الفهرس 
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Abstract
Ochratoxin-A is an important mycotoxin produced by different Aspergillus and Penicillium species. The presence of ochratoxin A (OTA) in animal feeds raises concerns in poultry and livestock industry due to subclinical intoxications and poor growth in animals (Gentles et al., 1999; Zia et al., 2010). OTA present in the poultry foods at low to moderate levels induces immunosuppression, decreased body weight gains and increased susceptibility to infectious diseases (Saleemi et al., 2010 and Mukhtar et al., 2010). OTA has gained considerable attention due to its intrinsic toxicity and its frequent occurrence in feed commodities used in livestock feeds. The main target organ of OTA in poultry, as in other species,appears to be the kidney, although liver, gastrointestinal tract, lymphoid organs,skeletal system, hematopoietic tissues and the reproductive organs can also be affected (Paterson and Lima, 2010).At higher toxic levels, the birds show clinical signs of disease, mortality,nephritis (Elaroussi et al., 2006), and hepatitis (Kumar et al., 2004).chratoxicosis developing from high degree of contamination of foods with OTA is a common condition in different avian species. OTA induces degenerative changes and an increase in the weight of kidneys and liver (Stoev et al., 2011).OTA is frequently presented in poultry foods (Saleemi et al., 2012). Its levels in the foods are kept minimum by different methods including use of ingredients having low levels of OTA, proper storage and use of toxin binders to bind the preformed mycotoxins and rendering them unabsorbable from the gut. All these methods work with a variable degree of efficiency. Ochratoxin A not only induces disease in chicken but also it may accumulate in the eggs and meat of the poultry and thus enters in human food chain. Therefore, all the efforts should be made to protect the commercial poultry birds from the toxic effects of ochratoxin. Another important strategy in case of clinical ochratoxicosis is to reduce the damage and losses by alleviating the deleterious effects of OTA by different hepato-protective and renal protective substances.Ochratoxin-A (OTA) is a nephrotoxic, hepatotoxic and teratogenic mycotoxin produced by storage molds on a variety of commodities. Ochratoxins affect many species including humans, dogs, pigs, dairy cattle, and chickens. The molecular mechanisms involved in OTA-induced nephrotoxicity (Purchase and Theron, 1998), carcinogenesis (Bendele, et al., 1985 and Pitt 2000), teratogenic effects (Zeb, 2004), immunosupression (Bondy and Pestka, 2000 and Creppy et al., 1983) were studied. Data regarding OTA metabolism are controversial. Several metabolites have been characterized in vitro and/or in vivo, whereas other metabolites remain to be characterized. Several major mechanisms have been shown as involved in the toxicity of OTA: inhibition of protein synthesis,promotion of membrane peroxidation, disruption of calcium homeostasis,inhibition of mitochondrial respiration and DNA damage. The genotoxic status of OTA is still controversial because contradictory results were obtained in various microbial and mammalian tests, notably regarding the formation of DNA adducts.More recent studies are focused on the OTA ability to disturb cellular signalling and regulation, to modulate physiological signals and thereby to influence cells viability and proliferation (Creppy et al.,1983 and Denli et al., 2008). Oxidative damage may be one of the manifestations of cellular damage in the toxicity of ochratoxin A. Reactive oxygen species (ROS) have a major role in the mediation of cell damage (Hoehler et al., 1997). Several defence mechanisms attempt to minimize the production and the action of harmful oxidants. Free radical damage initially induced by mycotoxins can be propagated and magnified by lipid peroxidation chain reactions (Rizzo et al., 1994).Antioxidants are substances that can inhibit reactions of free radicals, such as reactive oxygen species (ROS) by neutralizing oxidants and thus reducing oxidative damage. Thus antioxidants aid in the overall detoxification process in the liver and in cells and thus, may aid in alleviation of mycotoxicosis (Stańczyk et al.,2005 and Sakhare et al., 2007). Selenium, which is an antioxidant, enhances the formation of water soluble conjugated forms of ochratoxin A which promotes the clearance of the toxin and enhanced chick growth ( Santin et al., 2002).One of the most recent approaches involves the addition of adsorbents to animal food to bind the mycotoxins in the gastrointestinal tract for reducing their absorption (Ramos et al., 1996). Mannanoligosaccharides are derived from the cell wall of yeast (Saccharomyces cerevisiae); they have the ability to bind several pathogens and different chemical substances (i.e. aflatoxin B1 and zearalenone) in the gastrointestinal tract preventing their colonization or absorption, respectively (Devegowda et al., 1996, and 1998). Aravind et al. (2003) underlined that the addition of dietary esterified glucomannan (EGM) is effective in broilers to counteract in vivo toxic effects of feed naturally contaminated with aflatoxins,ochratoxin, zearalenone and T-2 toxin. On the other hand, another method for controlling mycotoxin hazards in animal husbandry is based on the use of specific yeast cultures, such as Saccharomyces cerevisiae (SC) strains, that are able to adsorb mycotoxins, thus limiting their gastrointestinal bioavailability (Yiannikouris et al.,2003).