Abstract
Hibiscus sabdariffa (HS) is an edible medicinal plant, indigenous to India, China and Thailand and is used in Ayurveda and traditional medicine. Alcoholic extract of HS leaves (HSEt) was studied for its anti-hyperammonemic and antioxidant effects in brain tissues of ammonium chloride-induced hyperammonemic rats. Oral administration of HSEt (250 mg kg−1 body weight) significantly normalizes the levels of ammonia, urea, uric acid, creatinine and non-protein nitrogen in the blood. HSEt significantly reduced brain levels of lipid peroxidation products such as thiobarbituric acid and reactive substances (TBARS) and hydroperoxides (HP). However, the administered extract significantly increased the levels of antioxidants such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and reduced glutathione (GSH) in brain tissues of hyperammonemic rats. This investigation demonstrates significant anti-hyperammonemic and antioxidant activity of HS.
Highlights
The neurological complications of hyperammonemia in the central nervous system (CNS) are receiving more attention
A concurrent increase of superoxide production and a reduction in the activities of various antioxidant enzymes have been shown in animal models of acute ammonia toxicity [4,5]
Blood Ammonia, Urea, Uric Acid and Creatinine were Restored to Normal Levels in Treated Rats
Summary
The neurological complications of hyperammonemia in the central nervous system (CNS) are receiving more attention. In spite of extensive investigations, the precise mechanisms involved in ammonia neurotoxicity are not completely understood. Oxidative stress is evolving concept in ammonia neurotoxicity. Its effect on the oxidative and nitrosative stress in the CNS has been recently reviewed [1]. Recent studies have reported an increased production of free radicals in cultured astrocytes after treatment with pathophysiological concentrations of ammonia [4]. A concurrent increase of superoxide production and a reduction in the activities of various antioxidant enzymes have been shown in animal models of acute ammonia toxicity [4,5]. Oxidative stress-mediated lipid peroxidation was shown as one of the characteristic features of hyperammonemia [5,6]
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