Abstract Title:

Aqueous date fruit extract protects against lipid peroxidation and improves antioxidant status in the liver of rats subchronically exposed to trichloroacetic acid.

Abstract Source:

J Physiol Biochem. 2014 Jun ;70(2):451-64. Epub 2014 Feb 27. PMID: 24573459

Abstract Author(s):

Amira El Arem, Emna Behija Saafi, Fatma Ghrairi, Amira Thouri, Mouna Zekri, Amel Ayed, Abdelfattah Zakhama, Lotfi Achour

Article Affiliation:

Amira El Arem

Abstract:

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, gamma-glutamyl 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 datepalm 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 damagein rat liver.

Study Type : Animal Study

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