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      Sub-chronic exposure to fipronil induced oxidative stress, biochemical and histopathological changes in the liver and kidney of male albino rats

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          Abstract

          Fipronil (FPN) is a broad-spectrum N-phenylpyrazole insecticide and has been used in agriculture and public health since the mid-1990s. The present study was designed to investigate the adverse effects of sub-chronic exposure to the FPN on the liver and kidney of male rats at three concentrations 0.1, 1 and 10 mg/L in drinking water for 45 days. Serum aspartate aminotransferases (AST), alanine aminotransferases (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) activity and levels of uric acid, creatinine and total protein were significantly increased in FPN-treated rats. Oxidative stress biomarkers such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and glutathione reduced (GSH) were significantly decreased, while lipid peroxidation (LPO) was significantly increased in treating rats in a concentration dependent manner. FPN caused histopathological alterations in liver and kidney of male rats. From our results, it can be concluded that FPN induced lipid peroxidation, oxidative stress, liver, and kidney injury in rats. These pathophysiological changes in liver and kidney tissues could be due to the toxic effect of FPN that associated with a generation of free radicals.

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          Role of quinones in toxicology.

          Quinones represent a class of toxicological intermediates which can create a variety of hazardous effects in vivo, including acute cytotoxicity, immunotoxicity, and carcinogenesis. The mechanisms by which quinones cause these effects can be quite complex. Quinones are Michael acceptors, and cellular damage can occur through alkylation of crucial cellular proteins and/or DNA. Alternatively, quinones are highly redox active molecules which can redox cycle with their semiquinone radicals, leading to formation of reactive oxygen species (ROS), including superoxide, hydrogen peroxide, and ultimately the hydroxyl radical. Production of ROS can cause severe oxidative stress within cells through the formation of oxidized cellular macromolecules, including lipids, proteins, and DNA. Formation of oxidatively damaged bases such as 8-oxodeoxyguanosine has been associated with aging and carcinogenesis. Furthermore, ROS can activate a number of signaling pathways, including protein kinase C and RAS. This review explores the varied cytotoxic effects of quinones using specific examples, including quinones produced from benzene, polycyclic aromatic hydrocarbons, estrogens, and catecholamines. The evidence strongly suggests that the numerous mechanisms of quinone toxicity (i.e., alkylation vs oxidative stress) can be correlated with the known pathology of the parent compound(s).
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            Serum lipid peroxide in cerebrovascular disorders determined by a new colorimetric method.

            K Satoh (1978)
            A new colorimetric method for quantitative analysis of serum lipid peroxide, free of interference from sialic acids, has been developed. We have used the thiobarbituric acid dissolved in sodium sulfate solution and both liberation of lipid peroxide and color reaction have been performed simultaneously by heating serum protein precipitate with this reagent in a weak acid solution. The new method is specific and facilitates the precise measurements of serum lipid peroxide. The average values determined by the new method increased slightly with age in healthy subjects. In patients with sequelae of cerebrovascular disorders, serum lipid peroxide values were higher than in healthy controls. These results may demonstrate the important role of lipid peroxide in aging and cerebrovascular disorders.
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              Free radicals as mediators of tissue injury and disease.

              A radical is any molecule that contains one or more unpaired electrons. Radicals are normally generated in many metabolic pathways. Some of these radicals can exist in a free form and subsequently interact with various tissue components resulting in dysfunction. The potential role of oxygen- or xenobiotic-derived free radicals in the pathology of several human diseases has stimulated extensive research linking the toxicity of numerous xenobiotics and disease processes to a free radical mechanism. However, because free radical-mediated changes are pervasive and often poorly understood, the question of whether such species are a major cause of tissue injury and human disease remains equivocal. This review discusses cellular sources of various radical species and their reactions with vital cellular constituents. Examples of purported free radical-mediated disorders are discussed in detail to provide insights into the controversy over whether free radicals are important mediators of tissue injury.
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                Author and article information

                Contributors
                Journal
                Toxicol Rep
                Toxicol Rep
                Toxicology Reports
                Elsevier
                2214-7500
                19 February 2015
                2015
                19 February 2015
                : 2
                : 775-784
                Affiliations
                [a ]Environmental Toxicology Research Unit (ETRU), Pesticide Chemistry Department, National Research Centre, 33 Bohouth Street, Dokki, Giza, Egypt
                [b ]Economic Entomology and Pesticides Department, Faculty of Agriculture, Cairo University, Egypt
                Author notes
                [* ]Corresponding author. Tel.: +20 2 33371211; fax: +20 2 33370931. abdeltawab.mossa@ 123456yahoo.com
                Article
                S2214-7500(15)00028-1
                10.1016/j.toxrep.2015.02.009
                5598362
                28962413
                b0d99a6f-f44a-44e0-ab5a-adf36d9fc6db
                © 2015 The Authors

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 1 October 2014
                : 25 January 2015
                : 11 February 2015
                Categories
                Article

                fipronil,rats,liver,kidney,oxidative stress,histopathology
                fipronil, rats, liver, kidney, oxidative stress, histopathology

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