Emna Behija Saafi

Protective effect of date palm fruit extract (Phoenix dactylifera L.) on dimethoate induced-oxidative stress in rat liver

Nowadays, peoples exposure to chemical compounds such as organophosphorus insecticides is continuously on the rise more and more. Theses compounds have induced an excessive production of free radicals which are responsible for several cell alterations in the organism. Recent investigations have proved the crucial role of nutritional antioxidants to prevent the damage caused by toxic compounds. In this study, we investigate the role of date palm fruit extract (Phoenix dactylifera L.) in protection against oxidative damage and hepatotoxicity induced by subchronic exposure to dimethoate (20mg/kg/day). Oral administration of dimethoate caused hepatotoxicity as monitored by the increase in the levels of hepatic markers enzymes (transaminases, alkaline phosphatase, gamma-glutamyl transferase and lactate dehydrogenase), as well as in hepatic malondialdehyde thus causing drastic alteration in antioxidant defence system. Particularly, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were found increased by dimethoate while catalase (CAT) activity was reduced significantly. These biochemical alterations were accompanied by histological changes marked by appearance of vacuolization, necrosis, congestion, inflammation, and enlargement of sinusoids in liver section. Pretreatment with date palm fruit extract restored the liver damage induced by dimethoate, as revealed by inhibition of hepatic lipid peroxidation, amelioration of SOD, GPx and CAT activities and improvement of histopathology changes. The present findings indicate that in vivo date palm fruit may be useful for the prevention of oxidative stress induced hepatotoxicity.

Nephroprotective effect of date fruit extract against dichloroacetic acid exposure in adult rats

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 417.71mg gallic acid equivalents/100g fresh weights (FW), while total flavonoid and tannins contents were 285.23 and 73.65mg catechin equivalents/100g FW, respectively. The ADE has strong scavenging activity. Ferulic, caffeic and p-coumaric acids are the majors compounds. Nephrotoxicity was induced in male Wistar rats by the administration of 0.5 and 2g/L DCA as drinking water. Some of these rats received also by gavage ADE (4mL/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.