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Chargui I.,University of Sfax | Grissa I.,University of Sfax | Bensassi F.,Laboratory of Research on Biologically Compatible Compounds | Bensassi F.,National Institute for Agricultural Research | And 4 more authors.
Biomedical and Environmental Sciences | Year: 2012

Objective: To evaluate histopathological alterations of the liver and kidney of female rats exposed to low doses of DM and its potential genotoxic activity. Methods: Female Wistar rats were randomly assigned to control (3 groups, 6 rats in each) and treatment groups (3 groups, 6 rats in each). They were subjected to subcutaneous injections of DM (at doses of 0.003, 0.03, and 0.3 mg/kg bw/d) after 30, 45, and 60 d, respectively. Results: Significant alterations were recorded in liver parenchyma induced by hepatic vacuolization, fragmented chromatin in nuclei, dilatation of sinusoids and congestions. Lesions within proximal and distal tubules were observed in the kidneys. Tissue congestions and severe alterations within glomeruli were visible. DM as a pyrethroid insecticide induced significant increase (P≤0.05) of plasma MDA concentrations after 45 d. A significant increase (P≤0.05) in plasma ALT (after 45 and 60 d) and AST (after 60 d) concentrations was recorded as compared to controls. During the whole experimental period the toxic agent provoked significant DNA damages (P≤0.05), especially in the dominance of classes 3 and 4 of obtained comet. Conclusion: DM even at a very low dose displays harmful effects by disrupting hepatic and renal function and causing DNA damages in puberscent female rats. Low doses of DM are hepatotoxic and nephrotoxic. © 2012 The Editorial Board of Biomedical and Environmental Sciences. Source

El Golli-Bennour E.,Laboratory of Research on Biologically Compatible Compounds
Turkish Journal of Biochemistry | Year: 2011

The decision to attend graduate school to get a PhD is an important one, and not one to be made lightly or without consideration. In Tunisia, typical doctoral programs take four to seven years to complete and in most science fields students then spend two to four years in postdoctoral training before beginning their professional career. Committing to a PhD means sacrifices as doctoral students are generally not well paid and doctoral training is a "job" that requires perseverance and very hard work. Survey on Tunisian doctoral education and career preparation is a national survey of doctoral students intended to provide a snapshot of their experiences and goals. About 200 students completed the 15- questions survey. These students were from 5 selected universities and represented Biomedicine and Health Sciences sectors. In this report, we have tried to explain the reasons making doctoral study as a real abnegation. Hence, there are three major causes (i) doctoral study may increase personal debt: relative to peers, it will forego many years of income (ii) limitation in the opportunity to get international research training courses that approve and finalise dissertations and (iii) Once they obtain their diploma it is too difficult for PhD graduates to get an appropriate work in universities, research or public health establishments. Nevertheless, doctoral work is still usually an exciting and positive experience. Source

El Golli-Bennour E.,Laboratory of Research on Biologically Compatible Compounds | Bacha H.,Laboratory of Research on Biologically Compatible Compounds
Toxicology | Year: 2011

The environment represents a key contributor to human health and disease. Exposure to many substances such as pollutants, toxins and chemicals, has detrimental effects on health and are considered to contribute substantially to most diseases of major public health significance. Environmental diseases as mycotoxicosis are those in general aroused or exacerbated by exposure to environmental stressors as mycotoxins. These hazardous compounds are secondary metabolites produced by fungi and occurred simultaneously in food, feed and raw materials. The present investigation was conducted to assess if (i) Hsp70 induction, a parameter of protective and adaptive response, is a systematic biomarker to mycotoxin intoxications and (ii) all mycotoxins undergo oxidative stress in there toxic signalling pathways, as the omnipresent process playing a role in the initiation or progression of numerous disorders. Overall, observations to date evoke that Hsp70 can act as biomarkers of oxidative injury instead they are not systematic to mycotoxin exposure. © 2011 Elsevier Ireland Ltd. Source

Brahmi D.,Laboratory of Research on Biologically Compatible Compounds | Brahmi D.,Research unit of Macromolecular Biochemistry and Genetic | Bouaziz C.,Laboratory of Research on Biologically Compatible Compounds | Ayed Y.,Laboratory of Research on Biologically Compatible Compounds | And 4 more authors.
Nutrition and Metabolism | Year: 2011

Background: Aflatoxin B1 (AFB1) is potent hepatotoxic and hepatocarcinogenic agent. In aflatoxicosis, oxidative stress is a common mechanism contributing to initiation and progression of hepatic damage. The aim of this work was to evaluate the hepatoprotective effect of cactus cladode extract (CCE) on aflatoxin B1-induced liver damage in mice by measuring malondialdehyde (MDA) level, the protein carbonyls generation and the heat shock proteins Hsp 70 and Hsp 27 expressions in liver. We also looked for an eventual protective effect against AFB1-induced genotoxicity as determined by chromosome aberrations test, SOS Chromotest and DNA fragmentation assay. We further evaluated the modulation of p53, bax and bcl2 protein expressions in liver. Methods. Adult, healthy balbC (20-25 g) male mice were pre-treated by intraperitonial administration of CCE (50 mg/Kg.b.w) for 2 weeks. Control animals were treated 3 days a week for 4 weeks by intraperitonial administration of 250 g/Kg.b.w AFB1. Animals treated by AFB1 and CCE were divided into two groups: the first group was administrated CCE 2 hours before each treatment with AFB1 3 days a week for 4 weeks. The second group was administrated without pre-treatment with CCE but this extract was administrated 24 hours after each treatment with AFB1 3 days a week for 4 weeks. Results: Our results clearly showed that AFB1 induced significant alterations in oxidative stress markers. In addition, it has a genotoxic potential and it increased the expression of pro apoptotic proteins p53 and bax and decreased the expression of bcl2. The treatment of CCE before or after treatment with AFB1, showed (i) a total reduction of AFB1 induced oxidative damage markers, (ii) an anti-genotoxic effect resulting in an efficient prevention of chromosomal aberrations and DNA fragmentation compared to the group treated with AFB1 alone (iii) restriction of the effect of AFB1 by differential modulation of the expression of p53 which decreased as well as its associated genes such as bax and bcl2. Conclusion: We concluded that CCE might have a hepatoprotective effect against aflatoxicosis in mice, probably acting by promoting the antioxidant defence systems. © 2011Brahmi et al; licensee BioMed Central Ltd. Source

Rjiba-Touati K.,Laboratory of Research on Biologically Compatible Compounds | Ayed-Boussema I.,Laboratory of Research on Biologically Compatible Compounds | Skhiri H.,University of Monastir | Belarbia A.,University of Sousse | And 3 more authors.
Mutation Research - Genetic Toxicology and Environmental Mutagenesis | Year: 2012

Cisplatin (Cisp) is one of the most effective chemotherapeutic agents. However, at higher doses several side effects may occur. Recombinant human erythropoietin (rhEPO), a glycoprotein regulating haematopoiesis, has recently been shown to exert an important cyto-protective effects in many tissues. The purpose of this study was to explore whether rhEPO protects against Cisp-induced genotoxicity in rat bone-marrow cells. Adult male Wistar rats were divided into six groups of 18 animals each: control group, rhEPO-alone group, Cisp-alone group and three rhEPO+Cisp-groups (pre-, co- and post-treatment condition, respectively). Our results show that Cisp induced a noticeable genotoxic effect in rat bone-marrow cells. In all types of treatment, rhEPO significantly decreased the frequency of micronuclei, the percentage of chromosome aberrations and the level of DNA damage. The protective effect of rhEPO was more efficient when it was administrated 24. h before exposure to Cisp. © 2012 Elsevier B.V. Source

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