ad libitum with semi-synthetic feed supplemented with 0, 3, 10 or 30% w/w lard. After 3 weeks, the mutation frequency, DNA repair gene expression, DNA damage and oxidative markers were determined in liver, colon and plasma. The mutation frequency of the λ gene cII did not increase with increased fat or energy intake in colon or liver. The DNA-adduct level measured by 32 P-postlabelling decreased in both liver and colon with increased fat intake. In liver, this was accompanied by a 2-fold increase of the mRNA level of nucleotide excision repair (NER) gene ERCC1. In colon, a non-statistically significant increase in the ERCC1 mRNA levels was observed. Intake of lard fat resulted in increased ascorbate synthesis and affected markers of oxidative damage to proteins in liver cytosol, but not in plasma. The effect was observed at all lard doses and was not dose-dependent. However, no evidence of increased oxidative DNA damage was found in liver, colon, or urine. Thus, lard intake at the expense of other nutrients and a large increase in the fat energy consumption affects the redox state locally in the liver cytosol, but does not induce DNA-damage, systemic oxidative stress or a dose-dependent increase in mutation frequency in rat colon or liver. [ABSTRACT FROM AUTHOR]

Phospholipid hydroperoxide glutathione peroxidase (PhGPx) is an antioxidant enzyme that reduces cellular phospholipid hydroperoxides (PLOOHs) to alcohols. Cellular peroxide tone has been implicated in cell growth and differentiation. By reducing the PLOOH level in the cell membrane, PhGPx regulates the peroxide tone and thereby might be involved in cell growth. We hypothesized that overexpression of PhGPx in human breast cancer cells would decrease their growth rate. We stably transfected MCF-7 cells (Wt) with L-PhGPx and measured cell doubling time, plating efficiency, and cell cycle phase transit times. P-4 cells (8-fold increase in PhGPx activity) showed a 2-fold increase in doubling time; doubling time increased directly with PhGPx activity ( r =0.95). The higher the PhGPx activity, the lower the plating efficiency ( r =-0.86). The profile of other antioxidant enzymes was unchanged. Overexpression of PhGPx lowered the steady-state level of PLOOH (by >60%). Results from bromodeoxyuridine pulse-chase experiments and flow cytometry indicate that PhGPx induced a delay in MCF-7 proliferation that was primarily due to a slower progression from G 1 to S. These results support the hypothesis that PhGPx plays a regulatory role in the progression of MCF-7 cells from G 1 to S possibly by regulating the steady-state levels of PLOOH. These data suggest that PhGPx can lower the peroxide tone, which might change the cellular redox environment resulting in a delay in G 1 transit. Thus, PhGPx could be an important factor in cell growth. [ABSTRACT FROM AUTHOR]