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      Effect of dietary turmeric and cinnamon powders on meat quality and lipid peroxidation of broiler chicken under heat stress condition

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          Two hundred and fifty male 1-day-old broiler chicks (Ross 308) were used to investigate the effects of dietary supplementation of turmeric and cinnamon powders on meat quality and lipid peroxidation of broilers under heat stress condition. The five treatment groups were control (recommended temperature for Ross 308), heat stressed (32 ± 1 ˚C from 9:00 AM to 5:00 PM during finisher period) and heat stressed birds fed with 0.50% turmeric, 0.50% cinnamon and a blend of cinnamon and turmeric (0.25% turmeric + 0.25% cinnamon). The results showed that there were no significant differences between the treatments for ether extract, ash and crude protein contents of thigh meat at 42 day of age ( p > 0.05). Heat stress decreased the pH value and dry matter (DM) content of thigh meat, whereas the consumption of all experimental diets (turmeric, cinnamon and both of them) compensated the decreased pH and DM values due to heat stress to some extent but could not restore them to the level of control treatment ( p < 0.01). Furthermore, the thigh meat lightness was increased under heat stress ( p < 0.05). The thiobarbituric acid reactive substances and free radicals scavenging activity were increased in thigh meat of broilers reared under heat stress ( p < 0.05), while these parameters were reduced by the combination of both plants ( p < 0.01). It was concluded that heat stress reduces antioxidant properties and quality of thigh meat and dietary supplementation of turmeric and cinnamon powders together can remove the detrimental effects of heat stress on meat quality.

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          Antioxidant Activity and Total Phenolics in Selected Fruits, Vegetables, and Grain Products

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            Molecular events associated with reactive oxygen species and cell cycle progression in mammalian cells.

            Cell cycle progression is regulated by a wide variety of external factors, amongst them are growth factors and extracellular matrix factors. During the last decades evidence has been obtained that reactive oxygen species (ROS) may also play an important role in cell cycle progression. ROS may be generated by external and internal factors. In this overview we describe briefly the generation of ROS and their effects on processes that have been demonstrated to play an essential role in cell cycle progression, including such systems as signal transduction cascades, protein ubiquitination and degradation, and the cytoskeleton. These different effects of ROS influence cell cycle progression dependent upon the amount and duration of ROS exposure. Activation of growth factor stimulated signaling cascades by low levels of ROS result in increased cell cycle progression, or, in case of prolonged exposure, to a differentiation like growth arrest. From many studies it seems clear that the cyclin kinase inhibitor protein p21 plays a prominent role, leading to cell cycle arrest at higher but not directly lethal levels of ROS. Dependent upon the nature of p21 induction, the cell cycle arrest may be transient, coupled to repair processes, or permanent. At high concentrations of ROS all of the above processes are activated, in combination with enhanced damage to the building blocks of the cell, leading to apoptosis or even necrosis.
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              Curcumin, an antioxidant and anti-inflammatory agent, induces heme oxygenase-1 and protects endothelial cells against oxidative stress.

              Curcumin, a widely used spice and coloring agent in food, has been shown to possess potent antioxidant, antitumor promoting and anti-inflammatory properties in vitro and in vivo. The mechanism(s) of such pleiotropic action by this yellow pigment is unknown; whether induction of distinct antioxidant genes contributes to the beneficial activities mediated by curcumin remains to be investigated. In the present study we examined the effect of curcumin on endothelial heme oxygenase-1 (HO-1 or HSP32), an inducible stress protein that degrades heme to the vasoactive molecule carbon monoxide and the antioxidant biliverdin. Exposure of bovine aortic endothelial cells to curcumin (5-15 microM) resulted in both a concentration- and time-dependent increase in HO-1 mRNA, protein expression and heme oxygenase activity. Hypoxia (18 h) also caused a significant (P < 0.05) increase in heme oxygenase activity which was markedly potentiated by the presence of low concentrations of curcumin (5 microM). Interestingly, prolonged incubation (18 h) with curcumin in normoxic or hypoxic conditions resulted in enhanced cellular resistance to oxidative damage; this cytoprotective effect was considerably attenuated by tin protoporphyrin IX, an inhibitor of heme oxygenase activity. In contrast, exposure of cells to curcumin for a period of time insufficient to up-regulate HO-1 (1.5 h) did not prevent oxidant-mediated injury. These data indicate that curcumin is a potent inducer of HO-1 in vascular endothelial cells and that increased heme oxygenase activity is an important component in curcumin-mediated cytoprotection against oxidative stress.

                Author and article information

                Vet Res Forum
                Vet Res Forum
                Veterinary Research Forum
                Urmia University Press (Urmia, Iran )
                Spring 2017
                15 June 2017
                : 8
                : 2
                : 163-169
                [1 ] Department of Animal Sciences, Faculty of Agriculture, Urmia University, Urmia, Iran;
                [2 ] Department of Food Hygiene and Quality Control, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran.
                Author notes
                [* ]Correspondence: Mohsen Daneshyar. PhD, Department of Animal Sciences, Faculty of Agriculture, Urmia University, Urmia, Iran. E-mail: m.daneshyar@urmia.ac.ir
                © 2017 Urmia University. All rights reserved.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, ( http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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