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El Arem A.,University of Monastir | Thouri A.,University of Monastir | Zekri M.,University of Monastir | Saafi E.B.,University of Monastir | And 3 more authors.
Food and Chemical Toxicology | Year: 2014

The aim of this study was to investigate the protective effects of aqueous date extract (ADE) on dichloroacetic acid (DCA)-induced nephrotoxicity. In vitro, total phenolic content estimated in the ADE were 417.71. mg gallic acid equivalents/100. g fresh weights (FW), while total flavonoid and tannins contents were 285.23 and 73.65. mg catechin equivalents/100. g FW, respectively. The ADE has strong scavenging activity. Ferulic, caffeic and p-coumaric acids are the major's compounds. Nephrotoxicity was induced in male Wistar rats by the administration of 0.5 and 2. g/L DCA as drinking water. Some of these rats received also by gavage ADE (4. mL/kg) before the administration of DCA. After two months of experiment, DCA administration caused elevated levels of renal MDA, significant depletion of GSH levels, altered the antioxidant enzyme activities and deteriorated the renal functions as assessed by the increased plasma urea, uric acid and creatinine levels compared to control rats. The treatment with the ADE significantly normalized the increased plasma levels of creatinine, urea and uric acid, reduced the elevated MDA levels, significantly normalized the antioxidant enzyme activities and GSH level and restored the altered kidney histology in rats treated with DCA. Therefore, it was speculated that ADE protects rats from kidney damage through its antioxidant capacity. © 2013 Elsevier Ltd. Source


El Arem A.,University of Monastir | Zekri M.,University of Monastir | Thouri A.,University of Monastir | Saafi E.B.,University of Monastir | And 4 more authors.
Journal of Physiology and Biochemistry | Year: 2014

In this study, we investigated the antioxidant and protective properties of date fruit aqueous extract (DFAE) on trichloroacetic acid (TCA)-induced nephrotoxicity in rat. Oral administration of TCA as drinking water (0.5 and 2 g/L) daily for 2 months caused nephrotoxicity as evident by elevated levels of plasma creatinine, urea, and uric acid. Activity of antioxidant enzymes, catalase (CAT) and glutathione peroxidase (GPx), was decreased, whereas superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were increased along with histopathological injuries. The oral administration of DFAE (4 mL/kg/day) to TCA-treated groups proved some significant correction by increasing the antioxidant activity of the CAT and GPx enzymes and normalizing the SOD activity and the MDA level (p <0.05). It also protected kidney's histology and normalized the functions of this organ. It could be concluded that DFAE has a protective role against TCA-induced oxidative stress in rat, thereby protecting the renal tissue from TCA-induced damage. © University of Navarra 2013. Source


El Arem A.,University of Monastir | Saafi E.B.,University of Monastir | Ghrairi F.,University of Sousse | Thouri A.,University of Monastir | And 4 more authors.
Journal of Physiology and Biochemistry | Year: 2014

Trichloroacetic acid (TCA) is a prominent by-product of the chlorination of drinking water. It induces cell damage by producing free radicals and reactive oxygen species. The present study was carried out to evaluate the potential hepatoprotective role of the aqueous date extract (ADE) against TCA-induced liver injury. Forty-eight male Wistar rats were randomly divided into six groups of eight: group I served as the control; group II was given ADE by gavage; groups III and IV received TCA as drinking water at 0.5 and 2 g/L, respectively; and groups V and VI were treated with ADE by gavage and then received TCA at 0.5 and 2 g/ L, respectively, as drinking water. The experiment was performed for 2 months. The hepatotoxicity of TCA administration was revealed by an increase in the levels of hepatic marker enzymes (transaminases, gammaglutamyl transferase, and lactate dehydrogenase) and conjugated bilirubin and a decrease in albumin level. The TCA administration induced also significant elevation of the malondialdehyde (MDA) level and the antioxidant activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) paralleled with a significant decline in catalase (CAT) activity. These biochemical alterations were accompanied by histological changes marked by the appearance of vacuolization, necrosis, congestion, inflammation, and enlargement of sinusoids in the liver section. Treatment with date palm fruit extract restored the liver damage induced by TCA, as demonstrated by inhibition of hepatic lipid peroxidation; amelioration of SOD, GPx, and CAT activities; and improvement of histopathology changes. These results suggest that ADE has a protective effect over TCA-induced oxidative damage in rat liver. © University of Navarra 2014. Source


Saafi-Ben Salah E.B.,Higher Institute of Biotechnology of Monastir | El Arem A.,Higher Institute of Biotechnology of Monastir | Louedi M.,Higher Institute of Biotechnology of Monastir | Saoudi M.,University of Sfax | And 6 more authors.
Journal of Physiology and Biochemistry | Year: 2012

Recent investigations have proved the crucial role of nutritional antioxidants to prevent the damage caused by toxic compounds. In this study, the antioxidant effect of date palm fruit extract on dimethoate-induced oxidative stress and nephrotoxicity in rat is investigated and compared with the effect of the well-known antioxidant vitamin C. Male Wistar rats were randomly divided into six groups of ten each: a control group (C), a group that received dimethoate (20 mg/kg body weight) (D), a group given Deglet Nour extract (DNE), a group treated with DNE 30 min before the administration of dimethoate (DNE + D), a group which received VitC (100 mg/kg body weight) plus dimethoate (Vit C + D), and a group given dimethoate for the first month and DNE 30 min after administration of dimethoate, during the second month (D + DNE). These components were daily administered by gavage for 2 months. After completing the treatment period, blood samples from rats were collected under inhaled diethyl ether anesthesia for serum urea, uric acid, and creatinine levels, while the rat kidneys were obtained for enzyme assays and histology. Oral administration of dimethoate in rats induced a marked renal failure characterized by a significant increase in serum creatinine and urea levels (p<0.01) in addition to a significant decrease in serum uric acid (p<0.05). Interestingly, these drastic modifications were accompanied by a marked enhancement of lipid peroxidation in kidney, indicating a significant induction of oxidative damage (p<0.01) and dysfunctions of enzymatic antioxidant defenses. These biochemical alterations were also accompanied by histological changes in kidney revealed by a narrowed Bowman's space, tubular degeneration, tubular cell desquamation, and tubular dilatation of proximal tubules. Treatment with date palm fruit extract (Deglet Nour) and also with vitamin C significantly (p<0.05) reversed the serum renal markers to their near-normal levels when compared with dimethoate-treated rats. In addition, Deglet Nour extract and vitamin C significantly reduced lipid peroxidation, restored the antioxidant defense enzymes in the kidney, and improved the histopathology changes. The present findings indicate that in vivo date palm fruit may be useful for the prevention of oxidative stress-induced nephrotoxicity. © 2011 University of Navarra. Source


El Arem A.,University of Monastir | Ghrairi F.,University of Sousse | Lahouar L.,University of Monastir | Thouri A.,University of Monastir | And 7 more authors.
Journal of Functional Foods | Year: 2014

The hepatoprotective activity of an aqueous date extract (ADE) against dichloroacetic acid (DCA) induced liver damage in rats was investigated. The free radical scavenging activity of ADE was evaluated using the DPPH assay. The total carbohydrate phenolic, flavonoid and condensed tannins contents of the ADE were determined. Different polyphenolic compounds, namely gallic, chlorogenic, protocatechuic, ferulic, caffeic, syringic, m-hydroxybenzoic, coumaric and phenylacetic acids, and catechin, were indentified. Oral administration of the ADE to male Wistar intoxicated with DCA at 0.5 and 2 g/l as drinking water for 2 months, demonstrated a significant protective effect by lowering the levels of hepatic marker enzymes (AST, ALT, LDH and GGT) and conjugated bilirubin, and by improving the histological architecture of the rat liver. ADE attenuated oxidative stress by decreasing the extent of hepatic TBARS (thiobarbituric acid reactive substances) formation, restoring the activities of SOD, CAT and GPx and by reducing the hepatic DNA fragmentation. This study demonstrated that ADE protects rat liver from DCA-induced injury and suggests a potential therapeutic use for ADE. © 2014 Elsevier Ltd. Source

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