Abstract

Food is essential to provide sustenance but may also be an important factor in the genesis of human diseases. An association between the intake of grilled or broiled meat and development of cancer was recorded by Thomson et al. (1996). Grilling meat, fish or other foods with intense heat over a direct flame result in fat dripping on the hot fire and yielding flames containing a number of polycyclic hydrocarbons (PAHs), these chemicals adhere to the surface of the food. The more intense the heat, the more PAHs are present (Larsson, 1986). PAHs are produced from organic compounds by condensation of smaller units at high temperatures forming stable polynuclear aromatic compounds. At high temperature, organic compounds are easily fragmented into smaller compounds, mostly free radicals, which may then recombine to form a number of relatively stable PAHs (Lijinsky, 1991). Lin et al. (1996) showed that, mice fed high fat diet developed more serve disease and had a shorter life span. Weisburger et al. (1994) found that the use of grilled meats in diet, where compounds formed on the surface of meat may be associated with increased risk of genotoxicity and cancer. They also showed that, normal intestinal bacteria can convert one of these compounds, 2-amino-3-methyl-3H-imidazo [4, 5-f] quinoline (IQ) to the 7-hydroxy metabolite, 2-amino-3,6-dihydro-3-methyl-7H-imida-zolo[4, 5-f] quinolin-7-one(7-OHIQ),a directacting mutagen. The surface of fried and grilled meat or fish contain powerful mutagens, Sugimura et al. (1977) isolated these mutagens and identified them as heterocyclic aromatic compounds with an exocyclic amino group and often an O-methyl group. The heterocyclic amines formed by partial pyrolysis of amino acids, sugar or creatinine at high temperatures has been shown to be carcinogenic and mutagenic in mice and rats (Ohgaki et al., 1991). Food mutagens cause different types of DNA damage, nucleotide alterations and gross chromosomal aberrations. Most mutagens begin their action at the DNA level by forming carcinogen-DNA adducts, which result from the covalent binding of a carcinogen or part of a carcinogen to a nucleotide. However, the effect of food mutagens in carcinogenesis can be modified by heritable traits, namely, low penetrant genes that affect mutagen exposure of DNA through metabolic activation and detoxification or cellular responses to DNA damage through DNA repair mechanisms or cell death (Goldman and Shields, 2003) The single cell gel electrophoresis (SCGE) assay, also known as the comet assay, is a rapid, simple, visual and sensitive technique for detecting and analyzing DNA strand breakage in a variety of organs and various mammalian cells (Olive et al., 1990). The advantage of the comet assay is that it allows any viable eukaryote cells to be analyzed. For these reasons, the comet assay is now widely used in researches of biomonitoring and DNA damage processes to routine assessments of genotoxicity. Quantitative analysis for DNA damage has yielded several parameters, including tailed nuclei, tail length, DNA % in the tail, and tail moment in the comet assay (Tice et al., 2000). Singh et al. (1988) made microgels slides and electrophoresing under alkaline conditions and removed the DNA supercoiling and denaturated the DS DNA to SS DNA .With this modification they obtained a dose response curve with respect to length of DNA migration. The resulting images were subsequently named ‘Comet ‘because of their appearance and their total length was considered directly related to the DNA damage. From that moment a range of applications of the Comet assay have been used in investigations of the physiochemical behavior of DNA, through studies of cellular responses of DNA damage, to biomonitoring of human population. When the Comet assay technique is used to detect in vivo genotoxicity, the most important advantage is that DNA lesions can be measured in cells not engaged in mitotic activity, making it possible to assay many organs (Fairbairn et al., 1995). The grilled chicken fat was used by low income people in Egypt and used to prepare Howawshi. Thus the aim of this study was to evaluate the genotoxic and histopathologic effects on liver and kidney of rats fed on diet contained fats of grilled chicken.

Highlights

  • The damage was clear in the liver of treated rats. This may be due to ingest of genotoxic compounds from grilled –processed chicken. Such compounds cause different DNA damage, most of genotoxic compounds begin their action at the DNA level by forming DNAadducts, which bind mutagen to a nucleotide (Goldman and Shields, 2003)

  • An increase in DNA damage was indicated by an increase in migration length of the stained DNA

  • The results in Table (2) and Figs. (2, 3 and 4) showed that grilled chicken fat induced a significant concentrationdependent increase in the tail length, tail intensity%, tail migration and tail moments in the liver, kidneys and lymphocytes respectively. These results suggested that DNA damage observed was due to genotoxicity and comet assay might be used to detect the DNA damage induced by grilled fat in rat liver, kidneys and lymphocytes

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Summary

Objectives

The aim of this study was to evaluate the genotoxic and histopathologic effects on liver and kidney of rats fed on diet contained fats of grilled chicken

Methods
Results
Conclusion
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