Oral nanoparticulate curcumin combating arsenic-induced oxidative damage in kidney and brain of rats

• Published in: Toxicology and industrial health 2016-03, Vol.32 (3), p.410-421
• Main Authors: Sankar, Palanisamy, Telang, Avinash Gopal, Kalaivanan, Ramya, Karunakaran, Vijayakaran, Suresh, Subramaniyam, Kesavan, Manickam
• Format: Article
• Language: English
• Subjects: Administration, Oral; Animals; Antioxidants - administration & dosage; Antioxidants - pharmacology; Arsenic; Arsenic - toxicity; Brain; Brain Chemistry - drug effects; Brain Diseases - chemically induced; Curcumin - administration & dosage; Curcumin - pharmacology; Damage; Drinking water; Exposure; Glutathione; Kidney - chemistry; Kidney - drug effects; Kidney Diseases - chemically induced; Kidneys; Male; Nanoparticles - chemistry; Oxidative Stress - drug effects; Particle Size; Rats; Rats, Wistar
• ISSN: 0748-2337; 1477-0393
• DOI: 10.1177/0748233713498455

Arsenic exposure through drinking water causes oxidative stress and tissue damage in the kidney and brain. Curcumin (CUR) is a good antioxidant with limited clinical application because of its hydrophobic nature and limited bioavailability, which can be overcome by the encapsulation of CUR with nanoparticles (NPs). The present study investigates the therapeutic efficacy of free CUR and NP-encapsulated CUR (CUR-NP) against sodium arsenite-induced renal and neuronal oxidative damage in rat. The CUR-NP prepared by emulsion technique and particle size ranged between 120 and 140 nm, with the mean particle size being 130.8 nm. Rats were divided into five groups (groups 1–5) with six animals in each group. Group 1 served as control. Group 2 rats were exposed to sodium arsenite (25 ppm) daily through drinking water for 42 days. Groups 3, 4, and 5 were treated with arsenic as in Group 2; however, these animals were also administered with empty NPs, CUR (100 mg/kg body weight), and CUR-NP (100 mg/kg), respectively, by oral gavage during the last 14 days of arsenic exposure. Arsenic exposure significantly increased serum urea nitrogen and creatinine levels. Arsenic increased lipid peroxidation (LPO), reduced glutathione content and the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were depleted significantly in both kidney and brain. Treatment with free CUR and CUR-NP decreased the LPO and increased the enzymatic and nonenzymatic antioxidant system in kidney and brain. Histopathological examination showed that kidney and brain injury mediated by arsenic was ameliorated by treatment. However, the amelioration percentage indicates that CUR-NP had marked therapeutic effect on arsenic-induced oxidative damage in kidney and brain tissues.